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Your task is to summarize this medical case report into a title
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A 65-year-old female was referred to the Department of Neurosurgery from the Department of General Surgery with progressive bitemporal hemianopsia and loss of visual acuity in the left eye for three months. She had undergone a left radical mastectomy for invasive ductal carcinoma five years earlier and received four cycles of adjuvant chemotherapy using adriamycin/cyclophosphamide (AC) and radiation therapy. Twenty-eight months postoperatively, there was local left thoracic wall recurrence, and she underwent four additional cycles of docetaxel chemotherapy. Nine months later, after she developed new back pain, a bone scan and spine magnetic resonance imaging (MRI) were performed, which showed multiple metastases of breast cancer to the 4th and 5th lumbar vertebrae, right sacrum, and pelvis. The patient received radiation therapy to the metastases ten times and was prescribed letrozole. She had also been taking medication for hypertension.\nDue to progressive left visual loss, brain MRI was performed. A 1.1×2.2×2 cm pituitary mass was found, with intermediate signal intensity on T1- and T2-weighted images and a well-enhancing nature. The mass was dumbbell shaped, compressed the optic chiasm, and displaced the pituitary stalk to the left (). Blood and urine tests were all normal, except for elevated prolactin measuring 42.60 ng/mL (). On visual field examination, bitemporal hemianopsia was noted with decreased visual acuity on the left side.\nAlthough the patient had a history of multiple metastases from breast cancer, the MRI findings and laboratory results suggested that the pituitary mass was a primary macroadenoma; therefore, we performed a surgical tumor removal via sublabial-transsphenoidal approach. Since the intraoperative findings of the mass were similar to a benign pituitary macroadenoma, no frozen pathological examination was performed ().\nThe patient's postoperative course was uneventful and the prolactin level determined three days postoperatively was 10.50 ng/mL, which was within the normal range (). Seven days postoperatively, her urine output increased to 130 mL hourly. A water restriction test was performed, and she was diagnosed with central DI. After administering vasopressin, the central DI improved and the left visual acuity improved both subjectively and objectively, from 0.16 preoperatively to 0.20 postoperatively.\nThe pathology report seven days postoperatively showed moderately differentiated adenocarcinoma; immunohistochemical staining with MOC-31 was positive. The final diagnosis was that the tumor was metastasized from breast invasive ductal carcinoma ().\nThe patient underwent CyberKnife treatment for the remnant mass in the pituitary gland one month after the initial operation. Central DI occurred one week after the CyberKnife treatment, but improved with vasopressin. Following the CyberKnife treatment, the patient's hormone levels were within the normal ranges, so the vasopressin replacement was maintained (). The patient returned for follow-up five months after the initial surgery and four months after the CyberKnife surgery, with no signs of metastasis. Subsequently, she was lost to follow-up.
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A Case of Pituitary Metastasis from Breast Cancer That Presented as Left Visual Disturbance
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You are tasked with extracting and summarizing the essential information from this case report
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A 72-year-old male, smoker with a past medical history of arterial hypertension, high blood cholesterol and ischemic cardiomyopathy, had suffered a transient episode of slurred speech a week earlier that resolved within 4 hours.\nThe patient presented to the emergency department with gait instability and unclear speech. Physical examination of the patient revealed blood pressure 130/60 on the right arm and 150/75 on the left, weak pulse in both legs and no radial pulse in the arms. Neurological examination showed unclear speech and gait instability without other abnormalities. The National Institute of Health Stroke Scale (NIHSS) was 2. The Canadian scale was 10.\nElectrocardiogram revealed sinus rhythm. Computed tomography (CT) of the brain showed prior lacunar infarcts in both basal ganglia and a subacute lacunar infarction affecting left paramedian thalamus.\nTranscranial Doppler ultrasound was normal. Extracranial Duplex ultrasound showed diffuse cervical atheromatosis including non-relevant (< 50%) carotid plaques and indirect hemodynamic signs of bilateral subclavian artery (SA) stenosis (delayed increase in systolic flow with monophasic flow profile instead of a normal triphasic profile). Interestingly, both vertebral arteries (VA) also showed delayed systolic flow increase (Fig. ). A bilateral subclavian steal phenomenon was then suspected and arm compression test with a blood-pressure cuff was performed. The test was repeated on both arms; release of the pressure cuff led to reverse flow in the right VA and loss of diastolic flow in the left VA (Fig. ). The arm compression test was repeated because of the patient's neurological symptoms while we recorded basilar artery (BA) waveforms (Fig. ) by means of transcranial Doppler. The normal anterograde BA flow became retrograde following the causative ischemia test in either arm (Fig. ).\nThe suspected diagnosis was athero-embolic stroke affecting left thalamus due to proximal left subclavian atheromatosis. Additionally, the patient suffered bilateral subclavian steal phenomenon, mainly on the right side. The patient was admitted to the stroke unit. A CT angiography performed 24 hours later confirmed the data from the ultrasound study. It showed stenosis about 77% of the right subclavian artery and 50% of the left.\nStenting was performed on both subclavian arteries in the same procedure free of complications. Pharmacological double anti-aggregation treatment was established; acetylsalicylic acid 150 mg/d and clopidogrel 75 mg/d.\nAfter two months, the patient was asymptomatic. Cervical ultrasonography confirmed permeability of stents in the subclavian arteries and absence of steal phenomenon.
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Relevance of Basilar Artery Study in Patients with Subclavian Steal Phenomenon
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As a medical summarizer, your job is to condense this case report into its key points
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Case 2, a 31-year-old male Siberian crane (Leucogeranus leucogeranus), was presented for altered behavior per animal care staff. On physical exam, the third digit of the right foot was swollen with the distal interphalangeal joint markedly swollen and warm to the touch. Radiographs showed bony lysis and soft tissue swelling of the distal aspect of the third phalanx of the right third digit (). An RLP was performed in the same manner as Case 1, but with 5 mg/kg amikacin sulfate (50 mg/mL; Wedgewood Pharmacy) and 0.5 mg/kg meloxicam (5 mg/mL; Boehringer Ingelheim Animal Health). The bird was then started on ceftiofur (Excede, Zoetis; 20 mg/kg IM q7d). On day 6, the third digit appeared unchanged, so RLP was repeated under manual restraint. Following the procedure, the bird was started on enrofloxacin (Baytril, Bayer Corp; 10 mg/kg PO q24h for 14 days) and piroxicam (Greenstone LLC, Peapack, NJ 07977, USA; 0.9 mg/kg PO q24 for 14 days). The third digit swelling had improved slightly and RLP was repeated on day 13 under manual restraint. On day 20, the soft tissue swelling had resolved, although the distal aspect of the third phalanx was still mildly enlarged. The bird’s lameness had also resolved and oral antibiotics and anti-inflammatories were discontinued. The digital enlargement persists 3 years following treatment with no recurrence of soft tissue swelling or lameness.
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Adjunctive Use of Intravenous Antibiotic Regional Limb Perfusion in Three Cranes with Distal Limb Infections
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You are tasked with extracting and summarizing the essential information from this case report
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A 31-year-old right-handed woman with implantation of a VNS 3 years prior to her MEG recording presented for further evaluation. Since age 5 years old the patient had focal seizures that began with a “funny feeling,” flushing, and head turning to the right. Some seizures terminated at this point, while at other times her seizures progressed to impair awareness and/or evolved into a bilateral convulsive seizure. Treatment with acetazolamide, carbamazepine, valproic acid, and levetiracetam failed to improve the woman’s seizure frequency. An MRI did not demonstrate any structural brain abnormalities. An epilepsy monitoring unit (EMU) evaluation captured seizures with a broad, right hemispheric onset. An initial MEG recording prior to VNS implantation captured epileptiform activity, which was originally and unsuccessfully analyzed using ECD modeling. The interpretation at the time was that the MEG study did not provide localizing information.\nSynthetic aperture magnetometry (g2) was used to analyze a second MEG recording after the VNS implantation, as well as the previous recording performed prior to VNS implantation. Even though the second recording was separated from the first by 6 years and the raw MEG sensor data were strongly contaminated by artifact from the VNS during the second recording, an equivalent right frontal focus was identified on both recordings (Figure A). This indicates that SAM can reproducibly localize interictal epileptiform activity despite the presence of large artifacts due to the VNS implant. Examination of the source signal series reconstructed from the focus demonstrated MEG discharges that correlated with the simultaneously recorded scalp EEG during the second recording (Figure C), and, importantly, that lacked the high-amplitude fluctuations present in the raw MEG data that were induced by the VNS (Figure B). (For comparison, the raw MEG sensor data prior to VNS implantation are depicted in the top part of Figure B.) Furthermore, during the patient’s second MEG recording an electrographic seizure was recorded by EEG, with a preceding MEG-recorded discharge detected in the source signal series (Figure D). The SNR for the virtual electrodes was at least 50:1.\nGiven the new localizing information provided by the MEG recordings, the patient was determined to be a candidate for invasive monitoring and possible resection. A subdural grid was placed over the right frontal lobe, covering the focus identified on MEG (Figure F). Seizures captured during the invasive monitoring demonstrated electrographic onset (Figure E) very close to the focus of peak kurtosis identified by SAM(g2) on the MEG recordings (Figure F). Following resection, which included the focus identified by SAM(g2), the patient experienced a significant improvement in her seizures, improving from four to six focal seizures with loss of awareness and sometimes evolution to bilateral convulsive seizures monthly to two to four focal seizures with retained awareness monthly. Her scalp EEG recordings demonstrated a greatly reduced frequency of interictal epileptiform activity.
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Localization of Interictal Epileptiform Activity Using Magnetoencephalography with Synthetic Aperture Magnetometry in Patients with a Vagus Nerve Stimulator
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Your job is to distill the important information into a title from this case report
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A 72-year-old Caucasian male with an 8-year history of PD (HY stage 2) whose PD symptoms consisted of mild right and slight left rest tremor, mildly decreased co-ordination on the right, slightly decreased coordination on the left, mildly increased tone on the right, and slightly increased tone on the left. The patient previously received levodopa therapy for 5 years: one LC 100/25 mg tablet five times per day, switched to one LCE 150 tablet four times per day and CR-LC 200/50 mg administered at bedtime. Over the course of his disease, PD medication consisted of selegiline, pergolide mesylate, amantadine and rasagiline. All were stopped due to side effects or lack of efficacy. His current medications included LCE 150 mg, four times per day and ropinirole 3 mg, three times per day. The patient experienced no motor complications on his current therapy. The patient noted no clear OFF time, but felt that his ON time was not as good as it had been. He also noticed an increased difficulty in performing activities of daily living (ADL) throughout the day, and the physician found a worsening of symptoms upon examination. As a result of these patient and physician assessments, treatment was switched to one LCE 200 tablet four times per day. No screening diagnostic tests were used before switching. Following the switch to LCE 200, the patient has experienced no AEs. He reports that his physical functioning has improved, in terms of walking, ADL and personal care. Although he noticed no change in function during the night, he notes that he is turning ON much quicker in the morning. He reports that he turns ON in about 30 minutes now where it used to take 60-90 minutes.
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Levodopa/carbidopa/entacapone 200/50/200 mg (Stalevo® 200) in the treatment of Parkinson’s disease: a case series
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Your role is to provide a brief, accurate title of this medical case report
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A 70-year-old man presented with a 3-day history of acute upper abdominal pain. He had a fever of 38.1°C and tenderness in the upper abdomen. The patient had not been taking medications and his past history was unremarkable. Laboratory data showed a white blood cell count of 14,000/mm3 and C-reactive protein level of 11.8 mg/dl. A contrast-enhanced CT scan of the abdomen revealed a mass of mixed solid and fluid components, measuring 5.5 cm, adjacent to the lesser curvature of the stomach (fig. ). He underwent gastrointestinal endoscopy, which revealed a submucosal tumor near the gastric angle without an ulcer or fistula. According to these findings, he was diagnosed as having an intra-abdominal abscess, and sulbactam/cefoperazone sodium 2 g/day was administered for 10 days. Consequently, the fever decreased, his symptoms relieved and the laboratory data improved. A contrast-enhanced CT scan on the 7th day showed mass reduction (5.5–3.5 cm) (fig. ). An endoscopic ultrasound examination was performed on the 30th day, which showed a submucosal tumor with mixed hypoechoic changes (fig. ). A fine-needle aspiration biopsy was performed, and the tumor was diagnosed as GIST.\nLaparoscopic surgery with the 5-port approach (fig. ) was performed to excise the tumor on the 70th day from the first presentation. Laparoscopic findings showed that the tumor existed in the lesser curvature of the stomach and adhered to the omentum. Wedge resection of the stomach was performed using a linear stapler, and the tumor was excised en bloc with the omentum and gastric wall (fig. ).\nThe excised tumor measured 3.0 × 2.5 cm in diameter and originated from the serosal layer of the stomach, without an obvious fistula between the gastric lumen and the tumor. Histological findings showed spindle cells with a stromal growth pattern without necrosis (fig. ). The tumor was positive for c-kit (CD 117) and CD 34 (fig. ), with a Ki-67 index of 8% and mitosis of <5/50 HPF, and was accordingly diagnosed as low-risk GIST. The postoperative course was uneventful, and the patient was discharged on postoperative day 12. Imatinib mesylate was administered as adjuvant treatment, and no recurrence has been noted for 2 years after operation.
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Gastrointestinal Stromal Tumor of the Stomach with an Abscess Excised by Laparoscopic Surgery
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Your role is to extract the core information from this case report
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A 50-year-old man with past history of hypertension and chronic renal failure was admitted to our hospital complaining of high grade fever, vomiting and diarrhoea for the past week. On examination he was lethargic, with slow eye photomotor reflexes, confused on arousal, with poorly coordinated movements and speech. He appeared malnourished, dehydrated, and oliguric. The relevant laboratory investigations and clinical picture reflected severe chloride-potassium-fluid depletion with metabolic alkalosis (pH 7.69), compensatory hypoventilation, hypercapnia, hypoxemia and acute-on-chronic renal failure [Tables , ]. Computer tomography of the brain was normal.\nUnder careful monitoring, replacement of normal free fluid, potassium and sodium chloride was started. Milk based enteral nutrition (up to 2 litres per day) along with supplementation of magnesium, phosphate, vitamins and trace elements were started.\nUrinary tract infection (E. coli growth in urine) was treated with antibiotics according to sensivity reports. Inspite of improvement in presenting complains of fever, vomiting and diarrhoea, his renal function deteriorated progressively over the next two days (serum urea 90 mg/dl, creatinine 5.2 meq/dl). Extreme alkalemia persisted. Oral acetazolamide 250 mg per day was started and the frequency of the proton pump blocker was increased to twice a day. Haemodialysis with dialysate containing 25-28 meq/dl of bicarbonate was tried twice. Lower bicarbonate containing dialysate was unavailable. Intravenous calcium gluconate (10 mg) followed by 1500mg calcium carbonate per day was administered for hypocalcemia (corrected serum calcium levels 7 gm/dl). On the fourth day he developed further deterioration in level of consciousness and developed myoclonic jerks, tetany and seizures. CT scan revealed an acute subdural hemorrhage in the right parietal region. Procurement of medical grade hydrochloric acid was attempted. However, patient was shifted to a government hospital due to financial constraints where he expired after two days.
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Extreme metabolic alkalosis in intensive care
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Your role is to extract the core information from this case report
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A 70-year-old gentleman with a past medical history of chronic obstructive airways disease and cor-pulmonale was referred to the Surgical Admissions Unit by his General Practioner with a 2-week history of progressively worsening painful and swollen right scrotum with associated vomiting and fever for the last 1 day. The patient reported no preceding factors and no history of trauma/injury to his genitalia.\nOn admission, history and examination (consisting of a full systemic review and detailed urological examination) was performed. No lower urinary tract symptoms were reported other than long-standing nocturia (twice). Examination revealed a swollen right hemiscrotum and a visible and palpable hydrocele, which transilluminated. The hydrocele was pre-existing, with a symptom--free interval. No other structures were palpable. A per-rectum examination revealed a slightly enlarged prostate but no evidence of tenderness to suggest prostatitis. No evidence of epididymo-orchitis was suggested. No crepitus or areas of gangrene were noticed. A preliminary diagnosis of an infected hydrocele was made and intravenous antibiotics, including Gentamycin and Augmentin, were started. Blood samples taken on admission showed a white cell count (WCC) of 22.3 × 109/l, with marked neutrophil leucocytosis.\nThe following day, the patient reported much less pain and felt much better. Because of the grossly swollen hemiscrotum, the right testicle could not be palpated nor could a fluid level be elicited. An ultrasound scan confirmed the presence of a tense 7 cm hydrocele. In addition, echogenic material was identified, which was reported as possibly due to a haemorrhage or infection. No comment was made regarding the epidydymis or right testicle, thereby suggesting that this was not affected. The left testicle was reported as normal. Monitoring of the patient's fluid input and output suggested adequate amounts of urine voiding with no symptoms reported by the patient of hesitancy, dysuria, haematuria or frequency.\nThree days post-admission, the patient developed a pyrexia of 38°C, with a C-reactive protein (CRP) level of 491.8 mg/L and a leucocytosis of 21.3 × 109/l. Four days post-admission, the pyrexia had settled and the antibiotics were changed to oral preparations of Augmentin with a view to the patient being discharged the same day. However, the patient reported difficulty with micturition and, therefore, an ultrasound scan of his bladder was arranged, which showed a large residual of 999 ml of urine. The patient was catheterised. A urine specimen obtained subsequently showed no significant growth. The patient continued to spike a temperature reading of >38°C and became hypotensive (systolic 74 mmHg; diastolic 54 mmHg – usually >120 mmHg systolic) and further blood cultures were taken. A CRP of 472.5 mg/L was obtained however, the WCC improved to 15.9 × 109/l. It was decided to keep the patient in the hospital for further monitoring of his urinary retention.\nSeven days post-admission, the patient reported a sizeable reduction in the scrotal swelling. However, on examination, two discrete black lesions were noticed on the scrotum, prompting the diagnosis of FG. A further review of the patient later in the day showed further areas of superficial necrosis as well as a spreading cellulitis (approximately 5 cm proximally toward his abdomen in 6 hours). Repeat blood tests showed a rise in the WCC to 27.4 × 109/l, which was predominantly a neutrophil leucocytosis of 25.7 × 109/L. IV antibiotics including Tazocin, Metronidazole and Clindamycin were started after discussion with the microbiologists. The patient was taken to the operating theatre for urgent debridement.\nDuring the operation, the skin and subcutaneous tissue was radically debrided (extending throughout the perineum and lower anterior abdomen) to healthy tissue and a right orchidectomy performed due to the non-viable necrotic testicle. Pus and skin obtained was sent to the microbiology department for microscopy, culture and sensitivity. Culture later revealed a heavy growth of E. coli and anaerobes, all sensitive to the current antibiotic regimen. Dressings consisted of Jelonet, gauze padding and crepe bandage.\nFollowing the initial debridement, the patient was transferred to the Post-Operative Surgical Unit, where he continued to improve. Two days post-operatively, the patient was taken back to theatre for a second look. Further debridement of additional necrotic material took place.\nThe patient continued to improve postoperatively and, 5 days post-surgery, his WCC was 12.7 × 109/l, with a CRP of 61.3 mg/l. Following microbiology advice, all antibiotics were stopped 7 days post-surgery as the WCC had normalised at 8.8 × 109, and his CRP came down to 38.6 mg/l. He eventually underwent skin grafting, under the care of the Plastic Surgeons, to his perineum, medial thigh and anterior abdomen.\nNo typical risk factors, typical for the development of Fourniers were identified on review of the patient's notes.
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Fournier's gangrene developing secondary to infected hydrocele: A unique clinical scenario
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Your task is to summarize this medical case report into a title
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A thirty-seven-year-old female patient presented with abdominal pain and fever. Two weeks ago, she underwent LSG in a state hospital. Physical examination revealed minimal sensitivity by palpation localized to the left upper quadrant. Her body temperature was 39°C. White blood cell count was 11,600mm3/dL, and the C-reactive protein (CRP) value was 166. The chest X-ray showed blunting of the left costa-phrenic angle with minimal left sided pleural effusion (). An oral contrast given esophago-dueodenography was performed to rule out a staple line leak under scope which did not show extra-luminal contrast extravasations (). Abdominal computerized tomography (CT) revealed a unilocular pyogenic liver abscess measured 12x7cm in diameter which was localized to the left lobe (). A history of LSG from two weeks ago and a left sided pleural effusion on chest X-Ray were suggestive of pyogenic liver abscess secondary to staple line leak. The patient was hospitalized and an Ultrasound guided percutaneous drainage catheter was placed. Intravenous antibiotic therapy (piperacillin-tazobactam3x4.5gr/day) was started immediately. The course of the patient was uneventful. The liver abscess resolved and she was discharged on the 22th day with oral antibiotic therapy.
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Pyogenic liver abscess after laparoscopic sleeve gastrectomy
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You are to provide a brief yet comprehensive title of this case report
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A 47-year-old female complained of vertigo caused by head rotation. Approximately 2 months prior to visiting a neighborhood clinic, vertigo, nausea and dullness of the right arm had begun when she turned her face to the left. Bow Hunter’s Syndrome (BHS) was suspected at that clinic and she was referred to our hospital for scrutiny. Medical history: she had been prescribed antihypertensive agents. She and her family did not have any genetic past history.\nThere were no abnormalities concerning neurological examinations and she did not reveal any dysmetria at her initial visit to our hospital. However, when she turned her head leftward for approximately 15 s, leftward nystagmus appeared, and this was followed by dullness of the right arm. Approximately 25 s after the onset of dullness, the patient complained of severe nausea. After the head was returned to the central position, downbeat nystagmus appeared, which changed to rightward nystagmus, then disappeared after 30 s. These transitional nystagmus and symptoms were observed both in the sitting and supine positions.\nHer nystagmus at her first visit was unrecordable, therefore Fig. A (and Additional file video) shows the nystagmus at her second visit in a sitting position using infrared CCD video-oculography.\nThe routine electronystagmography and equilibrium tests were normal. MRI showed no abnormal findings in the brain, but MR Angiography and 3D-CT detected right vertebral artery (VA) hypoplasia (Fig. B, C) and carotid ultrasonography showed the reduction of blood flow of the right VA. (Fig. D). There was no bony deformation which was responsible for pressing on the right VA with head rotation on CT. “In addition, there were no symptoms or reduction in flow in the dominant left vertebral artery on turning the head to the contralateral side. We could not record the nystagmus and the carotid doppler concurrently.\nAccording to these symptoms and findings, BHS was diagnosed, and we consulted with the neurosurgery and orthopedic surgery departments. Conservative therapy was advised and she was told to avoid rotating her neck leftward in her daily life.\nAfterwards, she noticed that her systolic blood pressure was too low, i.e., 80–90 mmHg every evening under the medication for her hypertension. At last, the prescription modified by a new physician elevated her blood pressure and the vertigo symptoms also improved. Her systolic blood pressure after her hypertensive medication was stopped was about 120–130 mmHg. She has not suffered a vertigo attack since.
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Transitional nystagmus in a Bow Hunter’s Syndrome case report
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Your role is to provide a brief, accurate title of this medical case report
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40-year-old male patient with a diagnosis of HIV infection since 2006 in low-adherence antiretroviral therapy, who presents a two-year history of the appearance of four painful, slow-growing lesions in the limbs and abdomen, associated with low back pain. The physical examination showed well defined subcutaneous nodules, mobile, of a rubbery consistency and very painful, located in the left forearm (1 × 1.5 cm), abdomen (0.5 × 0.5 cm), left thigh (1 × 0.5 cm), and one of larger size and linear shape on the dorsum of the right hand (2 × 1 cm) (). Within the relevant laboratory, 2,200 leukocytes, 920 lymphocytes, with CD4 of 6 cells/mcL and a viral load of 36,600 copies are reported. In the magnetic resonance imaging (MRI) of the contrasted spine, an extensive epidural infiltration with foraminal involvement of T4-T5, T7, T11, and T12 with compression and displacement of the spinal cord is evident (). A biopsy of one of the skin lesions () and of the epidural mass () were taken with findings similar to histology, finding a positive fusocellular neoplasm for H-caldesmon and smooth muscle actin (SMA) a diagnosis of smooth muscle tumor. Subsequently, an in situ hybridization study was performed for the detection of the Epstein-Barr virus encoding region (EBER), which was positive ().
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Cutaneous smooth muscle tumors associated with Epstein-Barr virus in an adult patient with HIV
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 69-year-old woman was admitted to our hospital with a 5-day history of macroscopic hematuria and AKI. She was diagnosed with IgAN on renal biopsy 6 years prior. Following this diagnosis, she was administered prednisolone because she had persistent microscopic hematuria and proteinuria of approximately 1.0 g/day. Proteinuria remitted after treatment; however, microscopic hematuria persisted (over 100 RBCs per high power field). Prednisolone was discontinued 1 year ago. Five days prior to admission, she developed an upper respiratory tract infection, accompanied by gross hematuria. The gross hematuria persisted; however, the color became lighter after admission. Her past medical history included hypertension, diabetes, and dyslipidemia. She was not receiving any antithrombotic medication. On admission, her body temperature, blood pressure, and heart rate were 36.6℃, 144/64 mmHg, and 65 beats/min, respectively. She had no abnormal findings on examination of her tonsils, pharynx, extremities, and skin. Laboratory data are presented in Table . Her serum creatinine level increased to 4.9 mg/dl from 1.1 mg/dl at the last visit. Urinalysis revealed that the urinary protein excretion level was 1.25 g/day; the sediments contained 30–49 RBCs and ≥ 100 white blood cells per high-power field. There were no signs of dehydration. Abdominal ultrasound showed that both kidneys were of normal size, excluding hydronephrosis.\nA renal biopsy was performed 7 days after admission. Light microscopy showed that nine out of 29 (31 %) glomeruli were globally sclerotic, and five out of 29 (17 %) had cellular crescents. Most glomeruli showed moderate mesangial proliferation. The proximal tubule epithelial cells were edematous, showed detachment from the tubular basement membrane, and contained granules of various colors (ranging from yellow to brown). Some tubules showed dilation and loss of the brush border. There was no obvious hemorrhage or obstructive RBC casts in the tubules. There was interstitial fibrosis and inflammatory cells were present around the injured tubules (Fig. a–c). Immunofluorescence showed granular mesangial staining for IgA and C3 (Fig. d, e). Electron microscopy showed mesangial electron-dense deposits (Fig. g). Perls’ Prussian blue staining showed hemosiderin deposition in the renal proximal tubular cells, which was not observed 6 years ago when first renal biopsy was performed (Fig. ). Low vacuum scanning electron microscopy, a novel method for rapid three-dimensional pathological analysis [, ], showed the electron-dense particles in tubular epithelial cells. Furthermore, transmission electron microscopy revealed that these particles were located in lysosomes (Fig. ). Based on these findings, she was diagnosed with ATN with a concurrent IgAN flare-up. After confirming the results of the renal biopsy, she was treated with intravenous pulse methylprednisolone, followed by oral prednisolone. The gross hematuria gradually faded, and the serum creatinine levels decreased. After 3 months, the serum creatinine and urinary protein excretion levels were 1.8 mg/dl and 0.24 g/day, respectively.
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Renal hemosiderosis presenting with acute kidney Injury and macroscopic hematuria in Immunoglobulin A nephropathy: a case report
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You are tasked with extracting and summarizing the essential information from this case report
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A 1-day-old female African newborn weighing 3500 g was referred for management of a large oral mass that protruded from the mouth and caused maxillary protrusion and flattening of the nose. The patient was having difficulty breathing (Fig. ).\nShe was born by spontaneous vaginal delivery to a mother who was unaware of the date of her last menstrual period. She had no prenatal medical care, so there was no opportunity for prenatal diagnosis.\nInitial examination revealed a mass that occupied the majority of the oral cavity and protruded from the mouth. On palpation, the mass appeared to arise from one side of the palate, and there was an adjacent palpable cleft. No other congenital anomalies were evident on physical examination.\nThe patient had some breathing difficulty, but the airway was patent. She was administered oxygen and intravenous fluids, and a nasogastric feeding tube was successfully placed. Feeding was commenced at 35 ml, eight times per day, and she stabilized.\nOn day 5, she was taken to surgery. Laryngoscopy was performed using a standard Macintosh blade size 1, and an easy intubation with a 2.5 endotracheal tube. The mass was excised under general anesthesia, Good hemostasis was achieved, and complete resection of the tumor was accomplished. There were no immediate postoperative complications.\nGross examination revealed a large fibrocystic tumor involving the oral and nasal cavities with its base originating from the hard palate. It measured 6 × 5 × 4.5 cm and was well circumscribed (Fig. ).\nHistopathologic examination revealed a congenital primarily epidermal teratoma.\nShe had an uneventful postoperative course, although a palatal defect remained (Fig. ). She had no difficulty opening or closing her mouth. Bottle feeding with expressed breast milk was initiated shortly after surgery and was well tolerated. She was able to breastfeed by postoperative day 5.\nOn postoperative day 30, the patient was taken back to surgery, where she underwent successful palatoplasty (Fig. ). She was discharged home with her mother on postoperative day 9 after palatoplasty (Fig. ).
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Congenital epignathus associated with a cleft palate: a case report
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Your task is to provide a clear and precise title of this case report
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A 66-year-old retired female patient was admitted with left-sided hemiplegia, dysarthria, and hemineglect 30 min after symptom onset. The National Institutes of Health Stroke Scale (NIHSS) score was 13. Medical history included coronary heart disease, hypertension, diabetes, and smoking. Notably, she had a history of hemithyroidectomy 1 week prior because of goiter.\nAcute non-contrast computed tomography (CT) was unremarkable. CT angiography revealed right-sided middle cerebral artery (MCA) M1 occlusion. IVT was contraindicated because of the recent surgery, and MT was initiated.\nMechanical thrombectomy was successfully performed using a Solitaire stent retriever (thrombolysis in cerebral infarction scale 3, Figures A–B). Symptom-to-recanalization time was 130 min.\nAfter the procedure, the patient showed rapid major neurological improvement. Brain MRI on day 4 demonstrated small ischemic infarcts in the right posterior basal ganglia region and right temporal cortex (Figure C). While thorough cardiac work-up including stroke unit ECG monitoring, 24-h ECG and transesophageal echocardiography showed no cardioembolic source, duplex sonography revealed an irregular-shaped ulcerated plaque formation in the right internal carotid artery (ICA) origin but without relevant stenosis (peak systolic velocity of 66 cm/s on doppler sonography compared to 57 cm/s contralaterally; luminal stenosis of 40% on CT angiography). Therefore, only antiplatelet and statin therapy was initiated and the patient was discharged home with an excellent outcome on day 8 [NIHSS: 0, modified Rankin scale (mRS): 1].\nOn the next morning (day 9 after the index stroke), she was re-admitted with wake-up-stroke (last seen well 10 h before) and had again a right total anterior circulation stroke syndrome (NIHSS: 16).\nMultimodal MRI was performed. Aside from the past infarction, no new diffusion or FLAIR-positive lesions were found. However, a right-sided proximal MCA occlusion was present again and was associated with severe hypoperfusion (Figures A–C).\nAs thrombolysis was contraindicated (both because of recent surgery and recent stroke) and MRI showed an extensive diffusion–perfusion mismatch, MT was again successfully performed with a Solitaire stent retriever (door-to-recanalization time: 149 min, thrombolysis in cerebral infarction scale 3, Figures D–E).\nThe neurological exam on the following day showed once more remarkable recovery (NIHSS: 0). Postinterventional duplex sonography and contrast-enhanced MR-angiography did not show any signs of vasospasm or vessel dissection.\nDetailed etiological re-evaluation including CT angiography of the aortic arch, repeated echocardiography, and 24-h ECG revealed no new findings. The already known ulcerated plaque at the right ICA origin (Figure ) was, therefore, considered as the most likely cause of the two strokes, and uneventful carotid thrombendarteriectomy was performed. The patient was discharged home with only minimal clumsiness of the left hand (NIHSS: 0, mRS: 1).\nRepeated neurological follow-up examinations were performed at 3, 6, and 18 months, each showing no further vascular events and stable neurosonographic findings.
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Repeated Endovascular Treatment of Early Recurrent Proximal Middle Cerebral Artery Occlusion: Case Report and Brief Review of the Literature
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As a clinical title specialist, your goal is to synthesize the key elements of this case report
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An 18-year-old Burmese man, with no significant medical history at the time, visited the Emergency Department for intermittent abdominal pain that had acutely worsened. He reported no fevers, shortness of breath, lightheadedness, fatigue, blood in the stool, tarry stools, changes in bowel habits, weight loss, nor any other symptoms other than severe abdominal pain. His vital signs were normal. Physical examination was remarkable for left upper quadrant abdominal tenderness and mild abdominal distention. Also, small, dark blue-colored spots on the lips () as well as the fingers were noted (). Laboratory testing was notable for hemoglobin of 8.3 g/dL with an unknown baseline. He had a mean corpuscular volume of 74 fL, a red blood cell distribution width of 17.2%, as well as an iron panel with iron level of 18 µg/dL, iron-binding capacity of 362 µg/dL, and ferritin of 35 µg/dL findings consistent with iron-deficiency anemia.\nAbdominal computerized tomography (CT) scan was performed and showed findings of a segment of large intestine invaginating into the adjoining intestinal lumen at the level of the splenic flexure (). The patient was taken to the operating room where he underwent exploratory laparoscopic bowel resection in order to surgically treat an intussusception that had caused large bowel obstruction. He was found to have multiple large polyps of varying sizes which were sent for histopathological evaluation. The pathology report showed hamartomatous polyps consistent with Peutz-Jeghers polyposis. There was no malignancy and the margins were negative. The patient was started on oral iron supplementation and referred to a gastroenterologist for further evaluation. He underwent colonoscopy where he was found to have many polyps throughout the colon and rectum (), the largest of which were removed and sent for histopathological evaluation. The histology revealed a polyp with proliferation of the smooth muscle bundle () on hematoxylin and eosin stain (× 400). Immunohistochemistry (IHC) stained positive for smooth muscle actin (SMA) (× 100) indicating smooth muscle origin with central core branching of the smooth muscle () consistent with hamartomatous polyps. Also, the patient underwent genetic testing, which was positive for a germline mutation in the STK11 (LKB1) gene, confirming the diagnosis of Peutz-Jeghers syndrome. His family members have since been referred for genetic testing and colonoscopy as they none of the family members had a colonoscopy done.
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Peutz-Jeghers Syndrome Presenting as Colonic Intussusception: A Rare Entity
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Your task is to summarize this medical case report into a title
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Patient 5, a 21-yr-old Korean female, had severe dyspnea and a pulmonary AVM. She had a history of cyanosis, dyspnea, and clubbing of her fingers at birth, as well as multiple AVM in the lung. She underwent a segmentectomy of both lungs at the age of nine. A visual inspection revealed an acneiform eruption on her face, microtelangiectasia on the tongue, and clubbing fingers with one small telangiectasia (). The chest CT and pulmonary angiography revealed extensive peripheral AVM in both lungs () and a probable arterioportal shunt involving the liver. Selective coil embolization of the AVM in the lung was performed twice, and the dyspnea was ameliorated.
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Clinical Features and Mutations in the ENG, ACVRL1, and SMAD4 genes in Korean Patients with Hereditary Hemorrhagic Telangiectasia
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As a medical summarizer, your job is to condense this case report into its key points
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A 30-day-old female baby, born at full-term, to nonconsanguinous parents, presented with a history of feeding difficulty and failure to thrive. There was a history of respiratory distress and cyanosis at birth. The antenatal period was uneventful. Clinical examination revealed dysmorphic features, with microcephaly, a cone-shaped occiput, microphthalmia, proptosis, bilateral simian crease, and a depressed nasal bridge. The child was noted to have mouth-breathing. There was no evidence of a cleft palate. A flexible nasopharyngolaryngoscopy was attempted, but the scope could not be negotiated toward the choanae. A No.6 nasogastric tube also could not be passed through the nostrils.\nA CT scan was performed as the next step to evaluate the upper airways. This was negative for choanal atresia, but revealed multiple typical findings, which led to the diagnosis of CNPAS. The nasal cavity showed medial approximation of the nasal processes of the maxilla, causing marked narrowing of the pyriform apertures, which measured 3 mm in width on an axial image, at the level of the inferior meatus []. There was associated thinning of the anterior nasal septum. Additional findings included hypotelorism, a single maxillary central incisor tooth (megaincisor) [], and a triangular hard palate [] with a prominent median inferior palatal bony ridge []. The maxillary sinuses were hypoplastic. The perpendicular plate of the ethmoid and nasal bone was absent, as were the cribriform plate, the crista galli, and the fovea ethmoidalis on the left side, with a resultant nasoethmoid encephalocele in the superior left nasal cavity [].\nMRI was recommended to exclude known associated anomalies such as holoprosencephaly and anterior pituitary abnormalities, as well as for a detailed evaluation of the encephalocele. However, this was deferred to a follow-up visit. The child improved symptomatically with conservative measures such as insertion of an oral airway and feeding in the upright position. No active intervention was undertaken during this visit and the patient was asked to report for review earlier, in case there was any symptomatic worsening.
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Congenital nasal pyriform aperture stenosis: A rare cause of nasal airway obstruction in a neonate
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You are required to deliver a compact title of this case report, outlining the significant findings
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AB is a 12 year old boy admitted to the paediatric hospital following precipitous weight loss as a result of increased exercise, in an otherwise very active and sporty boy. According to his mother, this commenced the ‘day after lockdown’ and was not linked with any intentional reduction in food intake or body image dissatisfaction. In fact AB maintained the position that he was too thin. AB joined the family for meals as per norm with no reduction in usual amounts or variety consumed and there was no obvious change in his mood state.\nDuring Covid-19 restrictions, AB missed attending school, socialising with peers and his training routine. He recreated this with a self-initiated exercise schedule. At the time of lockdown, AB’s father had been abroad and his absence from the family home was further prolonged by a two-week enforced post-holiday quarantine. AB’s mother was balancing a heavy work-at-home schedule with providing for her other children and the extent of AB’s exercise and associated weight loss, in the presence of usual eating and general demeanour had gone unnoticed until father’s return. It was at that point that AB’s mother attended her family physician, and was advised to seek hospital admission due to significant weight loss.\nAB was described by his mother as pre-morbidly being a ‘faddy eater’, showing little interest in food and eating much less than his younger siblings, but without any adverse effects. An example given was during their pre-Covid ski holiday, all the family increased their food intake apart from AB. Although AB ate fast food when out with friends, at home he preferred simple, minimally flavoured, bland foods and rarely ate treats. For ease of meal preparation, AB’s mother had a scheduled weekly meal plan which all the family, including AB, followed. He never expressed any concern over his body image and there were never any deviations from his growth trajectory. Mother estimated his typical daily intake to be 1300–1500 cal/day.\nAB was talented athletically, played soccer and football competitively, with a heavy but structured schedule of daily soccer training and weekend competitive games with two different clubs. He also spent time on the family trampoline at home. This amounted to 6 h strenuous exercise per week, plus routine school sports. In the days immediately after lockdown, to replace his previously structured day, AB started running for up to an hour a day, covering 10-11 k, initially alongside his mother’s daily walk, and later independently and much faster. He later joined his brother in cycling 10-20 k daily and spent 1–2 h each evening on the family trampoline, irrespective of weather. The estimated daily calories expenditure was around 2600 cal/day, and greater than the reference range of 1800–2200 for an active 9–13 year old boy.\nPre-morbidly AB’s weight was estimated at 33.1 kg, corresponding to a Body Mass Index (BMI) of 15.6 (15th %) or 90% Ideal Body Weight (IBW). He had lost almost 5 k in 2 months and was medically comprised on admission. His admission weight was 27.5Kg, BMI 12.9 (0.03%) corresponding IBW 70.35%. At the time of admission and based on maternal report and discussion with the hospital dietician, AB’s daily calorie intake was estimated to be between 1300 and 1500 Calories/day, giving an overall deficit of 1100–1300 cal/day. (A sample daily intake in included in Table .)\nAB’s developmental milestones are within normal boundaries. He was perceived to be popular at school with many friends and academically very able. He engaged well with his family, was generally very active but not considered to have difficulties with attention or impulsivity. There was no suggestion of any pre-morbid anxiety, obsessional features or low mood. Although he generally liked routines, schedules and well planned activities, his mother was adamant that there were no social communication difficulties. He was self-sufficient, empathetic and not overly emotional, tending to deal with difficulties or upsets himself. Given his mother’s work with children with special needs, she felt that this was a precise and accurate reflection of his development. Teacher reports described a biddable boy, who excelled in school and sports, with a close circle of friends. He was described as helpful and considerate. There were no concerns expressed by teachers regarding mood, social communication difficulties, or ADHD. There was no prior contact with mental health services and no history of substance misuse. There was no medical history of note, he was up to date with all his vaccinations, had no allergies and was not on any medication.\nAB is the middle of 5 healthy children aged from 17 to 10. Mother describes some personal difficulties with weight maintenance and past dieting behaviour, with weight fluctuation of 2 stone. At the time of presentation, she was happy with her weight and had a structured exercise routine built into her day to facilitate weight maintenance. Father, like his siblings, is tall and thin. All AB’s family are sporty, of slim physique and his older brother was a national athlete for many years. Mother described the family to follow a ‘healthy diet of home based and natural ingredients’ by which she meant that she prepared fresh meals daily using fresh produce and limited her use of processed foods (Table ). She also reported she limited her childrens’ use of social media. AB parents describe a happy marriage and no difficulties with co-parenting. Parents described an authoritative parenting style, with low levels of expressed emotions and a preference for advanced planning, routine and structure. By way of example, holidays aboard were planned well ahead of time including scheduling and booking activities on various days. There were no other family stressors reported. There was a history of bipolar disorder on the paternal side, and depression in maternal first degree relative.\nAB was pre-pubertal, with no expressed concern regarding male gender. He was perceived favourably by peers and had not experienced any bullying at school. Although the clinicians felt father’s absence and forced quarantine during the immediate lockdown might have triggered additional anxiety for AB and his family, and contributed to his presentation, this was disputed by both AB and his mother.\nAB was extremely thin, gaunt with a very visible skeletal frame. He found it hard to engage and eye contact was generally poor. Speech was low in volume and conversation restricted. AB described his mood as mostly ‘sad’ and ‘bored’, he reported difficulty adjusting to lockdown, he missed his friends and soccer training and found the days at home long and uneventful. He reported a preference to have ‘things planned’ and felt better when he joined his mother or brother on their activities. He denied his pursuit of exercise was driven by any wish to alter his body shape or to lose weight. He acknowledged he was underweight and stated he ‘did not like being this skinny’. He perceived that his engagement in exercise was ‘80% to stop being bored and 20% to keep fit’ and felt it aligned with the behaviour of his other family members. He recognised that he had become ‘obsessed’ with a desire to exercise and its mood elevating component. If he did not exercise for any reason, which he reported was very seldom, he reported feeling ‘sad’. He volunteered that immediately pre- admission he exercised less because he was too tired. AB denied any fear of an untoward outcome if he did not exercise as planned and allowed his brother to choose their cycle route, distance and timing. Although he chose his exact running route, his start time was linked to that of his mother’s walk. During this time, he denied any attempt to limit his calorie intake and stated he enjoyed his meals. He denied any feelings of hunger; ‘it had never occurred to me to eat more, and no one told me’. He described his mood as good unless he was unable to exercise for any reason and denied any ideas or behaviours linked to self-harm. There was no evidence of any abnormal thought form or perceptual abnormalities. His thought content was very much focussed on his desire to return to his routine of school, sports and time with friends. He was eager to follow the hospital treatment plan and be discharged.\nPhysical examination revealed a cachectic boy, with low body temperature (35.8–36, Normal 37.) There was evidence of cardiac insufficiency; low heart rate (30s at night time) and orthostatic changes of 22 bpm (lying HR 38/ standing HR 60). His blood pressure was variable; systolic ranging from 81 to 105 mmHg, diastolic from 52 to 76 mmHg, but with minimum orthostatic changes (< 10 mmHg). His electro-cardiograph revealed sinus bradycardia with normal QTc. There were some initial abnormalities in his biochemistry and haematology results (Table ).\nChild Behaviour Check List (CBCL) completed by parents suggested no areas of clinical concern. AB completed the Rosenberg Self-Esteem scale, a self-esteem measure widely used in social-science research and helpful to examine self-esteem. Scores below 15 indicate problematic low self-esteem []. AB scored 40/40. The exercise addiction scale was also completed. This is a short screening tool used clinically to examine the possibility of exercise addiction, with scores above 24 being considered clinically relevant. AB scored 29/30, indicating significant difficulties. By contrast his global score on the Eating Disorder Examination Questionnaire (EDE-Q) was 0.39, with very low scores on each of the subscales: Restrain: 0; Shape: 0.75 and Weight 0.8, suggesting no eating disordered pathology.\nAt the time of admission AB was severely undernourished, having lost an excessive amount of body weight in a short time. This was due to a significant imbalance between energy expenditure and intake but without any evidence of eating disordered psychopathology. Specifically, AB did not endorse a fear of fatness or weight gain, body image dissatisfaction, or a distorted view of body shape. His excessive engagement in exercise was driven by a desire to impose structure on his day and fight boredom. It was subsequently reinforced by an improvement in his mood. He did not meet criteria for AN or Atypical AN, included in Other Specified Feeding or Eating Disorders (OSFED). A working diagnosis of exercise addition was made (Table ).\nAB treatment plan was devised following multi-professional input from child psychiatry, paediatrics and dietetics. He commenced on a refeeding program, with a gradual increase from 1400 to 2000-2400 cal/day during hospital stay with phosphate and thiamine supplements. He found it very difficult to eat all the food offered, initially eating as little as 400–500 cal/ day. This low intake was driven by severe abdominal discomfort, reflux and severe constipation upon refeeding. Replacement with a nutritional supplement, Fortisip, was given. AB had no bowel movements over a 4 week period despite heavy doses of laxatives. Clinical examinations and plain film of abdomen did not reveal any evidence of impaction. His mood dropped significantly as he struggled to adhere to his meal plan, tolerate painful abdominal peristaltic movements and gain the necessary weight needed for discharge. One-one nursing was provided at meal times to support AB with oral intake, ensure postprandial bed rest and observe if any desire to exercise. His parents also struggled with what they perceived to be the multi-disciplinary team’s over focus on weight restoration and a fear that AB’s complaints were misinterpreted as wilful refusal, rather than an inability to eat. They considered discharge against medical advice.\nAn early intensive transitional out-patient plan was progressed to facilitate family engagement and assist with careful weight restoration. This followed an adapted version of Family based treatment, with psycho-education offered, provision of structured meal plans, and establishing parental role in all aspects of food preparation, presentation and supervision. AB was allowed trials home for family meals and over-nights, despite being medically compromised, and these were carefully monitoring by his mother and clinical team. A detailed record of all food offered and eaten was kept and reviewed at hospital reviews, along with estimated daily calories (circa 2100 cal/day). Initial progress was followed by a significant drop in weight and low sodium which precipitated a medical re-admission and a need for cardiac monitoring. AB admitted he had been spitting out half of the food plated by his mother for fear of a return of his abdominal pain.\nAfter one week of medical stabilization as an in-patient, transitional care continued with twice weekly psychiatry/medical review and heightened maternal supervision. AB was discharged to community child and adolescent mental health services (CAMHS) after 2 weeks. His weight at discharge was 30.4 kg, BMI 14.5 and IBW 82.6%, still below his pre-morbid levels. Zoom out-patient sessions were planned with CAMHS given the reduced face-to-face contact during Covid-19. AB found these sessions very difficult, finding it hard to engage and missing out on non-verbal cues. Subsequent Zoom calls continued with his mother who reported on weekly weights and the degree of adherence to the meal plan. This allowed daily calorie intake to be estimated and he was eating 1800–2000 cal per day without resistance. AB’s mother also reported on the return of any physical symptoms and the degree of AB’s re-engagement with family and social life. Casual sporting activities were gradually re-introduced, alongside additional snacks. With time, and restoration of initial weight lost, additional snacks were dictated by preference rather than imposed. AB was discharged from CAMHS eight weeks post-hospital discharge. Two months post-discharge and 6 months post- initial presentation, AB’s mother wrote a letter updating the clinical team as to AB’s ongoing progress. She enclosed a photo of AB enjoying a ‘McDonalds’ equivalent. She reported he was ‘back to his normal self’ with resumption of pre-morbid eating habits and reaching his pre-morbid weight. AB did not receive any neuroleptic medication during admission, and prescription of thiamine and laxatives had been discontinued.\nAB had created a daily routine immediately following the imposed lock down and loss of his previously busy schedule of football training and competitive matches. Initially his pursuit of physical activity followed the family’s engagement in health optimisation during Covid-19 and was pursued as a shared activity. Within a few weeks it surpassed it and seemed to take primacy over other activities. AB reported being increasing driven to, and rewarded by, the mood boosting effects of his exercise, and being unaware of any hunger sensations, continued with his previous scheduled meal and snack routines. He maintained contact with some friends through social media, but had not socialised with any face to face. The family coped as best they could with the additional stressors of parents and children working and studying from home. The delay in AB’s presentation was most likely due to mother having to manage on her own while her husband was in quarantine. The reduced ability of face-to-face clinical sessions made engagement with ongoing mental health services difficult for AB, due to his difficulty picking up subtle non-verbal cues and his difficulty with emotional intelligence. A decision to work flexibly and independently with his mother, using principles from FBT approach, supporting and empowering her to monitor AB’s nutritional intake and physical state, allowed safe medical monitoring.
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Childhood onset exercise addiction or atypical anorexia nervosa during Covid-19: case report
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Your task is to provide an accurate and brief title of this case report
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This 35 years old indigenous man, with no stable accommodation for 10 years, identified the street as where he most frequently sleeps. His highest level of schooling was year 8. His first contact with the adult hospital healthcare system was in 2005 when he was hit by a car at the age of 22 years old, causing severe injuries. By this time, he already had severe ataxia (unsteady gait) and intellectual impairment from heavy solvent and alcohol abuse during his teenage years. In 2012 he had a further major car accident causing multiple leg fractures and by 2013, he was permanently wheelchair bound, homeless and a frequent user of street drugs, solvents and alcohol. He reports being regularly assaulted and having had multiple interactions with police, at the age of 30 years old, he was approved for permanent supported care but always left hospital to return to the streets before this could be found. His combination of permanent physical disability, lack of mobility, brain injury and vulnerability to attack and coercion resulted in him scoring 14 on the VI-SPDAT questionnaire in August 2016, reflecting high vulnerability. When asked ‘what do you need to be safe and well’ he simply answered ‘a house’.\nHospital use by this patient for a 27 months period (January 2015 to March 2017) is summarised in and the costs of these ED presentations and inpatient admissions have been computed using the sources described in the methods section. His total estimated costs for the 51 ED presentations over the 27 months period January 2015 to March 2017 was $33,456, and the cost of the 28 inpatient admissions amounted to $299,460. In total, this represents a cost to the health system of almost $333,000 or $12,333 per month over a 27 months period.\nIn early April 2017, this patient was found a place in a supported psychiatric care facility. Since then, he has not presented to any hospital or been admitted as an inpatient in the 7 months since being housed. The comparative cost of his past hospital use with the cost of case worker support and housing is discussed at the end of this results section.
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Tackling Health Disparities for People Who Are Homeless? Start with Social Determinants
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 72-year-old woman presented 3 h after a sudden onset of a right arm palsy. Her only stroke risk factor was hyperlipidemia. She reported no chest or back pain, and her arm paralysis had improved prior to the presentation. Neurologic examination revealed no symptoms on arrival; the National Institutes of Health Stroke Scale score was 0. The left arm blood pressure was 128/49 mmHg, and heart rate was 64 beats per minute. The right arm blood pressure was not checked because aortic dissection was not suspected. She was fully awake (Glasgow Coma Scale score = 15). She had normal heart sounds. The pretibial pitting edema and jugular venous distension were not observed. Laboratory tests revealed elevated D-dimer (50.5 μg/mL, normal <0.5 μg/mL). Electrocardiography showed normal sinus rhythm. Brain magnetic resonance imaging (MRI) showed no areas of restricted diffusion consistent with acute cerebral infarction. The distal right vertebral artery was not clearly visualized, and the right internal carotid artery showed a slightly lower signal intensity than the left internal carotid artery on the cervical and brain MRA. The course of the right brachiocephalic artery was not visible (A–B), which made us suspect the existence of aortic dissection in the time-of-flight MRA (TOF-MRA), but the definitive diagnosis could not be established (C). The subsequent pulse-gated noncontrast thoracic bSSFP-MRA revealed a dissection flap in the ascending aorta (D–E). Eventually, radiographs demonstrated mediastinal widening, and the chest CTA revealed Stanford TAAAD (F).\nEmergency surgical aortic repair with the ascending aorta and arch replacement were performed. The patient was discharged in an ambulatory state without residual neurologic deficits.
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Pulse-gated noncontrast thoracic magnetic resonance angiography for acute aortic dissection with transient ischemic attack: A case report
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You are to provide a brief yet comprehensive title of this case report
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A 40-year-old man suffering from fibular and medial malleolus fracture of the left leg underwent surgical reduction with plates and screws. Twenty days after the orthopedic surgery, wound dehiscence and exposure of the distal part of the fibular plate were observed. Swabs revealed an infection with Staphylococcusaureus. Before any further surgical procedure the patient underwent hyperbaric oxygen therapy, antibiotic therapy and local debridement until cultures were negative. The flap healed uneventfully in 20 days, and full weight bearing was allowed 30 days after surgery. The patient kept smoking during the whole period.
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Distally based sural fasciomusculocutaneous flap for treatment of wounds of the distal third of the leg and ankle with exposed internal hardware
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Your task is to provide a clear and precise title of this case report
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A 90-year-old man presented for evaluation of asymptomatic pigmented lesions on his soles. His past medical history is significant for prostate cancer. He receives leuprolide acetate (Lupron) depot suspension 22.5 mg injection every three months.\nCutaneous examination showed black macules on his feet. An 8 x 8-mm black macule was present on his left plantar foot near the heel. A 10 x 10-mm black macule was present on the right plantar midfoot.\nA 3-mm punch biopsy was performed at each site. Antibiotic prophylaxis, cephalexin 500 mg twice daily, was prescribed for 15 days. Topical mupirocin ointment (2%) was applied to the biopsy sites three times daily.\nHe returned for suture removal after two weeks. The left foot showed a combined (blue and junctional) nevus that was present in the lateral margins of the specimen; since this is a benign lesion, no further treatment was necessary. However, the right foot showed a junctional nevus with dysplastic features that also extended to the specimen’s lateral margins; the dermatopathologist recommended an additional biopsy.\nA broader biopsy, using the shave technique, was done and included most of the residual pigmented lesions on his right foot. Cephalexin 500 mg twice daily was continued for an additional two weeks. He also continued to apply the mupirocin ointment (2%) to the area three times daily.\nAfter an additional week of cephalexin—his third consecutive week receiving the antibiotic—he began to experience tenderness of his left Achilles tendon when walking. He was scheduled to return to the office one week later. He continued to take the antibiotic and his tendon pain progressively increased.\nFollow-up examination, two weeks after the second biopsy (and four weeks after starting cephalexin), showed partial healing of the biopsy site on his left foot; there was neither inflammation nor tenderness. Pathology evaluation of the larger biopsy specimen demonstrated a benign compound nevus, having features consistent with congenital onset, and without any atypia. Based on the revised diagnosis, no further intervention was necessary for the residual lesion that extended to the deep and lateral margins of the specimen.\nExamination of his Achilles tendons was also performed. His right tendon was asymptomatic. Similarly, at rest, his left tendon had no pain. However, on ambulation, the left Achilles tendon was very tender.\nCephalexin was discontinued; he had received four weeks of treatment. Ibuprofen was prescribed for symptomatic relief; however, the patient decided not to initiate oral therapy with the nonsteroidal anti-inflammatory drug. Within one week after stopping cephalexin, the left Achilles tendon pain spontaneously resolved and has not recurred. Subsequently, during the evaluation of his Achilles tendons two weeks after cephalexin had been withdrawn, there was no pain when walking.
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Cephalexin-associated Achilles Tendonitis: Case Report and Review of Drug-induced Tendinopathy
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You are to provide a brief yet comprehensive title of this case report
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An 18-year-old girl reported to our hospital with sudden onset diminution of vision in her left eye with pain for the past one week. She gave a history of injury to her left eye with her younger brother's fist while playing.\nShe was a known case of keratoconus for the past 4 years and had undergone isotonic collagen cross-linking in the right eye following Dresden protocol. Initial records prior to cross linking showed best corrected visual acuity (BCVA) right eye 20/60 (-1.00 Dsph/-6.00 Dcylx 700) and left eye 20/200 (+4.00 Dsph/-12.00 Dcylx 1300) with pachymetric values of 409 μm in right eye and 273 μm in the left eye. She was intolerant to semisoft contact lenses and a DALK was performed under general anesthesia in the left eye. Manual dissection was done due to the failed big bubble technique. While dissecting the thinnest portion of the host bed, 2 inadvertent micro-perforations of the DM occurred, which were sealed with fibrin glue. On the second postoperative day, a slight nasal separation of the DM was seen, so 14% perfluoropropane (C3F8) was injected intracamerally one week after the DALK. Postoperatively, the patient was advised topical prednisolone acetate (1%) 8 times a day, to be tapered weekly, and then once a day to continue. BCVA at one month post C3F8 injection was recorded as 20/80 (+6.00Dsph/-8.00Dcylx 800). Intraocular pressure (IOP) recorded was 14 mm of Hg in both eyes. She was counseled for regular visits for suture removal in the left eye.\nAt the present visit, posttrauma in her left eye, BCVA in the right eye was 20/50 (-10.00Dsph/-6.00Dcylx 200) and 20/2000 in the left eye. Inferonasal graft dehiscence with broken sutures and localized graft edema was seen []. Underneath the edematous graft, an intact host DM was seen. Anterior chamber was deep and the crystalline lens was intact. Irregular pupil with intermittent posterior synechia suggesting traumatic mydriasis was also seen. Anterior segment optical coherence tomography (ASOCT) showed separation of the donor graft from the host bed and an intact host bed []. Under general anesthesia, a paracentesis was made to reduce anterior chamber pressure and the surface of the host Descemet's membrane and of the graft was washed to remove any debris or epithelial cells. The broken sutures were removed and the area of graft dehiscence was re-sutured to the host bed with interrupted 10-0 nylon sutures. At 3 weeks, the uncorrected visual acuity (UCVA) in left eye improved to 20/400 (20/200 with pinhole). A month later, BCVA in left eye was 20/60 (-3.50 Dsph) with a clear graft and intact sutures []. Fundus examination was normal in both eyes.\nA year later she reported with mild decrease in vision in left eye 20/80 (-3.00 Dsph/-3.50 Dcylx 1200), N 36 due to a posterior subcapsular cataract. Specular microscopy (Tomey EM 3000) at 2-year follow-up showed central density 1833 sq. mm, CV 46, hexagonality 36%, standard deviation of 249 and polymegathism. At 2-year follow-up post-DALK topography was done guiding suture removal. [] Lens aspiration with foldable intraocular lens (IOL) implantation was performed successfully. Three weeks later BCVA improved to 20/40 (+3.00Dsph/-3.00Dcylx 1200) [].\nShe continued to maintain good vision till her last follow-up with a BCVA of 20/40 (+2.50 Dsph/-6.00 Dcylx 1300, +3.00 Dsph N6), 4 years after the resuturing with a clear corneal graft showing mild interface scarring and a stable intraocular lens. BCVA with scleral contact lens was 20/20 in right eye and 20/30 in the left eye. Anterior segment ocular coherence tomography (ASOCT) done at the last visit showed well-apposed graft with central corneal thickness of 620 μm [].
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Posttraumatic deep anterior lamellar keratoplasty dehiscence: Descemet's resistance
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As a clinical title specialist, your goal is to synthesize the key elements of this case report
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This case report was confirmed by the patient and the patient signed the informed consent form, A 16-year-old female visited our clinic complaining about progressive neck pain and left arm abduction weakness (grade III) over the past 2 years. She was examined by plain X-ray, three-dimensional (3D)-computed tomography, magnetic resonance imaging, and vertebral artery angiogram. The analyses indicated a calcified extradural mass with a size of about 3 cm×2.4 cm, ill-defined, compressing the cord in the C3–4 portion, and extending into the neural foramen with eroded vertebral body. A vertebral angiography showed a left side hypoplastic vertebral artery ().\nThere was no evidence of family history and long bone deformities revealing the multiple hereditary exostosis.\nThe tumor was successfully excised using a modified combined anterior oblique and posterior approach. In this approach, the extraforaminal portion of the tumor was first removed through the anterior oblique approach. For this, the patient’s body including the neck was tilted to the right side for a proper surgical view to avoid vertebral artery injury using an intraoperative doppler. In the second part, the intracanal portion of the tumor was removed via a posterior approach with C3/C4 laminoplasty under intraoperative neuro-monitoring (). The tumor showed a dark-red colored leather-like consistency with some calcification.\nA histopathologic study of the resected material showed a cartilaginous cap and an underlying bone with enchondral ossification. The cartilaginous cap demonstrated chondrocytes without cytologic atypia comparable with osteochondroma ().\nPostoperative, the symptoms of the female were improved. Clinical and radiological assessments were performed in the 5 years after the operation. Clinically, she was symptom-free and there was neither a spinal instability nor kyphosis or tumor recurrence in the imaging studies ().
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Solitary Osteochondroma Presenting as a Dumbbell Tumor Compressing the Cervical Spinal Cord
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Your role is to provide a brief, accurate title of this medical case report
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A 14-year-old female presented to the family physician for paleness. She had menorrhagia without complaints of abdominal pain or fatigue. She was the second of three children of healthy, non-consanguineous Bulgarian-Belgian parents. Medical history and family history were unremarkable, except that her sister and mother also suffered from menorrhagia. Physical examination revealed normal parameters and besides paleness no clinical abnormalities. The blood test showed severe microcytic anemia (Hb 6.7 g/dL, MCV 62 fL) and mild thrombocytopenia (platelets 87×10E9/L) with low ferritin (2 ng/mL). Additional blood work, including folic acid, vitamin B12, coagulation tests, and hemoglobin electrophoresis, was normal. Serology for cytomegalovirus, Epstein-Barr virus, and parvovirus did not show any active disease. Oral iron medication was started (6 mg/kg/daily) and the platelet count improved quickly. On D27 after the start of oral iron treatment, the hemoglobin did not show any improvement, therefore, a red blood transfusion was given, and oral anti-conceptive medication was added. Her hemoglobin recuperated to normal levels.
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Thrombocytopenia in severe iron deficiency anemia in children
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You are tasked with extracting and summarizing the essential information from this case report
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A 42-year-old woman presented with a right breast lump, lower back pain, loss of height, marked kyphosis and hepatomegaly. Core biopsies from the breast lump showed ductal carcinoma in situ (sample labelled P1.1; and ). An additional biopsy from an ipsilateral axillary lymph node (P1.2) revealed metastatic ductal adenocarcinoma (ER+ (8/8) and HER2+ (3+)). Computed tomography scan revealed widespread metastatic disease in bones, pleura and liver ( and ). The patient was started on treatment with trastuzumab and taxane-based chemotherapy, with a significant partial response (). After induction chemotherapy, she was maintained on tamoxifen and trastuzumab. After 19 months on treatment, she presented with seizures and head computed tomography revealed a large metastasis in the left frontal lobe (), which was resected (M2.1). Therapy with tamoxifen and trastuzumab was continued and collection of plasma samples was initiated (samples T1–T9). Four months after surgery, she had enlarging liver lesions and a new metastatic deposit in the left ovary (). Treatment was switched to a combination of lapatinib and capecitabine, resulting in stable disease for 12 months (). General deterioration then occurred, with disease progression in the chest (new pulmonary nodules, bilateral pleural effusions and posterior chest wall mass, ; Eastern Cooperative Oncology Group performance status 2–3). Treatment was stopped and the patient died ∼4 months later.\nTumour samples were obtained at diagnosis from the primary breast site (P1.1) and an axillary lymph node (P1.2); after 19 months from the brain metastasis area (M2.1); and at autopsy after 3 years on treatment (from the primary breast site, and from metastatic deposits in the chest, liver, ovary and vertebrae, labelled P3.1 and M3.1–M3.4, respectively). Serial plasma samples were obtained over the last 500 days of clinical follow-up (T1–T9). Tumour and plasma samples collected and the clinical course are summarized in .
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Multifocal clonal evolution characterized using circulating tumour DNA in a case of metastatic breast cancer
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You are to provide a brief yet comprehensive title of this case report
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Case C-II-1 (upper panel in ), a 3-year-old male with DD and congenital agenesis of the radius noted at birth, was referred for genetic diagnosis. The pregnancy was uneventful, and his parents are both healthy and non-consanguineous. During pregnancy, there was no exposure to drugs, alcohol, or tobacco. He was born at 39 + 5 weeks via normal spontaneous delivery, and his birth weight was 2590 g. After the birth, he revealed congenital agenesis radius and hypoplastic carpal bones of both forearms. He exhibited torticollis, and a neck sonogram identified sternocleidomastoid muscle thickening. An echocardiogram showed a known cause of cardiac murmur and showed an atrial septal defect (type: ostium secundum). The atrial septal defect was closed 4 weeks after the birth. Special evaluation for skeletal dysplasia including laboratory tests and imaging was within the normal range. We examined him using the Bayley-III scale at the age of 39 months and found global DD (cognitive, motor, and language developmental ages: 19–22 months, 23–26 months, and 15–19 months, respectively). He had fine motor impairment in throwing a small ball, stacking small blocks, and making a mark on paper with a crayon at 42 months. His body weight was 13.5 kg (3rd percentile), height was 100 cm (10 to 25th percentile), and head circumference was 48.5 cm (10th percentile) at age 4. He attended additional education programs, including speech therapy, fine motor exercise, and social skill training. The boy inherited the 15q11.2 BP1–BP2 deletion from his unaffected mother. His sister (age of 32 months) also has this deletion, but is phenotypically unaffected ().
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Phenotypic Diversity of 15q11.2 BP1–BP2 Deletion in Three Korean Families with Development Delay and/or Intellectual Disability: A Case Series and Literature Review
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Your task is to summarize this medical case report into a title
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A 53-year-old Caucasian woman presented to eye casualty with a 6-week history of gradual worsening of vision of her left eye. The Snellen best-corrected VA (BCVA) of the right eye was 6/18 (unaided) improving to 6/9 (pinhole), whereas the BCVA of the left eye was 6/24 (unaided) but no improvement through pinhole. The intraocular pressure (IOP) was 16 mmHg in both eyes. There was no ocular history of surgery, but a history of left orbital fracture after a car accident was reported. There was no significant family history of ophthalmic disease. Anterior segment examination did not reveal any significant findings apart from dry eyes and a small meibomian cyst of the left eye. Both eyes were phakic with no cataracts. Dilated fundal examination showed an ODP in the left eye accompanied by some macular abnormality. An OCT scan was carried out illustrating a serous macular detachment of the symptomatic eye []. No pathological findings of the fellow retina were detected. Four weeks after the initial assessment, BCVA of the left eye was 2/60, improving to 6/60 (pinhole). Fundoscopy of the affected eye showed a significant maculopathy with subretinal fluid. A left pars plana vitrectomy (PPV) combined with inner retinal fenestration, endolaser, and perfluoropropane (C3F8) gas tamponade was performed. Facedown posture was adopted postoperatively for a week. There were no complications reported from the surgery. Two months following the surgery, her BCVA improved to 6/36. On clinical examination and imaging, the central fovea was flat with substantially reduced subretinal fluid in the macular area []. Six months postoperatively, the BCVA continued to improve to 6/12. OCT scan illustrated a significant regression of subretinal fluid, while the fovea was clear of fluid []. On her last visit, unaided VA was 6/6 and 6/9 in the right and left eyes, respectively.
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Optic Disc Pit Maculopathy – Case Series, Clinical Approach, and Management
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Your role is to extract the core information from this case report
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Our patient was a three-year-old previously healthy African American male, with history of intermittent asthma, eczema, and intermittent constipation. He presented to the emergency department with hematemesis and melena. He had no surgical history other than a circumcision in infancy. The only medications he took were Ibuprofen, approximately twice monthly, and an albuterol inhaler as needed. His mother denied any ingestions, chemicals or foreign bodies, or previous history of hematemesis. There were no known significant GI conditions within the family.\nOn the morning of admission, the patient woke up with diffuse abdominal pain and subsequent emesis containing multiple blood clots. Upon arrival, his weight and height were 15 kg and 94 cm, respectively. His vital signs were within normal limits for age, and he was afebrile. Upon physical exam, he was in no acute distress, with moist mucus membranes, no respiratory distress or cardiac abnormalities. He did not have any abnormal skin findings or signs of bleeding. His initial laboratory studies included white blood cell count of 11.1×103/µL, hemoglobin 9.6 g/dL, hematocrit 27.6%, mean corpuscular volume 78.1 fL, platelets 307×103/µL, prothrombin time 13.9, international normalized ratio 1.07, partial thromboplastin time 27.5.\nTherapeutic endoscopy was performed in an endoscopy unit in a free standing children's hospital (Johns Hopkins All Children's Hospital) with anesthesiologist administered intravenous propofol. Endoscopy revealed clotted blood and debris consistent with recent bleeding. Inspection of the stomach body revealed four individual lesions that appeared to be Dieulafoy in origin. The lesions were injected with 1:10,000 epinephrine; the first identified lesion was injected with 2 mL, and subsequent lesions with 0.1 to 0.3 mL aliquots (, , ). Elective endo-clipping was not performed at that session due to adequate hemostasis.\nLater that evening, he had a subsequent episode of hematemesis with a low-grade fever. His hemoglobin decreased to 6.9 mg/dL, and he received a packed red blood cell transfusion. Repeat endoscopy showed no active bleeding. The four previously injected lesions were easily visualized; therefore, the endoscopist did not provide further hemostatic therapy. Hematemesis was felt to be related to old blood. The patient was discharged home and prescribed sucralfate every 8 hours, ranitidine twice daily, and lactulose as needed for constipation.\nHe was seen in clinic two weeks after discharge and appeared to be doing well with no further complaints of nausea, vomiting, or abdominal pain. The patient subsequently had recurrent non-bloody emesis four months after his hospitalization with simultaneous fecal retention and constipation. The patient underwent a bowel clean out with lactulose and esophagogastroduodenoscopy was negative for GI bleeding.
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Three Year Old Male with Multiple Dieulafoy Lesions Treated with Epinephrine Injections via Therapeutic Endoscopy
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You are required to condense this medical case report into a title
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A 35-year-old female patient was presented with a right elbow joint pain and swelling for a duration of six months. The patient's blood investigation revealed elevated C-reactive protein (60 mg/ml) and diagnosed to have rheumatoid arthritis. The patient was treated with anti-rheumatoid drugs and had no symptom relief. The patient was referred for three phase bone scintigraphy and radiosynovectomy. Perfusion phase images [] demonstrates increased perfusion in the right elbow joint and blood pool images [] shows increased blood pooling consistent with synovitis. Whole body images [] showed increased uptake in the right elbow joint. The patient was then administered intraarticular injection of Lu-177 HA and images of the elbow joint was acquired in a dual head gamma camera (Siemens Symbia True point) in high energy general purpose collimator with multiple windows of 113 Kev and 208 Kev. Lu 177 HA images [] showed good distribution of tracer in the elbow joint. Her elbow was immobilized for 48 hours. She is on follow-up.
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Radiosynovectomy of the elbow joint synovitis in rheumatoid arthritis treated with Lutetium - 177 labeled hydroxylapatite (Lu-177 HA) particulates; first case report and image of Lu -177 HA in the elbow joint
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You are tasked with extracting and summarizing the essential information from this case report
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A 48-year-old HIV-positive white male was admitted in our proctology outpatient clinic due to proctorrhagia arisen a few weeks before. Digital rectal examination revealed a palpable mass extended for 3 cm on the right-anterior wall of the rectum, 5 cm away from the anal verge.\nInvestigating patient's clinical history and his sexual preferences, we knew he had no relevant medical history, had an ongoing homosexual relationship, and denied recent unsafe sexual behaviour.\nAn urgent colonoscopy was arranged and confirmed a single large ulcerated lesion, occupying one-third of the visceral circumference; biopsy specimens were sent for histological analysis.\nThe patient underwent a complete staging in the suspect of rectal malignancy; the computed tomography was negative for metastases to thoracic and abdominal parenchymal organs. The MRI showed a pathological, 2 cm deep thickening of the rectal wall, starting at 4 cm from the anal verge and extended proximally for about 6 cm, with a possible infiltrative behaviour to the mesorectal fat and significant postcontrast signal enhancement but no hyper intensity in the diffusion-weighted images (b = 800, 1000); two centimetric lymphadenopathies were also identified in the perirectal fat, a possible expression of nodal metastases. A Positron Emission Tomography reported a focal [F-18]FDG accumulation in the rectal wall, expression of a lesion with high glucose metabolism, and in five spots in the mesorectal space, suggestive for nodal spread.\nAt last a transanal ultrasound was performed and documented a uT3 level of invasion and an N+ involvement, without involvement of levator ani muscle.\nNo evidence of neoplastic cells was found in bioptic specimen; subsequently the patient underwent two more endoscopic procedures with extensive sampling of the ulcerated lesion, always obtaining the result of a chronic inflammatory process, with a negative research for HSV 1/2, CMV, and HHV-8 antigens.\nOnly at this point the patient was screened for genitourinary infectious diseases; he was positive for syphilis on serological testing, and Warthin-Starry stain allowed direct visualization of spirochetes on biopsy specimen; thus diagnosis of rectal syphilitic ulcer was made.\nThe patient was then addressed to the Infectious Diseases Division where he was treated with 2.4 mega units of Benzathine Penicillin with subsequent complete remission of the disease.
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The Great Pretender: Rectal Syphilis Mimic a Cancer
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Summarize this medical case report, ensuring to cover the initial presentation
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A 55-year-old woman with triple negative invasive ductal breast cancer, who achieved remission 10 years ago presented with progressive weakness. She was found to have relapsed disease involving the liver, lung, and bone (vertebral, acetabulum, and ilium) 1 year ago (), and subsequently received chemotherapy including palbociclib, nivolumab, and abraxane as well as 4 monthly doses of zoledronate, followed by 10 monthly treatments of denosumab. She last received bone-stimulating therapy and chemotherapy 3 months prior to admission. She had no other comorbidities, nor a history of additional medications or herbal supplements. She was a lifetime nonsmoker. She was admitted for obstructive jaundice due to progression of disease. During the course of her admission, she complained of severe lower extremity bone pain limiting ambulation. Prior to admission, the patient’s electrolytes were within normal limits.\nUpon admission, she was cachectic (body mass index < 18), with hypophosphatemia of 1.6 mmol/L (2.5 – 4.5 mmol/L). Nephrology was called for further evaluation. Remainder of lab studies are shown in and include a normal corrected calcium of 9.5 mmol/L (8.5 – 10.5 mmol/L), low 25-hydroxyvitamin D of 15 ng/dL (20 – 50 ng/dL), elevated PTH of 287.3 pg/mL (12 – 88 pg/mL), and elevated ALP of 635 U/L (≤ 130U/L). FePhos was 78% (< 5 – 10%), consistent with phosphate wasting. Of note, 1,25-dihydroxyvitamin D was elevated at 83 pg/mL (20 – 50 pg/mL) despite not being on calcitriol.\nGiven elevated urine phosphate, an oncologic osteomalacia was suspected and FGF23 was checked and was elevated at 548 (< 180) RU/mL. Due to aggressive supplementation, serum phosphate increased to a peak value of 3.8 mmol/L; PTH decreased to 44, but FGF23 and FePhos remained elevated at 424 and 72%, respectively. The patient continued to decline and passed away within 2 weeks.
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Hypophosphatemia and FGF23 tumor-induced osteomalacia in two cases of metastatic breast cancer
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You are required to condense this medical case report into a title
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A 34-year-old asymptomatic man was found to have an ampullary adenoma with a normal biliopancreatic duct on ERCP. EP was performed using a reported method., After the excision was completed, a 5 Fr, 9-cm Geenen PD stent was placed immediately and the distal end protruded into the duodenum. After taking up the resected specimen, the PD stent was not seen in the duodenum. Fluoroscopy confirmed that the stent had migrated into the proximal duct. Several attempts to retrieve the stent via the papillae using a rat-tooth forceps, snare, or basket were unsuccessful. The next day, we performed ERCP to retrieve the proximally migrated PD stent. The migrated stent was removed successfully with a minisnare (Soft AcuSnare; Wilson-Cook). Unfortunately, the patient developed severe pancreatitis and required hospitalization for 1 month to recover from the postprocedure pancreatitis.
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Wire-Guided Endoscopic Snare Retrieval of Proximally Migrated Pancreatic Stents after Endoscopic Papillectomy for Ampullary Adenoma
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Your objective is to distill this medical case report into a succinct title
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A 34-year-old man presented with intermittent right flank pain for 6 months. Preliminary ultrasound for suspected calculus disease showed right hydroureteronephrosis with a dilated proximal ureter but no evidence of calculi. Excretory urography showed right-sided grade 4 hydroureteronephrosis, the ureter being dilated up to the L4 vertebral level, with a tapered segment seen coursing superiomedially. A diagnosis of circumcaval ureter was suggested, and MRU was performed. MRU showed grade 4 hydronephrosis with the medialized segment of the ureter coursing around the IVC, and axial sections clearly depicted the anatomy [].
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Appearances of the circumcaval ureter on excretory urography and MR urography: A single-center case series
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Your role is to extract the core information from this case report
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An 18-year-old male patient was admitted to our institution with principal complaints of short stature, prepubertal sexual maturation, and exertional dyspnea, for 1 year. He was severely anemic, with a hemoglobin level of 3.3 g/dL. He had a history of small bowel resection from 50 cm below the Treitz ligament to 5 cm above the ileocecal valve, necessitated by midgut volvulus in the neonatal period. No other abnormal congenital or genetic condition was detected. After surgery he experienced short bowel syndrome (SBS) as a sequela, and total parenteral nutrition had been supplied, which was gradually replaced by enteral feeding. Chronic abdominal pain, intermittent diarrhea, and vomiting had persisted for several years but eventually improved. At 4 years of age, his feeding mode was entirely enteral, and he was lost to follow-up until his recent visit. His family history was unremarkable. He denied use of any abusive substance and was not sexually active.\nReview of system on admission revealed long-lasting dizziness and dyspnea on exertion, and these symptoms had become aggravated in the past year. He also complained of early satiety during meals, but denied gastrointestinal symptoms such as abdominal pain, constipation, or diarrhea.\nOn physical examination, he was alert, but chronically ill-looking and very pale. His blood pressure was 113/77 mmHg, his pulse rate 95/min, his respiratory rate 20/min, and his body temperature 36.1℃. His height was 137.7 cm (below the 3rd percentile for his age) and his weight 28.9 kg (also below the 3rd percentile for his age). His pubic hair was of Tanner stage I, as was his genital development (testis volume <4 mL). Other physical and neurologic examination findings were unremarkable.\nThe results of initial laboratory studies are listed in . The complete blood count showed hemoglobin of 3.3 g/dL, hematocrit of 12.5%, mean corpuscular volume (MCV) of 86.2 fl, mean corpuscular hemoglobin (MCH) of 22.8 pg, red cell distribution width (RDW) of 22.2%, and reticulocyte count of 0.59% (reticulocyte production index 0.16). The white blood cell count was 4,900/mm3 with a differential count of 45% neutrophils, 47% lymphocytes, 7% monocytes, and 1% eosinophils. The platelet count was 182,000/mm3. Serum iron was 23 µg/dL (normal 50-170 µg/dL), TIBC was 534 µg/dL (normal 280-400 µg/dL), and serum ferritin was 2.5 ng/mL (normal 20-320 ng/mL). Serum vitamin B12 was 60 pg/mL (normal 211-911 pg/mL) and serum folic acid was 11.3 ng/mL (normal >5.4 ng/mL). Peripheral blood cell morphology () showed normocytic hypochromic anemia, marked anisocytosis, mild poikilocytosis, hypersegmented neutrophils, and mild thrombocytopenia. Bone marrow aspiration and biopsy revealed normal cellularity (90%) with an myeloid : erythroid (M : E) ratio of 2:1. Dyserythropoiesis, including changes in megaloblastoid levels, decreased amounts of hemosiderin particles, and sideroblasts, were also found. The cytogenetic study revealed a normal 46,XY karyotype. Because our patient was of short stature and was sexually underdeveloped, we performed a hormonal evaluation. Luteinizing hormone (LH) and follicular stimulating hormone (FSH) levels were 3.1 mIU/mL (normal 1.5-9.0 mIU/mL) and 2.0 mIU/mL (normal 2.0-9.2 mIU/mL) respectively, both of which were at prepubertal levels. Testosterone was 0.34 ng/mL (normal 3.5-9.7 ng/mL), insulin-like growth factor-1 (IGF-1) 83.6 ng/mL (normal 239-630 ng/mL), and insulin-like growth factor binding protein (IGFBP-1) 3,565 ng/mL (normal 1,820-6,990 ng/mL). On simple chest radiography, the heart size was normal. Bone age was about 12 years by wrist x-ray (). Bone mineral density (BMD) measured by dual energy x-ray absorptiometry was very low, and the Z score (with respect to bone age) of the BMD of the lumbar spine was -3.9.\nBased on these findings, the patient was diagnosed with anemia caused by a combined vitamin B12 and iron deficiency attributable to impaired absorption caused by SBS. Parenteral vitamin B12 and iron treatment was initiated. Vitamin B12, as cobalamin, was administrated via intramuscular injection of 100 µg daily for 14 days, followed by 50 µg every other week. Our patient was also given 3 mg/kg elemental iron (ferric form) intravenously every other day for 14 days, followed by the same dose weekly. He was initially placed on a high potassium diet to avoid the transient hypokalemia that could result from rapid erythropoiesis.\nThe hematologic indices responded immediately to therapy (). The reticulocyte count peaked at 14.9% on the 6th day of parenteral vitamin B12 and iron therapy. Ten days after treatment began, the hemoglobin concentration had increased to 7.7 g/dL, the hematocrit to 29.2%, vitamin B12 to 1,389 pg/mL, and serum iron to 47 µg/dL. He was discharged on the 10th day after admission with improvement in his dizziness and exertional dyspnea. After discharge, he was maintained on parenteral vitamin B12 and iron supplementation in the outpatient clinic. At 3 months after discharge, his hemoglobin level and hematocrit were 12.3 g/dL and 39%, respectively. Treatment was maintained for 17 months and the level of hemoglobin stabilized at around 12 g/dL. Two years after treatment began, the patient's weight and height had increased to 42.3 kg and 154.2 cm (below the 3rd percentile for his age). He has also attained puberty, with Tanner stage 4 pubic hair and a testicular volume of more than 10 mL.
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A case of anemia caused by combined vitamin B12 and iron deficiency manifesting as short stature and delayed puberty
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Your role is to provide a brief, accurate title of this medical case report
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A 56-year-old male presented to the emergency department of a regional hospital with a 5-day history of headache and dysarthria. On examination, mild asymmetry of his lower face was appreciable, with the remainder of the physical examination being unremarkable apart from a large ventral hernia palpable on abdominal examination. He had a past medical history of type 2 diabetes mellitus, hypertension, hypercholesterolaemia, chronic obstructive pulmonary disease, gastro-oesophageal reflux disease, past hepatitis C infection, and depression. His surgical history was significant with a laparoscopic cholecystectomy 7 years prior, complicated by a bile leak and intra-abdominal sepsis requiring laparotomy and washout, and a subsequent large ventral hernia. He had a significant smoking history of approximately 50 years along with intermittent cannabis use, and a previous history of intravenous drug use 20 years prior to presentation.\nA non-contrast brain computed tomography (CT) in the emergency department demonstrated a large area of low density in the right frontoparietal region, with subsequent brain MRI revealing a rounded subcortical enhancing lesion in the right precentral gyrus with surrounding vasogenic oedema.\nA CT of the chest, abdomen and pelvis demonstrated a 6.5-cm mass in the left upper zone medially with streaky surrounding inflammatory changes in the thorax, along with several enlarged mediastinal and periportal lymph nodes. Staging FDG PET/CT revealed an area of photopenia involving the right cerebral cortex in association with a hypodensity on the low-dose CT scan due to the known brain metastasis. He had an intensely avid (SUVmax 10.3) large mass in the left upper lobe, with heterogenous distribution of tracer with a central area of photopenia suggestive of central necrosis, as indicated by the green arrow in Figure . There were multiple FDG-avid mediastinal, supraclavicular, and peri-portal lymph nodes, as well as an FDG-avid left adrenal mass. An intense area of FDG avidity in the distal duodenal (D2) region (SUVmax 11.8) was identified as indicated by the blue arrow in Figure . The patient had no symptoms attributable to the duodenal mass at the time of the FDG PET/CT scan.\nThe patient was commenced on regular dexamethasone 4 mg and a proton pump inhibitor and subsequently underwent a right frontal lobe biopsy under stereotactic guidance. Histopathology of the brain metastasis demonstrated a metastatic tumour with solid sheets of malignant cells with atypical nuclei, eosinophilic cytoplasm, and frequent mitosis. Immunohistochemistry showed the tumour cells were positive for CK7 and TTF-1, consistent with a metastatic adenocarcinoma from a primary lung tumour. There was no targetable mutation detected in exon 19–21 of the epithelial growth factor receptor (EGFR) gene, and ALK, ROS-1, and BRAF immunohistochemistry were negative. Expression of the programmed cell death ligand-1 (PD-L1) was high (>95%), suggesting sensitivity to immunotherapy with checkpoint inhibitors.\nThe patient underwent gastroscopy to investigate the FDG-avid duodenal lesion, which demonstrated a large semi-circumferential stenosing lesion in the second part of the duodenum, with ampullary orifice not visualised (Fig. ). Endoscopic ultrasound showed significant peri-portal and peri-pancreatic lymphadenopathy, and a suspicious left adrenal gland nodule, confirming the finding of the PET scan. Biopsy of the duodenal mass demonstrated a TTF-1-positive adenocarcinoma consistent with metastatic lung adenocarcinoma and concordant with the resected brain metastasis.\nThe patient was discharged with the intention for treatment with post-operative cranial radiation and immunotherapy with pembrolizumab. He subsequently presented to the emergency department 12 days post initial discharge with a 4-day history of abdominal pain, dark urine, nausea, vomiting, and was jaundiced on clinical assessment. His liver function tests had become deranged in a predominately cholestatic pattern. Bilirubin was 74 μmol/L, lipase was 654 U/L, alkaline phosphatase (ALP) 427 U/L, gamma-glutamyl transferase (GGT) 671 U/L, alanine aminotransferase (ALT) 279 U/L, and aspartate aminotransferase (AST) 108 U/L. Abdominal CT demonstrated low-grade biliary dilatation due to the rapid increase in the size of the duodenal lesion. Inpatient duodenoscopy revealed a large fungating mass involving the ampulla of the duodenum with the bulk of the mass at the biliary orifice (Fig. ), and ERCP demonstrated extrinsic compression of the CBD with extrahepatic bile duct dilatation with tapering to the level of the ampullary tumour involvement, requiring the insertion of a distal CBD fully uncovered metal stent (Fig. ).\nThe patient had an unremarkable admission after distal CBD metal stent insertion and was discharged without complications. His bilirubin normalised on discharge with corresponding improvement of other liver function tests. The increase in the duodenal mass was deemed most likely due to disease flare at the commencement of immunotherapy, so he was continued on pembrolizumab. At the time of submission, he has completed cranial radiotherapy and 36 weeks of immunotherapy with progression imaging demonstrating an ongoing treatment response.
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Pancreatitis and Biliary Obstruction Secondary to Duodenal Metastasis from Rapidly Progressing Lung Adenocarcinoma Treated with Common Bile Duct Stenting
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Your objective is to distill this medical case report into a succinct title
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A 53-year-old Caucasian woman was referred to our institution because of the suspicion of peritoneal carcinomatosis, raised by the findings of ascites at a transvaginal ultrasound performed as a yearly routine exam; a pre-surgical staging exam with computed tomography (CT) scan show thickening of the gastric walls, multiple omental nodules and ascites ().\nHer previous personal history was unremarkable and she denied any clinical symptom or cancer history.\nAt our hospital, she underwent an esophagogastroduodenoscopy and colonoscopy, with results negative for gastric/colon cancer.\nHer comprehensive metabolic profile revealed mild liver dysfunction with an alanine transaminase of 77 U/L and aspartate transaminase of 71 U/L. When tumour markers were assessed, CA125 demonstrated increased levels of 290 U/mL (normal values <35 U/mL), whereas carcinoembryonic antigen, CA 19.9 and other immunohistochemical markers were within the normal ranges. Serological assessment of HIV, hepatitis C virus and hepatitis B virus were negative.\nTen days later, the patient underwent an ultrasound-guided biopsy () with a diagnosis of suspicious carcinoma from the an unknown primary site.\nAfter 2 weeks, the patient received a CT scan of the thorax (to complete pre-operative staging), demonstrating a spontaneous (with no therapy) dimensional and numerical reduction of peritoneal lesions in the upper abdomen, partially included in the chest CT scan, as well as resolution of peri-hepatic and peri-splenic ascites ().\nSince there was no evidence of primary cancer at pre-operative examinations and the second CT scan revealed a partial resolution of peritoneal implants and ascites without therapy, the suspicion of an infectious disease was raised.\nThe pathological evaluation of the biopsies performed on the omentum and peritoneum revealed the presence of lymphoid aggregates with a central core of epithelioid cells with large eosinophilic cytoplasm, without atypia or mitosis () and with no immunohistochemical marker of oncologic malignancy. Due to the presence of necrotic nodules with histiocytes and giant cells, a Ziehl–Neelsen stain was performed to identify bacilli (), whose presence was then confirmed with molecular assays.\nBecause of the uncertain result of the biopsy and the conflicting results of the 2 CT scans, in order to rule out malignancy with certainty, the patient underwent a laparoscopic surgery in 2 weeks.\nDefinitive histological diagnosis excluded the presence of malignant cells and reported a necrotising inflammation caused by non-tuberculous mycobacteria. Hence, the patient was sent to a hospital with expertise in infectious diseases.\nA follow-up CT scan performed 1 year later confirmed a complete recovery of peritoneal findings.
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A cancer-mimicking diagnosis of peritoneal carcinosis: report of a case of abdominal non-tuberculous mycobacterial infection
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Your task is to provide an accurate and brief title of this case report
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Α 78-year-old man was referred to our hospital for hematemesis and melena. The patient had undergone a partial gastrectomy with Billroth II gastroenterostomy because of duodenal ulcer disease 30 years ago. His history, however, included splenectomy caused by trauma, cholecystectomy, and hypertension. His physical exam and blood tests were unremarkable except for the presence of a normocromic anemia. He underwent an upper-gastrointestinal endoscopy, which identified a sizable ulcer crater at the beginning of the efferent jejunal loop, about 4 cm from the anastomosis, with unsuccessful attempts of permanent hemostasis. A laparotomy was decided upon. A large tumor of the efferent jejunal loop was identified with multiple small infiltrations in the afferent loop of 15-20 cm. The rest of the small intestine was free. The Helicobacter pylori examination was positive. A segmental resection of the gastric pouch and the infiltrated jejunal loops was performed, followed by a Roux-en-Y reconstruction.\nOn histopathologic examination, the reported ulcer was part of a grayish intramural lesion that infiltrated the entire wall of the intestine. Microscopically, large undifferentiated neoplastic cells were widely disseminated. The cells contained a moderate amount of cytoplasm and sizable, oval, frequently irregular pleomorphic nuclei with multiple prominent nucleoli. Binucleate, abnormal multinucleate, and multilobed nuclei formats were observed (Figure ). By immunohistochemistry, the large cells were strongly positive for CD30. They were also positive for vimentin, epithelial membrane antigen (EMA), CD7, CD43, and MUM1. Partial positivity was for the antigens CD138, p53, CD38, CD45RO (LCA), perforin, and AE1/AE3 (cytokeratin). The large cells were negative for the expression of CD2, CD3, CD5, CD4, CD8, ALK, CD56, CD20, CD79a, PAX5, CD45RA, TIA1, CD15, myeloperoxidase (MPO), lysozyme, and EBV-LMP1.\nThe findings are consistent with anaplastic large cell lymphoma (ALCL) ALK-negative (anaplastic lymphoma kinase), a rare type of non-Hodgkin lymphoma. The resection boundaries were free of neoplastic infiltration, and no lymph node involvement (17 in total) was found. The patient has been referred to the hematology department for further treatment and follow-up.
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Atypical anastomotic malignancies of small bowel after subtotal gastrectomy with Billorth II gastroenterostomy for peptic ulcer: Report of three cases and review of the literature
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You are required to deliver a compact title of this case report, outlining the significant findings
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The third patient is a 48-year-old woman who presented with about three months of back pain. CRP and ESR were 4.16 mg/dL and 115 mm/h, respectively (the indices have changed with the development and improvement of the fistula). Infectious spondylitis on T8–9 with paravertebral abscesses was confirmed on the MRI, and the result of the percutaneous needle biopsy showed positive AFB, PCR, and caseation necrosis, finally confirmed as tuberculous spondylitis. At the same time, active pulmonary TB was also confirmed and anti-TB medication therapy (daily isoniazid, rifampicin, pyrazinamide, and ethambutol for initial two-month, followed by a ten-month daily isoniazid, rifampicin, and ethambutol) started. Afterwards, a fistula was formed along the biopsy tract between deep lesion and skin, which resulted in repeated wound debridement and closure. Discontinuation of anti-TB medication therapy was considered after 12-month, because there were improvements in the pulmonary lesions and overall clinical features with healing of fistula. However, PET/MRI at 12-month anti-TB medication therapy showed sustained abscesses around the paravertebral space with intra-abscess SUVmax (from 6.67 to 7.02) even though decreased bone marrow edema and epidural abscess compared with PET/MRI at diagnosis (Fig. ). After additional three months of anti-TB medication, the leak of the tuberculous abscess through the fistula developed again. However, there was no drug resistance on DST of the pus through the repeated fistula.\nCulture-based phenotypic DST and GenoType MTBDRplus (a reverse hybridization line probe assay, Hain Lifesciences, Nehren Germany) are performed on the samples positive for M. tuberculosis. Phenotypic DST will be determined by the absolute concentration method using Lowenstein-Jensen media as recommended by WHO [] at the supranational reference laboratory. The drugs and their critical concentrations for resistance in the patients are as follows: isoniazid 0.2 μg/mL, rifampin 40 μg/mL, and ethambutol 2.0 μg/mL. Pyrazinamide susceptibility was determined by a pyrazinamide test [].\nClinical characteristics and assessment for therapeutic response of the patients are summarized in Table .
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Simultaneous 18F-FDG PET/MRI in tuberculous spondylitis: an independent method for assessing therapeutic response - case series
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You are to provide a brief yet comprehensive title of this case report
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A 54-year-old man with biopsy-proven IgA nephropathy on peritoneal dialysis (PD) presented with a complaint of abdominal pain similar to previous episodes of peritonitis. Consequent to persistent emesis and volume depletion, he was admitted to the hospital. He had had outpatient treatment for four episodes of peritonitis over the past 5 years; the last, culture positive for Citrobacter koseri, 18 months prior to admission.\nHe initiated PD in June 1997, but received a kidney transplant with a donor kidney from his brother 6 months later. In January 2005, he returned to PD due to chronic rejection and failure of his transplant kidney. After 3 years on PD, he underwent bilateral nephrectomy in March 2008, for persisting nausea and bilateral flank pain. A clear cell renal carcinoma (Stage T1, N0, Mx) was discovered in the right kidney and the left kidney had multicystic changes. Post-operatively, he was treated with hemodialysis via a tunneled dialysis catheter for 8 months when a peritoneal catheter was reinserted. He returned to PD in January 2009.\nIn July 2011, the index admission, his temperature was 96.7° with a peripheral white blood cell count (WBC) of 15,700/mm3 (normal differential count) and PD effluent cell count of 5,680/mm3 (a majority of neutrophils) (). A CT scan of the abdomen () demonstrated freely communicating intra-abdominal fluid and initial fluid samples grew Pseudomonas aeruginosa. Initial and subsequent therapy were not accomplished according to guidelines []. The patient was treated only with intra-peritoneal tobramycin (0.6 mg/kg/d), but experienced rapid resolution of his pain, clearing of fluid leukocytosis, and he was discharged on Day 4 to continue daily instillation of tobramycin.\nRecurrence of abdominal pain and nausea led to repeat hospitalization 2 weeks later with fluid again positive for Pseudomonas aeruginosa. Despite continuation of intra-peritoneal tobramycin and addition of oral levofloxacin, persisting symptoms led to removal of the PD catheter after 4 days (). A repeat CT scan of the abdomen again showed freely communicating intra-abdominal fluid. He improved on hemodialysis with continued intravenous ceftazadime and oral levofloxacin for 4 weeks.\nAfter 15 weeks, he had another episode of abdominal pain () and at that time (), CT scan of the abdomen demonstrated compartmentalization of abdominal fluid with the development of a thick wall or “rind” encapsulating a large right abdominal fluid collection. After 2 CT-guided drainage procedures and a 6-week course of parenteral ceftazadime and oral levofloxacin, he had complete resolution of symptoms.\nThree months later, a CT scan was performed and revealed persistence of a large peri-hepatic fluid collection enclosed within the same thick wall (). Fluid obtained via percutaneous drainage of the cavity was sterile (). A final CT examination of the abdomen 6 weeks later () showed continued diminution of the fluid collection, which again was sterile. Further problems have not recurred over 12 subsequent months.
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An intra-abdominal abscess or “rind” as a consequence of peritoneal dialysis-associated pseudomonas peritonitis
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As a medical summarizer, your job is to condense this case report into its key points
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A 44-year-old female was admitted to our department because of a 3-year history of headache and a progressive worsening of right exophthalmos with a brain MRI showing a giant enhancing right temporal mass with erosion of the sphenoid greater wing and extension toward infratemporal fossa and right orbit [Figure –]. Due to the large dimensions and the invasiveness of the lesion, the patient was submitted to brain DSA with embolization of external carotid artery feeders (middle meningeal artery, accessory meningeal artery, distal sphenopalatin branches) using contour particles (150–350 micron). During the procedure, a large pseudoaneurysm of right middle cerebral artery branch was evident and embolized using Glubran2 glue [Figure –].\nNo complication after the DSA was evident. Thus, 3 days later the patient underwent tumor removal by frontotemporal-transzygomatic approach. Postoperative course was uneventful. Histological diagnosis was meningioma (World Health Organization [WHO] I). The patient is in good clinical conditions with no recurrence of meningioma at 3-year follow-up.
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The role of preoperative angiography in the management of giant meningiomas associated to vascular malformation
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As a medical summarizer, your job is to condense this case report into its key points
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In October 2011, a 30-year-old man consulted his General Practitioner complaining of prolonged diarrhoea. His past medical history was unremarkable. He was subjected to faecal, urine and blood analysis and all results were negative with the exception of a relatively high TSH (16.97 μU/mL, reference interval 0.34–5.60) while the fT4 was within the reference range. Anti-peroxidase and anti-thyroglobulin antibodies were negative. One month later, these thyroid function test results were further confirmed by two repeat analyses. The patient did not have any personal or family history of known thyroid dysfunction. There was no goitre on examination. Neck ultrasonography showed an average-sized thyroid gland and an echo structure with no obvious abnormalities, no nodules and normal vascular flow.\nDespite the fact that the patient showed no clinical signs or symptoms of hypothyroidism and the unlikely possibility (below 1%) of a young male presenting with such a medical condition , he was diagnosed with subclinical hypothyroidism and prescribed 50 micrograms of Levothyroxine per day. Surprisingly, his serum TSH level did not decrease with the treatment but, in fact, it increased steadily (), despite the fact that his Levothyroxine dose was increased progressively to 200 micrograms per day. Patient non-compliance was initially suspected, but this was discounted. To rule out intestinal malabsorption, markers for celiac disease were requested and they were all negative. He was not taking any other drugs that might have interfered with the Levothyroxine absorption. Importantly, since having been prescribed 200 micrograms of Levothyroxine per day, the patient complained of headaches and insomnia but no weight loss or palpitations.\nIn June 2012 he presented again with a persistently elevated result for TSH. To rule out Addison's disease (in which a elevated TSH values are found in some untreated patients ) a request for adrenocorticotropic hormone (ACTH) and cortisol determination was received in the laboratory, and elevated results were obtained for the ACTH. Cushing's disease (due to an ACTH secreting pituitary tumour) was excluded by a low dose dexamethasone suppression test and Addison's disease (adrenocortical insufficiency) was excluded by normal results for a short Synacthen test.\nIn January 2013, a repeat complete hormonal study was requested. Results above the upper reference limit were obtained not only for TSH and ACTH, but also for luteinising hormone (LH), follicular stimulating hormone (FSH) and prolactin (see ). As a result of the abnormal endocrine profile, several diagnostic imaging procedures were ordered to exclude the possibility of a pituitary tumour. Unfortunately, the patient missed the next scheduled clinic visit and was next seen in February 2015. Repeat endocrine profile analysis confirmed the previous results. This profile also included measurement of glycoprotein hormone alpha-subunit, which was normal. A pituitary magnetic resonance imaging (MRI) scan was also performed and this was normal.\nAt that time, a new endocrinologist (author D. A-B) reviewed the patient's clinical history. Given the persistence of discordant values between pituitary and peripheral hormones, he suspected the presence of EA in the patient sera. When questioned about possible contacts with animals, the patient confirmed that he had lived and worked on a farm during his childhood and adolescence, where he had direct contact with various animal species, including goats, sheep, cows, rabbits and pigs.
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Serum sample containing endogenous antibodies interfering with multiple hormone immunoassays. Laboratory strategies to detect interference
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You are tasked with extracting and summarizing the essential information from this case report
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A 50-year-old woman was involved in a press machine accident resulting in a crush injury to her left index finger. Almost the entire sterile matrix was lost. A thenar fascial flap was applied, and subsequent nail bed grafting was performed. At the 20-month follow-up, the new nail was graded as “excellent” ().
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Nail bed defect reconstruction using a thenar fascial flap and subsequent nail bed grafting
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Please create a concise title of this case report, focusing on critical details
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Our patient was a 51-year-old white woman from the Rif region of Morocco (Amazigh ethnicity) that presented abdominal swelling and deterioration of her general conditions three months before her visit to a general practitioner. The patient was previously diagnosed with hypertension and is currently under angiotensin-converting enzyme inhibition without any family history of hereditary cancer or other diseases. Her physical examination revealed abdominal distension and diffuse dullness with initially highly elevated cancer antigen 125 (CA-125) at 461.7 U/mL. Diagnostic imaging based on contrast-enhanced thoracoabdominal-pelvic computed tomography (TAP-CT) (Figure ) showed a left-sided ovarian mass and abundant ascites and pleurisy.\nThe patient was then referred to our department for specialized management. Given the strong suspicion of advanced ovarian cancer, ex-lap diagnostic surgery was performed. During surgery, two large bilateral ovarian masses associated with peritoneal carcinomatosis and highly abundant ascites (approximately 4 L) but without liver and spleen dissemination were found upon exploration and an omental biopsy was performed. The postoperative course was uneventful. Microscopically (Figure ), the sections examined found an omental tissue infiltrated by an undifferentiated tumor proliferation made of layers of cells with unclear cytoplasmic limits. These tumor cells have a rounded or oval nucleus with slightly mottled chromatin. Cytonuclear atypia was mild to moderate and there were few mitoses.\nImmunohistochemistry (IHC) based on 13 antibodies covering the most known possible tissue origins of tumor infiltration was used for differential diagnosis on surgical biopsy (Table ). The IHC analysis was in favor of a secondary infiltration of an achromic malignant melanoma with positive staining of HMB-45 marker (Figure ). After the surgical biopsy was performed which confirmed the melanocytic nature of the tumor according to the local pathologist, no foci of primary malignant melanoma except for the ovary were found upon dermatological examination.\nGiven the advanced disease, the patient received a combination of neoadjuvant dacarbazine (DTIC, 800 mg/m2; day 1), cisplatin (CDDP, 20 mg/m2; days 1, 2 and 3), and paclitaxel (PTX, 80 mg/m2; days 1 and 8) every three weeks. After six months of NACT, there was a decrease in the size of the known left ovarian tumor (52 × 49 mm against 91 × 77 mm) in favor of a partial tumor response (Figure -). Moreover, a complete regression of pleural effusion and peritoneal carcinomatosis and a marked decrease of CA-125 (9.19 U/mL against previous initial 461.7 U/mL) were also noted. The patient continued her treatment under NACT until the sixth cycle and she was reevaluated. TAP-CT showed a partial response (Figure ) (51 × 37 against 52 × 49 mm) without the appearance of new metastases. During the third cycle of NACT, accidental drug extravasation occurred in the left forearm and it was successfully managed with topical corticosteroids. The patient tolerated NACT well without any unanticipated adverse events that require reducing dose schedule or changes in interventions.\nFollowing the multidisciplinary tumor board meeting, total abdominal hysterectomy and bilateral salpingo-oophorectomy with cytoreductive surgery were indicated (Figure ).\nSurprisingly, the final pathological examination of all surgical specimens by an expert pathologist based on a panel of several markers was in favor of an adult granulosa cell tumor with negative HMB-45 and positive Inhibin B marker (Table ). The other tumor markers of melanoma were also negative. Adjuvant chemotherapy based on bleomycin, etoposide, and cisplatin (BEP) combination is being programmed. Our patient remains alive at the time of this case writing with 13 months of overall survival.
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A Report of a Rare Case of an Advanced Adult Granulosa Cell Tumor Initially Diagnosed as Primary Ovarian Melanoma
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You are required to condense this medical case report into a title
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A 65-year-old female consulted our office for naturopathic primary-care support for a myriad of conditions, which included diabetes with weight gain, chronic fatigue, depression with emotional lability, frequent colds, and recurrent urinary tract infections. The latter was attributed to a medullary sponge kidney as was her history of kidney stones and hypertension. The patient also suffered with long-standing acid reflux and was prone to irritable bowel with diarrhea. She had also suffered with multiple abscesses in the past as well as poor generalized wound healing. A history of fibroadenomas was also noted. The patient recollected, “never being well”, even as a child. She described her diet as a child as “deficient” and consisted mostly of canned beans and bread, which she attributed to her poor socioeconomic status as a child.\nPharmacological management of her diabetic condition included the use of metformin/sitagliptin (1,000 mg/50 mg, taken twice per day) and gliclazide (30 mg), also taken twice per day.\nAdditional medications included ramipril (5 mg/day), ranitidine (150 mg, twice per day), low-dose aspirin (81 mg/ day), hydrochlorothiazide (25 mg/day), allopurinol (100 mg/ day), citalopram (40 mg/day), and mirabegron (50 mg/day).\nPhysical examination revealed a 1.69 m (66.5 inch), 88.5 kg (195.0 lb) female. Body mass index was calculated at 31.0 (Obese Class I) (32). Central waist measurement was 112 cm, while her hips measured 118 cm. Blood pressure was 114/64 mmHg, measured at the left brachial artery. Bioimpedance analysis revealed a lean body mass of 49.9 kg (111.0 lbs) and a fat mass of 38.0 kg (84.0 lbs).\nLaboratory assessment prior to date of initial consult (June 2017) revealed a HBA1C of 7.8% and a random glucose of 6.5 mmol/L. Total cholesterol (TC) was 4.68 mmol/L, triglycerides (TG) were 2.63 mmol/L, high-density lipoproteins (HDL) was 1.04 mmol/L, low-density lipoproteins (LDL) was 2.44 mmol/L, and TC:HDL was 4.5. Alanine aminotransferase was 55 U/L, while creatinine was 79 μmol/L.
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Optimizing glycemic control in type 2 diabetic patients through the use of a low-carbohydrate, high-fat, ketogenic diet: a review of two patients in primary care
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You are required to deliver a compact title of this case report, outlining the significant findings
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An 11-year-old male patient was referred for evaluation of a swelling evolving for approximately 3 months without any painful symptoms. Clinical examination showed facial asymmetry in the middle and lower third of the face without inflammatory signs [].\nThe panoramic radiograph examination revealed a radiolucent image of an expansive, multiloculated lesion with well-defined borders that affected the body and ramus of the right mandible and displaced teeth 46 and 47 toward the basal cortex [].\nOn computed tomography examination, a solid lesion with external and internal cortical expansion and cortical thinning of the right mandibular ramus associated with 47 as well as regions with cortical discontinuity was observed. The lesion had attenuation similar to the muscles and small foci of hypoattenuation in its interior region [].\nThe differential diagnoses included solid ameloblastoma, myxoma, and AF since all were benign tumors of odontogenic origin. After incisional biopsy, the diagnosis of AF was confirmed. The patient's mother signed the consent declaration for the minor.\nThe lesion was enucleated along with teeth 46 and 47 under general anesthesia through an intraoral approach. Tooth 45 was preserved [].\nAt the 7-year follow-up, there were no signs of relapse in the clinical and radiographic examinations. Tooth 45 had been extracted by orthodontic indication. After 10 years of AF excision [], three implants were placed in the right posterior mandible region with the IANL technique.\nIn the 7-day postoperative period, the patient presented with hypoesthesia of the IAN, who was treated with low-level laser therapy sessions. Four laser therapy sessions improved 97% of the IAN hypoesthesia.\nTwelve years after the tumor excision, there were no clinical or imaging signs of recurrence of the lesion, and the implants showed osseointegration for future fixed prosthetic rehabilitation [].
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Successful Management of a Gigantic Ameloblastic Fibroma: A 12-Year Follow-up
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Your job is to distill the important information into a title from this case report
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A 36-year-old Sudanese gentleman with mild haemophilia A (F VIII :\nC level 38 iu/dl/normal range > 50 iu/dl) presented with a\nfive-week history of an atraumatic cystic swelling in the anterior\naspect of the right thigh. Clinically this cystic lesion was\ntypical of a haemophilic pseudotumour.\nOn examination there was an 8 × 10 cm mass in the\nanterior compartment of the right thigh which was tender to\npalpation.\nUltrasound scan examination revealed a large\nheterogeneous mass of mixed echotexture with a central area of\nliquefaction consistent with an intramuscular haematoma. A\nsubsequent angiogram showed no evidence of vessels\nsupplying the lesion or the presence of arteriovenous\nmalformations. MRI scanning confirmed an 18 × \n10 × 11 cm loculated cystic lesion in the anterior\ncompartment of the thigh involving the vastus intermedius and\nvastus medialis muscles. T1 weighting (T1W) demonstrated a lesion\nwith peripheral high signal (). Gradient-echo\nT2-weighted images revealed marked signal drop out centrally due\nto magnetic susceptibility artefact from altered blood products,\nusually haemosiderin (). The mass was shown to\nextend posteriorly as far as the medial cortex of the femur and\nmedially to the femoral canal (). No extension\ninto bone was seen. It was concluded that appearances were\nconsistent with those of an organising haematoma. Given the past\nmedical history, a provisional diagnosis of haemophilic\npseudotumour was made.\nStandard conservative treatment was commenced with a continuous\ninfusion of factor VIII, analgesia, and bed rest. Despite this,\nthe pain and swelling increased over the next five days and it was\ndecided to evacuate the haematoma. The haematoma was excised and\napproximately one litre of freshly clotted and organised blood was\ndrained. Haemostasis was achieved and the entire cavity packed.\nHowever, over the following seven days the swelling in the right\nthigh recurred. A further MRI scan was performed and the findings\nwere once more consistent with further haematoma formation.\nApproximately 1 litre of clotted blood was drained under\nultrasound guidance.\nSix weeks after the initial presentation the swelling recurred\nwith an overall increase in size. It was decided to perform an\nopen exploration, and a biopsy was taken of the cyst wall.\nSubsequent histology revealed poorly differentiated synovial\nsarcoma. Staging of the tumour was performed with a CT of the\nthorax which demonstrated pulmonary metastatic disease.\nThe tumour was found to be unresectable and a complete\ndisarticulation of the hip was subsequently performed. The patient\nwent on to a course of combination chemotherapy.
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Synovial Sarcoma Mimicking Haemophilic Pseudotumour
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Your task is to provide a clear and precise title of this case report
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A 45-year-old lady presented with recurrent narrow QRS short-RP tachycardia. Baseline ECG was normal with no evidence of pre-excitation. Echocardiography was unremarkable. During her electrophysiology study, Para-Hisian pacing (PHP) maneuver was performed before induction of tachycardia. Both the RV catheter and His catheter were placed at His bundle (HB) region (Appendix ). Pacing at variable output at fixed cycle length was performed from RV distal (RVD) bipole. It was started at an output of 10 mA at a pulse width of 2 ms and the output was gradually reduced till there was widening of paced QRS complex suggestive of loss of HB capture. The measurement of Stim-to-A time interval (SAT) recorded in the proximal coronary sinus (PCS was positioned at CS ostium) bipole was only 42 ms (Figure ).\nWhat is the mechanism behind such a short SAT? Is it due to inadvertent simultaneous atrial capture at the high output (hence making the maneuver uninterpretable) or could this be a genuine VA conduction suggestive of nodal VA conduction?
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Unusually short VA time during Para-His pacing maneuver: Is it a simultaneous atrial capture?
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As a clinical title specialist, your goal is to synthesize the key elements of this case report
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The patient is a 75-year-old male who with chief complaints of repeated epigastralgia and body weight loss from about one month earlier visited our hospital. In November 2009, he was admitted to our hospital for detailed examination and treatment. At time of his admission, there was no evidence of anemia and jaundice, and his abdomen was flat without any tenderness. Laboratory data were normal.\nUltrasonography and computed tomography (CT) of the abdominal region revealed that the main gallbladder was normal without any stones. A cystic structure (40.l mm × 31.3 mm × 17.3 mm) was observed in the upper region of the main gallbladder. It was filled with stones and debris ().\nMagnetic resonance cholangiopancreatography (MRCP) showed findings similar to those of ultrasonography and CT, but the communication between the cystic structure and the hepatic duct could not be defined (). By endoscopic retrograde cholangiopancreatography (ERCP) the right hepatic duct and the left hepatic duct were compressed to the left and right, respectively, and with the supplementary injection of radiopaque material an accessory gallbladder with multiple stones was visualized between the left and right hepatic duct (Figures and ).\nBy cholangiography through the endoscopic nazobiliary drainage (ENBD) tube, cystic duct and accessory gallbladder arising from left hepatic duct could be visualized (Figures and ). By positron emission computed tomography (PET-CT) a cystic structure resembling a gallbladder between the left lobe and right lobe of the liver could be visualized together with accumulation of F18-fluroradeoxyglucose (F18-FDP) (). The cause of epigastralgia could not be determined by gastroendoscopy and colonoscopy.\nBased on the foregoing findings leading to the possibility of stones and carcinoma in the accessory gallbladder, open cholecystectomy was performed in November 2009.\nFollowing the surgical removal of the main gallbladder, one-half of the accessory gallbladder was found to be embedded in the liver. The accessory gallbladder could be separated from the liver, but as the separation of the accessory gallbladder from the left and right hepatic duct was difficult due to severe inflammation, the accessory gallbladder was opened and after excluding the stones therein, the wall of the accessory gallbladder was removed as much as possible. After confirming the exit of the cystic duct toward the accessory gallbladder, ligation was made (). The remaining gallbladder wall was coagulated by argon beam. Well differentiated tubular adenocarcinoma was observed in the resected accessory gallbladder with infiltration into the subserosal layer ().\nThe patient has been discharged, but is now under postoperative chemotherapy as an outpatient.
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A Case of Double Gallbladder with Adenocarcinoma \nArising from the Left Hepatic Duct: A Case Report and Review of the Literature
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You are tasked with extracting and summarizing the essential information from this case report
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A 63-year-old man was diagnosed with clinical T1cN3M1b stage IVA lung adenocarcinoma (according to the 8th edition of the TNM Classification of Malignant Tumors). There was a metastatic lesion on the left adrenal gland. After examination of the biopsy tissue, epidermal growth factor receptor mutations, anaplastic lymphoma kinase translocations, and c-ros oncogene 1 translocations were not present, and the programmed cell death protein-ligand 1 (PD-L1) tumor proportion score was 100%. Thus, pembrolizumab monotherapy was used as first-line treatment.\nAfter 9 cycles of 200 mg of pembrolizumab every 3 weeks, the patient achieved a CR (Fig. ). After 15 cycles of pembrolizumab (from day 319 after the initiation of pembrolizumab), the patient developed skin toxicity (grade 2), but the rash improved after treatment with a steroidal anti-inflammatory agent. After 17 cycles of pembrolizumab (day 369), the patient developed hypothyroidism (grade 2) and commenced 25 μg of levothyroxine daily. The thyroid-stimulating hormone level was 17.98 µIU/mL, the free T3 level was 2.98 pg/mL, and the free T4 level was 0.61 ng/dL. On day 434, the dose of levothyroxine was increased to 100 μg daily, adjusting for the thyroid-stimulating hormone level.\nAfter 20 cycles of pembrolizumab (day 434), anorexia occurred and did not improve. Therefore, pembrolizumab was discontinued. However, the condition of the patient did not improve and the patient gradually became malaise. On day 441, no abnormality was observed in the pituitary gland using magnetic resonance imaging.\nOn day 484, the patient was taken to the hospital in an ambulance owing to movement difficulty. Physical examination upon admission revealed consciousness at E4V5M6, a body temperature of 39.1°C, blood pressure of 126/76 mm Hg, regular pulse of 120 beats/min, respiratory rate of 12 breaths/min, and arterial blood oxygen saturation of 93% (nasal 1 L/min). The body weight was 11.2 kg lower than that at the initiation of pembrolizumab (from 70 to 58.8 kg). The laboratory findings are shown in Table . A blood analysis revealed an elevated inflammatory response: white blood cells at 13,220/µL, C-reactive protein at 9.97 mg/dL, hyponatremia (sodium concentration: 132 mEq/L), hypoglycemia (sugar concentration: 48 mg/dL), an elevated creatinine (Cre) level (1.11 mg/dL), and an elevated creatinine kinase (CK) level (440 U/L). A chest X-ray did not reveal any abnormalities. Therefore, the patient was diagnosed with dehydration owing to some infectious disease and fluid replacement and antibiotic treatment was commenced on hospitalization.\nOn day 2 after admission, a blood analysis revealed that the Cre level (1.74 mg/dL), CK level (5,054 U/L), and hyponatremia (sodium concentration: 128 mEq/L) were further exacerbated. Additionally, blood pressure had lowered to 65/50 mm Hg. On endocrine examination, low levels of cortisol and adrenocorticotropic hormone were revealed (3.8 μg/dL and 1.1 pg/mL, respectively). The patient was diagnosed with acute adrenal insufficiency (grade 4) with prerenal failure induced by pembrolizumab. Hydrocortisone (200 mg daily) and noradrenaline were added to the treatment. The clinical course is shown in Figure . On day 5 after admission, the patient experienced an improvement in appetite. Additionally, serum sodium, Cre, and CK levels had improved to within the normal range. On day 8 after admission, the dose of hydrocortisone was reduced to 30 mg daily (orally). The patient was discharged on day 21 after admission because there was no relapse of symptoms after a reduction of oral hydrocortisone to 20 mg daily.\nWith regard to the subsequent clinical course of the patient, pembrolizumab has been discontinued and the administration of oral hydrocortisone (reduced to 15 mg daily on day 733) has continued without relapse of adrenal insufficiency. On day 984, a chest computed tomography scan showed no recurrence of lung adenocarcinoma, and the patient is being monitored without treatment (Fig. ).
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A Case of Lung Adenocarcinoma with Long-Term Response after Late-Onset Pembrolizumab-Induced Acute Adrenal Insufficiency
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Your objective is to distill this medical case report into a succinct title
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A 58-year-old previously well Sri Lankan man was admitted to our general medical unit with two episodes of gross hematuria with no frothy urine, dysuria, colicky abdominal pain or reduction in urine output. He had no preceding history of illness, fever, any other bleeding diathesis, or any history suggestive of a connective tissue disease. Our patient was mildly pale with mild splenomegaly and an elevated blood pressure of 150/90mmHg, but rest of the physical examination was normal. Initial laboratory investigations revealed an elevated serum creatinine of 2.9mg/dL (normal range: 0.7 to 1.3mg/dL). A urinary microscopic examination was significant with 100 to 120 red cells per high power field: 30% of cells were dysmorphic and his protein level was 600mg/dL. His blood leucocyte count was 5800/μL (normal range: 4000 to 11,000/μL), hemoglobin was 8.6g/dL (normal range: 11 to 16g/dL), and platelet count was 124,000/μL (normal range: 150,000 to 450,000/μL). His erythrocyte sedimentation rate was 20mm/h, his level of C-reactive protein was 1.1mg/L (normal range: 0 to 5mg/L), and serum albumin was 3.3g/dL (normal range: 3.6 to 5.5g/dL).\nAn ultrasound examination of our patient’s abdomen revealed normal-sized kidneys with increased echogenicity with mild splenomegaly.Blood film was reported as suggestive of anaemia of chronic disorder. In view of the bicytopenia and mild splenomegaly with significant hematuria, we performed a renal biopsy and a bone marrow biopsy. Results from the bone marrow biopsy showed no evidence of marrow infiltration by leukemia, lymphoma, myeloma or secondary deposits. The specimen from the renal biopsy (Figures and ) had 14 glomeruli, seen on the formalin-fixed paraffin sections. The glomeruli showed a mild diffuse increase in mesangial cells and matrix, and occasional tuft adhesions. Occasional foci of endocapillary proliferation were seen. The capillary basement membranes were normal. There were no crescents. We found focal infiltrates of lymphocytes in the interstitium. There were red cell and granular casts. We also noted occasional foci with tubular atrophy, interstitial fibrosis, and periglomerular sclerosis.\nEight glomeruli were seen on frozen sections for immunofluorescence studies. Direct immunofluorescence staining showed fine granular deposits of immunoglobulin (Ig) G (3+) and complement 3 (4+) in capillaries in all glomeruli, and IgM (2+) in the capillaries and mesangium in two glomeruli segmentally. There was no positive staining for IgA . We did not perform electron microscopy because it was not available at our institution. Overall, this renal histology was consistent with immune complex-mediated acute glomerular nephritis.\nFollowing this initial presentation our patient defaulted on follow-up. Three months later, he presented with bilateral ankle edema with periorbital swelling. He also complained of loss of appetite but had no other constitutional symptoms. An examination revealed mild pallor, a left-side discrete axillary lymph node, and moderate splenomegaly.\nInvestigations demonstrated worsening of his renal function, with serum creatinine of 3.18mg/dL and a urine protein to creatinine ratio of 1432mg/g. A urinary microscopic examination revealed 180 to 200 red blood cells per high power field, of which 40% were dysmorphic, along with red cell casts and coarse granular casts. An ultrasound examination of his kidneys revealed normal-sized kidneys (left 13.1cm; right 11.1cm) with increased echogenicity. His blood leucocyte count was 2900/μL, hemoglobin was 8.8g/dL, and his platelet count was 104,000/μL. Serologic test results for hepatitis B and C, and human immunodeficiency virus were negative, as was a Venereal Disease Research Laboratory test. Tests for antinuclear antibody and antineutrophil cytoplasmic antibody were negative. His complement levels for both C3 and C4 were normal, with a C3 level of 115.2mg/dL (normal range: 90 to 180mg/dL) and a C4 level of 27mg/dL (normal range: 10 to 40mg/dL). Serum cryoglobulins were not detected. Serum protein electrophoresis did not show evidence of a monoclonal gammopathy and myeloma screening was negative. His lactate dehydrogenase level was 404.9U/L.\nWe performed an axillary lymph node biopsy, which showed sections of his lymph node with an effaced architecture, diffusely infiltrated by a monotonous population of small lymphoid cells (Figure ). These cells showed strong membrane staining with CD20. Cyclin D1 was strongly expressed in >90% of the tumor cells (Figure ). His Ki67 index was 10%. A CD23 stain highlighted nodular aggregates of follicular dendritic cells (Figure ). The tumor cells were negative for CD23. These findings led to a diagnosis of B-cell NHL MCL.\nTherefore a final diagnosis of NHL with immune complex-mediated glomerulonephritis was made and our patient referred for further oncological management.\nHis oncological management involved a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP). Follow-up at three months showed complete normalization of his renal function to a serum creatinine of 1.2mg/dL (normal range: 0.7 to 1.3mg/dL) and a normal urine full report (protein - trace; red cells - nil). One year after chemotherapy, his renal function remained normal (serum creatinine 1.0mg/dL) with a normal full blood count (white cell count 6100/μL, hemoglobin 13.2g/dL, platelet count 234,000/μL) and a serum albumin level of 3.9g/dL.
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Mantle cell lymphoma first presenting as immune complex-mediated glomerulonephritis: a case report
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Your task is to provide a clear and precise title of this case report
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A 68-year-old woman was referred to our department after gastroscopy, which showed a mass in the stomach. She had undergone total abdominal hysterectomy with bilateral salpingo-oophorectomy because of an ovarian serous carcinoma (stage IIIa) nine years ago. On routine workup, gastroscopy showed a round mass, approximately 3 cm in diameter, in the upper body on the greater curvature side of the stomach ().\nA biopsy was performed and histologic examination indicated a poorly differentiated adenocarcinoma. Tumor markers including carcinoembryonic antigen and carbohydrate antigen 19-9 were within the normal ranges. Contrast-enhanced computed tomography showed focal, eccentric, enhancing wall thickening in the greater curvature of the stomach body and no significantly enlarged perigastric lymph nodes (). We diagnosed the patient with gastric adenocarcinoma and performed a laparoscopic-assisted total gastrectomy with D2 lymphadenectomy. No ascites or peritoneal lesion was observed. Reconstruction was performed with a Roux-en-Y anastomosis.\nThe resected specimen contained a polypoid tumor with central ulceration 3 cm in diameter (). Tumor cells had spread through the submucosal layer of the stomach with clear resection margins (). None of the 44 resected lymph nodes were positive for metastasis, but lymphatic tumor emboli were detected by immunostaining with CD-31 and D2-40 antibodies (). The tumor cells showed atypical hyperchromatic nuclei () and accompanying melanin distribution within the tumor nest (). Immunohistochemical examination revealed a positive reaction to HMB-45 antibodies and S-100 proteins and a negative reaction to cytokeratin antibodies ().\nBased on these findings, we diagnosed the patient with malignant melanoma. In the pathologic examination, the depth of tumor involvement was to the submucosal level and no metastasis showed in 44 lymph nodes. Therefore, the final pathologic tumor's TNM stage was pT1bN0M0. Postoperatively, further examinations were performed to identify the primary tumor or other metastatic foci. Ophthalmologic, dermatologic, and oral examinations showed negative findings. Positron emission tomography/computed tomography was performed, but no hot spots were detected (). These results indicated a final diagnosis of primary malignant melanoma of the stomach. After total gastrectomy, a follow-up study was performed with abdominal computed tomography scans at 3, 6, 12, 18, and 24 months (5 times) over the course of 2 years and there was no recurrence. The TNM tumor stage was early (pT1bN0M0); therefore, we did not perform any adjuvant chemotherapy, but the patient has taken oral immunotherapeutic medication for 4 months.
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Primary Gastric Malignant Melanoma Mimicking Adenocarcinoma
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Your task is to provide a clear and precise title of this case report
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A 5-year-old girl with a history of nausea, vomiting, abdominal pain, and diarrhea, who had been hospitalized without a definite diagnosis of her illness on multiple occasions before her consultation, was admitted because of diarrhea and moderate dehydration.\nPhysical examination revealed asymptomatic large plaques of confluent papules, reddish brown on the groins, pubis, and gluteus fold, firm, and well demarcated, approximately 2 × 7 cm in size of four-week duration (Figures and ). Neither hepatosplenomegaly nor palpable lymphadenopathies were detected. The clinical diagnosis of skin lesions was xanthomas, histiocytosis, molluscum contagiosum, or nongenital warts. Laboratory tests on admission were normal, including hemogram with hemoglobin level of 11.5 g/dL, a white cell differential count of 70% neutrophils, and 25% lymphocytes as well as phosphorous and parathyroid hormone levels, but an abnormal high level of serum calcium of 17.9 mg/dL. A 4-mm punch skin biopsy was taken, and subsequent hematoxylin and eosin stain revealed an amorphous and basophilic deposit in reticular dermis, highly suggestive of calcium deposits (). Von Kossa staining was positive and the diagnosis of calcinosis cutis was confirmed. Chest X-ray was normal and kidney ultrasound suggested nephrocalcinosis; however renal function parameters remained normal. There was no evidence of other visceral calcifications.\nFinally, a bone marrow biopsy revealed a significant hypercellularity with over 90% blasts with L1 morphology (). Immunohistochemical exam detected neoplastic cells positive for CD20 and CD79a indicating an infiltrate of B cell precursors (). Flow cytometry of bone marrow was also consistent with early pre-B cell lymphoblastic leukemia as immunolabeling was negative for surface immunoglobulin but positive for CD10, CD20, and CD19 []. Two weeks after admission, follow-up blood work revealed hemoglobin 9.2 g/dL with a white blood count of 2710/μL, with 82% neutrophils and 15% lymphocytes and an elevated level of lactate dehydrogenase (LDH, 2440 U/L; normal < 213 U/L) was detected. The patient was treated with three cycles of vincristine, daunorubicin, and L-asparaginase. After that the level of serum calcium was 9.4 mg/dL and the level of lactate dehydrogenase was reduced to a normal level. Skin lesions did not regress but they did not expand either, as no particular treatment was offered for these lesions. One month after the last chemotherapy cycle, the patient developed central nervous system leukemia and intrathecal methotrexate was given; however there was no response for that and treatment with cranial radiotherapy was started. Four months after her diagnosis the patient presented pancytopenia and died from sepsis.
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Metastatic Calcinosis Cutis: A Case in a Child with Acute Pre-B Cell Lymphoblastic Leukemia
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You are to provide a brief yet comprehensive title of this case report
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A 45-year-old male with a medical history significant for morbid obesity (body mass index, BMI 53.75) seizure disorder, type 2 diabetes mellitus, chronic kidney disease (CKD) stage IV (reported history of immunoglobulin A, IgA nephropathy), obstructive sleep apnea on home continuous positive pressure machine (OSA on home CPAP) and protein C and antithrombin III deficiencies was transferred to our center for acute encephalopathy, bilateral wrist drop, and polyneuropathy. Upon arrival the patient was found to be somnolent but oriented, and complained of bilateral tingling and weakness in his hands as well as urinary incontinence. Prior to admission the patient was independent at baseline; despite being morbidly obese, the patient was able to perform activities of daily living without assistance.\nNeurologic exam of motor skills upon arrival was significant for decreased bilateral grip strength and decreased bilateral quadriceps strength (right>left). Sensory exam was notable for decreased light touch sensation of upper extremities (right>left), as well as diminished light touch sensation of lower extremities (left>right). Examination of reflexes demonstrated: diminished bilateral biceps, triceps, and brachioradialis response as well as diminished bilateral patellar reflexes and no plantar response (Table ). A lumbar puncture was performed with no significant findings (Table ). Plasma exchange therapy was started empirically as a presumptive diagnosis of autoimmune demyelinating polyneuropathy (AIDP) was made. He underwent five sessions of plasma exchange with no clinical improvement. MRI of thoracic spine did not reveal any spinal abnormalities. Electromyography was performed and not supportive of a demyelinating process; however, it was suggestive of mononeuritis multiplex or an acute motor axonal neuropathy.\nDue to a lack of clinical improvement and a finding of low folate acid values on admission laboratory studies, other vitamin and element levels were measured. The patient was found to have significant deficiencies in copper, vitamin A, vitamin E, and vitamin B1 (Table ). Further history obtained from the patient revealed no risk factors for malabsorption including proton pump inhibitor use, zinc supplementation, or bariatric surgery. Studies for celiac disease were also negative. There were no abnormal dietary habits, unconventional diets, or excessive alcohol drinking identified. Of note, the patient had undergone a colonoscopy, upper endoscopy, and abdominal CT scan prior to admission, all of which were unremarkable.\nNutritional repletion was initiated and the patient was started on copper infusion therapy (receiving a total of four doses and then switched to oral copper), as well as folic acid (which was started one week prior to copper infusion), Vitamin A, Vitamin E, and Vitamin B1 supplementation. Repeat copper levels were increased and essentially within normal range. Most notably, the patient showed clinical improvement with an increase in grip strength as well as decreased tingling and numbness, which was further supported by the decrease in use of PRN (from the latin Pro Re Nata) medications for symptom control as well as a significant improvement in the patient's mental status.\nNeurologic strength exam prior to discharge revealed increased grip strength bilaterally, increased elbow flexion bilaterally, and increased hip flexion bilaterally. Bilateral plantar and dorsiflexion were also improved (Table ). The patient was discharged to a skilled nursing facility and was instructed to follow up with neurology as well as obtain repeat nutritional labs to determine the length of supplementation.\nGiven the fact that the patient did not show any clinical improvement until copper infusion was started, it was deemed to be the main culprit of the patient's presentation. Also of note, the patient had a normal mean corpuscular volume (MCV) anemia (Table ), which does not correlate with folic acid deficiency. Therefore, the patient's symptoms were deemed most likely secondary to copper deficiency. However, it would be difficult to completely rule out that folic acid may have contributed to the patient's symptoms.\nUpon follow up with the rehab facility two months after discharge, the patient has had continued improvement with significantly increased strength in his bilateral wrists as well as marked reduction in neuropathic pain symptoms. He has demonstrated a significant increase in motor strength and is now able to eat independently.
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Idiopathic Copper Deficiency Induced Myeloneuropathy
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You are to provide a brief yet comprehensive title of this case report
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A 51-year-old woman complained of headache with vomiting and gait ataxia of 1 month duration. She also noted diminution of her vision during the course of illness. She denied any difficulties in chewing or swallowing. She had 6/36 visual acuity and mild papilledema bilaterally. Her gait was ataxic in nature and had positive cerebellar signs. Hermental status and other cranial nerve examinations were normal. Magnetic resonance imaging scan showed a left cerebellar intra-axial mass lesion near cerebellopontine angle with T1-weighted hypointensity and T2-weighted hyperintensity with mild perifocal edema and mass effect []. On contrast study, the lesion was enhancing homogeneously with area of unenhanced cystic component in it. Magnetic resonance (MR) spectroscopy showed choline peak with reduced N-acetyl aspartate (NAA) and choline: NAA ratio of 5.74. Lactate peak [] was also observed at some places. Metastatic tumor, malignant lymphoma, and GBM were considered for radiological differential diagnosis. Workups for common metastatic lesions from breast, lung, colon, and secondary central nervous system lymphoma were found to be negative.\nThrough a left retromastoid suboccipital craniectomy a greyish-pink, soft, noncapsulated, vascular tumor in the left cerebellar hemisphere was excised in piecemeal near totally []. Diagnosis of giant cell variant of GBM was made on histopathological section [Figure –]. Then the patient was referred for radiotherapy. At follow up after 2 months, the patient has been doing well without any cranial nerve deficit.
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Cerebellar giant cell glioblastoma multiforme in an adult
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You are required to condense this medical case report into a title
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This was a case report of a 6-year-old boy who was diagnosed with ALL-L2 (French American British Classification) in 2001 and was treated as per multi center protocol (MCP) 843 protocol. Prophylactic irradiation to whole brain with cobalt 60 γ rays to a total dose of 1800 cGy in 10 fractions at 180 cGy/fraction was given from 13th to 23rd September 2001. In December 2003, all medications were stopped after proving complete remission by bone marrow examination.\nIn April 2011, nearly 10 years post-radiotherapy, he presented with speech difficulty and gait ataxia of 3 months duration. On examination, apart from subnormal intelligence and cerebellar signs he had no other deficits. Magnetic resonance imaging-brain showed – An ill- marginated infiltrating mass lesion in postero-superior cerebellar hemisphere with extension across the midline to involve left cerebellar hemisphere, compressing and displacing the 4th ventricle [].\nHe underwent midline sub occipital craniotomy and gross total excision of the tumor. Histopathology examination showed a moderately cellular tumor with a fibrillary background infiltrating into the cerebellar parenchyma []. The tumor cells displayed moderate nuclear pleomorphism and frequent mitotic figures, including atypical forms []. Tumor cells were immunopositve for glial fibrillary acidic protein [] and p53. MIB-1 labeling index was approximately 25% in the highest proliferating areas []. A diagnosis of anaplastic astrocytoma, World Health Organization grade III, was made. Post-operatively he was treated with adjuvant radiation therapy with three dimensional conformal radiotherapy to a dose of 60 GY in 30 fractions at 2 Gy/fraction. Post- radiotherapy, at 6 weeks follow-up, he had residual disease and hence was started on salvage chemotherapy with temozolamide. Presently, patient has only cerebral ataxia and no evidence of ALL.
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Primary anaplastic astrocytoma of the brain after prophylactic cranial irradiation in a case of acute lymphoblastic leukemia: Case report and review of the literature
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As a medical summarizer, your job is to condense this case report into its key points
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A 12-year-old boy presented with abdominal pain, fever and vomiting for 2 days. O/E tenderness, guarding and rigidity were present in the right lower abdomen. Ultrasound was suggestive of perforated appendix with periappendiceal loculated collection of volume 34cc and extending up to the subhepatic region. On diagnostic laparoscopy, perforated CDC with localised collection was identified with infarction of adjacent caecum. After laparoscopic dissection ileocaecal junction and right colon, it was delivered out by right transverse incision and right hemicolectomy was done and ileotransverse anastomosis was done []. On biopsy, perforated CDC was identified with variable lining epithelium, including gastric mucosa, stratified columnar epithelium, and metaplastic squamous epithelium. Postoperative recovery was uneventful, and the patient is well in 3-year follow-up.
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Caecal duplication cyst: A rare disease with variable presentation and its management in the era of laparoscopy
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You need to condense this case report into a succinct title
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53-year-old female, with no antecedent medical or surgical history, recalled chronic episodes of epigastric pain, for which an esophagogastroduodenoscopy (EGD) and colonoscopy were done, 10 days prior to presentation, revealing a large duodenal diverticulum and multiple sigmoid diverticula. Two days after endoscopy, she underwent urgent surgical drainage of a large retroperitoneal collection with insertion of a Penrose drain within the right lower quadrant (RLQ). Upon transfer to our medical center, she was clinically stable, yet reporting occasional low-grade fever and alteration in consistency of the RLQ discharge to bilious in nature, over the past few days, with significant increase in its amount to around 1200 mL per 24 hrs. Physical examination was insignificant for any signs of peritonitis, but rather significant for biliary discharge from the RLQ drain.\nLaboratory workup showed leukocytosis of 17,200 with 86% left shift; serum liver and pancreatic function tests were normal. Amylase and lipase level, from the draining fluid, were significantly elevated, measuring 482 IU/Lit and 11243 U/Lit, respectively.\nFluoroscopic guided drainogram showed delineation of a retroperitoneal collection in the RLQ, with a fistulous tract in junction with a duodenal segment (), suggestive of a high output duodenal-retroperitoneal fistula. The fistula is likely secondary to diverticular perforation, after endoscopy. Patient was started on broad-spectrum antibiotics and TPN.\nGradually, her clinical status improved, and the output drainage started to decrease to around 350 mL/day. A feeding jejunostomy tube was then inserted and enteral feeding initiated (). Follow-up CT and gastrografin swallow imaging showed the evidence of two outpouching structures within the D2 and D3 segments of the duodenum with layering of contrast (), representing two wide-neck duodenal diverticula. Neither contrast collection within the peritoneal cavity nor any persistent fistulous tract was noted. She was then started on PO diet, which was advanced as tolerated. Forty days later, she was discharged home, off any drains.
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Perforated Duodenal Diverticulum Treated Conservatively: Another Two Successful Cases
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Your task is to provide an accurate and brief title of this case report
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A 31-year-old woman presented at our Department due to infertility. Her medical history was unremarkable except unsuccessful attempts for pregnancy for the past 2.5 years. She had regular menstrual cycles since the age of 13 years. On clinical examination, she was normotensive and normokalemic without clinical signs of Cushing’s syndrome or hyperandrogenism. Her height, BMI and glucose homeostasis and bone mineral density proved to be normal (height: 170 cm, BMI: 19.8 kg/m2, fasting serum glucose: 5.0 mmol/l and HbA1c: 5.2%), and galactorrhoea was absent. Family history was also unremarkable. Initial laboratory findings indicated an increased serum prolactin level (93 ng/ml; reference range: 1.4–24 ng/ml), but this was due to macroprolactinemia (prolactin recovery after polyethylene glycol: PEG precipitation was 76%). Magnetic resonance imaging did not reveal any pituitary abnormality. A paternal cause of infertility was unlikely because her husband already had two children from his previous marriage. Detailed hormone laboratory investigations of the index patient suggested a partial resistance against glucocorticoids (Table ). After genetic counseling and written informed consent, Sanger sequencing of the coding region of the GR gene (\n) was performed. After identification of a pathogenic GR mutation, a family screening was indicated for the first degree relatives. Her 35-year-old, clinically healthy sister, who has no fertility problems (mother of a 10-year-old girl) was also genetically tested.\nAll patients and family members underwent genetic counseling and informed consent for genetic testing was obtained from all individuals. Evaluation and treatment of human data have been performed in accordance with the Declaration of Helsinki and the study was approved by the Local Ethical Committee of Semmelweis University.\nLaboratory measurements were performed at the Central Laboratory of Semmelweis University. Fasting blood samples were obtained between 08:00 and 09:00 h. Plasma, salivary and urinary cortisol and plasma ACTH, serum estradiol, progesterone, sex hormone binding globulin (SHBG), testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), free thyroxin (fT4), prolactin and growth hormone (GH) concentrations were measured with an electrochemiluminescence immunoassay (Cobas E411, ROCHE, Indianapolis; Architect System, Lisnamuck, Longford, Ireland; IDS-iSYS, Immunodiagnostic Systems Ltd., Boldon, England), while serum dehydroepiandrosterone sulphate (DHEAS) and androstendione concentrations were determined with radioimmunoassay (Beckman Coulter Brea, California, USA).\nDNA was isolated from peripheral blood by a standard procedure using commercially available DNA isolation reagents (DNA Isolation kit from blood, Qiagen, San Diego, USA). The whole coding region of the GR was evaluated by Sanger sequencing as previously described by Koper et al. [].\nTable summarises the main hormone laboratory findings of the index patient. During repeated measurements, serum cortisol levels in the morning were always elevated (between 26 and 35.4 μg/dl; reference range: 8–25 μg/dl) while plasma ACTH concentration was slightly above the upper limit or within the normal range (between 28.5 and 65 pg/ml; reference range: 7.2–63.3). Morning salivary cortisol levels (determined two times) were also elevated (1.36 and 1,13 μg/dl; reference range: < 0.690) but salivary cortisol collected at midnight was within the reference range (0.21 and 0.23 μg/dl; reference range < 0.430 μg/dl). A low dose (1 mg) overnight dexamethasone suppression test was performed twice, and showed an inadequate suppression of morning serum cortisol (10 and 15 μg/dl; reference range: l < 1.8 μg/dl). Repeated 24 h urinary free cortisol (UFC) concentrations were between 280 and 513 nmol/day (reference range: 100–379). Serum DHEAS was slightly elevated or normal (342 and 163 μg/dl, reference range: 130–330), and serum androstendione was increased (344 ng/dl; reference range 80-280 ng/dl). GH, SHBG, TSH, fT4, LH, FSH, testosterone, progesterone and estradiol levels were all normal (not shown in Table ).\nAs shown in Fig. , a heterozygous missense mutation (c.2141G➔A) resulting in a Arg714Gln change was identified in exon 8 of the GR gene. The same mutation was found in the clinically healthy 35-year-old sister of the patient, who had normal steroid hormone levels. Other family members denied the clinical, genetic or hormonal screening. In addition, this variant was not detected in more than 60 patients and controls tested either for glucocorticoid resistance or Cushing’s syndrome in our Laboratory. Moreover it was not present in commonly used genetic databases including Exome Variant Server (), Exac () and SNPeffect ().\nMolecular modeling and analyses were performed using the UCSF Chimera package [] (Fig. ). The coordinates of the GR ligand binding domain have been obtained from PDB structure 4UDC. Arginine at the position 714 is the member of helix 10 of the ligand binding domain (LBD) of the GR. It locates opposite side of the ligand binding pocket and relatively far from any known functional region. However, arginine has a large, positively charged side chain, which protrudes into a space created by helices 7–10 (Fig. ), but glutamine has a smaller, uncharged side chain, which may release helix 10 from its original position, which may lead to further conformational changes in the ligand-binding pocket. Nader et al. performed a complex functional testing of this mutation and using the quantification of the thickness of both the wild type and mutant Cα showed that the mutant LBD had an increased distance in root mean square deviation over the duration of the simulation compared to the wild type receptor, suggesting that the mutant structure binds the peptide with less affinity [].
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An unexpected, mild phenotype of glucocorticoid resistance associated with glucocorticoid receptor gene mutation case report and review of the literature
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You are required to condense this medical case report into a title
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A 25-year-old Japanese nulligravida woman was referred to our hospital to evaluate the abnormal structure of her uterus from a nearby clinic. She had no history of gynecological diseases, procedures, or uterine trauma. Her menstrual cycle was regular without any symptoms. Magnetic resonance imaging (MRI) revealed a myomatous mass with homogenous intensity present on the posterior uterine wall close to the internal ostium of the uterus, which shaped the inner pouch structure that was filled with a small amount of fluid (Fig. a). Upon initial examination, it appeared to be a rudimentary uterine horn; however, hysterosalpingography showed the patency of bilateral fallopian tubes connected with the fundus of the anterior uterus.\nAlthough the pregnancy was uneventful after natural conception, the myomatous mass and the pouch had become enlarged (Fig. b). At 38 + 4 gestational weeks, the patient underwent an elective cesarean delivery because the enlarged mass interfered with a vaginal delivery. Although involution of the uterus was uneventful and her menstruation did not occur during the four months after delivery, she presented at our department again with lower abdominal pain. The normal uterus was empty and about 7 cm in size. MRI showed that the myomatous mass was just as large as it was during pregnancy, and the fluid inside the myomatous mass had increased (Fig. c).\nTo improve her abdominal symptoms, she underwent laparotomy six months after delivery. During laparotomy, the uterus was completely normal with normal fallopian tubes and ovaries. A hard mass was found behind the uterus covered by thin serosa (Fig. a) and connected to the posterior uterine wall in the mid-line (Fig. b). The root of the tumor was about 3 cm in diameter. The tumor was taken out after incision of the root. The resected mass was about 18 cm in diameter and weighed approximately 1100 g. Macroscopically, the mass was a homogenous white pink hard tumor. The microscopic histological diagnosis was leiomyoma. The inner pouch space was covered with inner cervical mucosa, with inner cervical glands filled with a brownish mucosal fluid (Fig. ). The final diagnosis was uterine fibroid and diverticulum. After surgery, her abdominal symptoms resolved, and her regular menstruation resumed for six months.
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Enlarged uterine fibroid forming uterine diverticulum during pregnancy: a case report
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Summarize this medical case report, ensuring to cover the initial presentation
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A 12-year-old boy with no known congenital anomaly presented with recurrent, self-limited, colicky, right upper quadrant abdominal pain which was aggravated after fatty meals and Associated with occasional nonbilious vomiting for the past 1.5 years. Physical examination was unremarkable and so was the routine workup (hematology and liver function tests).\nSonography of the abdomen revealed a distended gallbladder (GB) with 1.2 cm long, grossly dilated, and tortuous cystic duct [Figure and ]. There was focal dilatation of common bile duct (CBD) at the site of cystic duct insertion which was “wide.” The common hepatic duct (CHD) was dilated in its distal three-fourth, while the proximal CHDs as well as the right and left hepatic ducts were normal in appearance and caliber. The intrahepatic biliary radicles (IHBRs) were not dilated.\nMagnetic resonance cholangiopancreatography (MRCP) was peculiar with dilatation of the cystic duct (the widest transverse diameter being 14 mm) and the CHD [Figure and ].\nIntraoperative cholangiogram [] confirmed the findings on preoperative imaging: distended GB, dilated and tortuous cystic duct, and dilated CBD. The cystic duct was opening into the CBD through a wide orifice. The IHBR and CBD distal to insertion of the cystic duct were normal. The main pancreatic duct was well visualized and not dilated. The junction of the CBD and the pancreatic duct was anomalous and peculiar with a long common channel. Free flow of contrast into the duodenum was observed and so was the opacification of the main pancreatic duct.\nSimilar findings were noted upon surgical dissection []. Proximal CHD was found to be normal. Cholecystectomy, excision of choledochal cyst, and the extrahepatic biliary tree beyond the normal CHD were performed, and the continuity of the biliary tree was re-established through a Roux-en-Y hepaticojejunostomy.\nThe postoperative recovery was uneventful.\nThe histopathology was consistent with the diagnosis of choledochal cyst, with no evidence of atypia.\nThe patient continues to be in regular follow-up and asymptomatic at 2 years of follow-up.
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Choledochal Cyst of the Cystic Duct – A Supplement to Todani's Classification
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Your role is to provide a brief, accurate title of this medical case report
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A 1-year-old, spayed female domestic shorthair cat was presented to the emergency service with a history of mild lethargy, gagging and occasional sneezing for 24 h. The owner had taken the cat’s temperature at home, and brought the cat in for examination as the cat had a fever of 103.6ºF (39.8ºC). On physical examination, the cat had an elevated temperature of 103.9ºF (39.9ºC), and markedly inflamed, painful gingiva. The gingivitis was extending across multiple teeth, but was not generalized, and its degree was assessed as being particularly advanced for such a young cat. Mild, bilateral mucoid nasal discharge was noted, and the remainder of the physical examination was unremarkable. The possibility of an upper respiratory infection was discussed with the owner, as was proper dental care for cats. The cat was treated with amoxicillin-clavulanate 13.75 mg/kg PO q12h (Clavamox; Pfizer) and buprenorphine 0.01 mg/kg PO q12h and discharged. The owner was instructed to follow up with her regular veterinarian in 5–7 days.\nSix weeks later the cat was returned for an acute onset of reluctance to move or walk. The owner felt that the cat’s behavior had become markedly different. The owner reported no known history of trauma. The cat continued to have upper respiratory signs, including nasal discharge, which had become serous. On physical examination the cat had a normal gait, but was resentful of lateral flexion of its neck in either direction. The remainder of the physical examination was unremarkable. The patient was again sent home with buprenorphine and instructed to return if there was no improvement in 2–3 days.\nTwo days later, the cat was returned for progression of its clinical signs. The owner reported that the cat wasn’t walking normally, but that it would ‘army crawl’ to get around at home. The cat was vocalizing as if painful and was still reluctant to move around the house. The cat had become anorexic. On physical examination, it was obtunded and found to have a right-sided hemiparesis with extensor rigidity in both the fore- and hindlimb. On the right side the cat had no conscious proprioception, and no withdrawal reflex was able to be elicited. The cat also had a left head tilt. The cat’s cranial nerves were otherwise within normal limits. Radiographs were taken (), and interpreted by a board-certified veterinary radiologist. The radiographs showed a metallic foreign body, consistent in appearance with a sewing needle, extending into the C1 vertebral canal and the skull at the level of the foramen magnum. The cat was admitted to the hospital for analgesia (0.1 mg/kg IV q4h hydromorphone), monitoring and removal of the foreign body.\nSurgical exploration of the cat’s neck was performed the next day. The cat’s neurological condition had declined overnight, and it was now non-ambulatory tetraparetic with minimal motor function in the forelimbs. Preoperative bloodwork was within normal limits. Presurgical radiographs were repeated, which showed that the needle was in approximately the same location. In surgery, a left-sided dorsal approach was used. The surgeon bluntly dissected through the muscles and fascia until the tip of the needle was identified via palpation. The end of the needle was found to be located near the body of C1, embedded in the surrounding fascia. The needle was gently extracted. The surgeon noted a very small amount of tissue adhered to the other end of the needle after it was extracted, but no obvious trauma to the surrounding tissues was seen. The tissue was not submitted for culture and sensitivity testing. After surgery the cat was given a subcutaneous injection of 8 mg/kg cefovecin (Convenia; Zoetis) and postoperative analgesia (0.02 mg/kg IV q6h buprenorphine).\nIn the immediate postoperative period, the cat still had a left head tilt, but was beginning to use its limbs, particularly its right side, with more strength than before surgery. If assisted in standing, the cat attempted to walk, but was very ataxic. The cat was not able to support itself in a standing position. On day 3 of hospitalization, the cat’s head tilt had resolved and it was able to walk with a mildly ataxic gait. The cat began to eat again, and was discharged on day 4 of hospitalization, 2 days after surgery. The owner reported that the cat was doing well when a follow-up telephone call was made approximately 5 months after surgery.
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Migration of a sewing needle foreign body into the brainstem of a cat
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Summarize this medical case report, ensuring to cover the initial presentation
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A 60-year-old man with acute left lower abdominal pain and left thigh pain was admitted 1 day after an ‘uncomplicated’ colonoscopic polypectomy. He had undergone an endoscopic mucosal resection (EMR) to remove a 0.8-cm-sized, protruding, sessile polyp in the distal descending colon. Approximately 10 hours following that procedure, the patient complained of increasing left abdominal pain. He did not have any underlying diseases except chronic alcoholism.\nInitially, his body temperature, blood pressure, and pulse were 37.8℃, 120/80 mmHg, and 118 beats/min, respectively. His blood test showed a white blood cell (WBC) count of 18,300/µL, with a left shift (neutrophils, 91.7%). He showed direct and rebound tenderness on the left lower abdomen. His left thigh pain worsened when he extended his leg. He was administered intravenous (IV) antibiotics, ceftizoxime 1 g and metronidazole 500 mg, and IV crystalloid fluid at a rate of 2,400 mL/hr. After 2 hours, the WBC count had increased to 29,400/µL, and his left lower abdominal pain had intensified, with severe direct and rebound tenderness.\nA computed tomography (CT) scan showed extraluminal free air bubbles around the sigmoid and the descending (SD) colon junction, minimal pericolic infiltration, and a high air density along the left psoas muscle. However, a definite abscess cavity was not seen (). From these results, we suspected a secondary peritonitis due to colonic perforation after colonoscopy, so we performed a laparoscopic exploration. During the exploration, we mobilized the SD colon in the retroperitoneum and found small-sized ecchymoses on the SD colon junction, but no obvious macroscopic perforation or injury of colon was noted. Moreover, a severe bruise was observed in the retroperitoneum near the left psoas muscle. We explored the bruising site, but found no abscess, phlegmon, or necrotic tissue ().\nEight hours after the operation, the patient passed a large amount of dark red urine (myoglobulinuria) followed by oliguria (0.45 mL/kg/hr). The serum creatinine level had increased from 2.3 to 3.4 mg/dL. After examining the serum myoglobulin level (), we diagnosed the condition to be rhabdomyolysis. The patient was transferred to the intensive care unit, and continuous renal replacement therapy was started for rhabdomyolysis-induced acute renal failure.\nDespite acute renal failure, the patient was alert, and his vital signs were stable until the third postoperative day when his systolic blood pressure (SBP) decreased to 70 mmHg, at which time norepinephrine IV infusion was started. However, it was soon tapered and stopped because the SBP had stabilized by the fifth postoperative day. Additionally, the bilirubin levels were also rising, and jaundice and acute liver failure had developed. On the fourth postoperative day, the total bilirubin level had increased to 22.9 mg/dL, and the aspartate aminotransferase/alanine aminotransferase levels had increased to 5,890/1,092 U/L (). Thereafter, he lapsed into a drowsy mental state. He became hemodynamically unstable, and his respiratory function clearly decreased on the eighth postoperative day. Finally, on the tenth postoperative day, the patient expired due to multiple organ failure.\nThis case report was approved by the Institutional Review Board.
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Rhabdomyolysis Following Colonoscopy: A Case Report
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You are tasked with extracting and summarizing the essential information from this case report
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A 68-year-old female with a body mass index (BMI) of 98.1 kg/m2presented with diabetes mellitus type 2, chronic kidney disease, hypothyroidism, and atrial fibrillation who suffered from left femur supracondylar extraarticular long oblique fracture 32-A2 (AO Muller classification) with a displacement of 31 mm ()after stepping out of the vehicle twisting her left leg accompanied by a short distance fall to the ground. The patient has been transferred from another hospital 1 month since injury to King Khaled National Guard Hospital of Jeddah city in Saudi Arabia for evaluation and management. After looking at patient’s file, taking full history and using a portable X-ray machine for evaluation in authors’ institute, it was decided to consult concerning specialties to reevaluate patient’s general health and condition. The patient was at high risk of developing a thrombus, using warfarin with a 4 mg dose, and thus, it was advised to withdraw the warfarin and to insert an inferior vena cava (IVC) filter. Unfortunately, in accordance with the interventional radiologist, the patient was not eligible for an IVC filter due to mainly to her chronic kidney disease status, weight, and size. Regardless of such limitations, it was important to proceed for preparation of open reduction internal fixation after considering all risk factors and her medical condition.\nStandard pre-operative protocols and screening were performed according to international standard. However, it was of high importance to establish extra adjustments for our patient to operate in the safest environment as possible. First, it was advised to book an extra-wide bariatric intensive care unit (ICU) bed for post-operative care and second, to prepare two surgical bariatric tables that would fit her size (). The surgical room door was small for the extra-wide bariatric ICU bed to pass through, so she entered the room with one bariatric bed with side support. Once the patient was in theater, twelve staff members helped to transfer the patient to the two-attached bariatric surgical table (). Third, two consultants and two specialists were prepared to participate in the surgery. Finally, an electromagnetic guidance device (TRIGEN SURESHOT, Electromagnetic targeting system, Smith and Nephew, USA) was prepared to facilitate imaging since C-arm by itself is limited to rotate freely around the patient.\nThe patient ideally underwent a retrograde interlocked closed intramedullary nail (TRIGEN meta-retrograde, Smith and Nephew, retrograde intramedullary nail, USA) fixation of the femur. The surgery was performed by two experienced consultants in trauma surgery and two orthopedic specialists to assist. Extensive prep and drape preparation performed with the patient in supine position, a percutaneous entry point using guide wire achieved closed reduction. A free hand insertion of distal locking screws was established under image intensifier guidance, while proximal locking was achieved by the electromagnetic distal targeting device.\nThe patient post-operative imaging showed satisfactory reduction on X-ray ().The patient did not develop any major early complication post-operatively. Surgical site infection (SSI) 6 days post-operatively was observed when patient started oozing serous fluid. Accordingly, the patient was not discharged until 4 weeks after operation due to the delay in wound closure. Meanwhile, laboratory culture result showed Staphylococcus aureus colonization, and the patient was treated efficiently with a 12-day course of vancomycin 5 mg/ml under infectious disease recommendations and changing of wound dressing (Mepilex Border, Safetac, all in one, USA) every 3 days with no necessity for debridement. Day of discharge imaging showed no infection of bone and a well-placed nail with a reduced fracture but minor delay in soft callus formation ().
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A Case Report and Literature Analysis:A Supracondylar Femur Fracture in a Super-Obese Patient
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.
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Phlegmasia cerulea dolens superimposed on disseminated intravascular coagulation in COVID-19
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Your objective is to distill this medical case report into a succinct title
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On 2018.01.24, a 19-year-old woman was admitted to the emergency room after taking 80 colchicine tablets (0.5 mg per tablet) 44 h previously. She had an argument with her boyfriend and ingested the colchicine to commit suicide. She was previously healthy and had no history of drug allergies. The clinical symptoms were abdominal pain, watery diarrhea and profuse vomiting. Other symptoms were muscle weakness and palpitations.\nOn physical examination, the temperature was 38.7 °C, pulse rate was 145, and respiration rate was 39. Her blood pressure was 122/60 mmHg, and she weighed 43 kg. Physical examination indicated upper abdominal pain.\nLaboratory test results before treatment indicated the following: a white blood cell (WBC) count of 28.2 × 109/L, and other values such as red blood cell (RBC) count, hemoglobin (HGB) level and platelet (PLT) count were within the normal ranges. The levels of α-L-fructosidase (AFU), adenosine deaminase (ADA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were increased to 98, 57, 84, 408, 378 and 3494 respectively from reference values (reference range were 12–40 U/L, 0–50 U/L, 5–40 U/L, 8–40 U/L, 40–150 U/L, 109.0–245.0 U/L, respectively). Biochemical abnormalities also included hypokalemia and hypoglycemia. Plasma prothrombin time (PT) and activate part plasma prothrombin time (APTT) were significantly prolonged at 23.50 s and 52.40 s respectively. The level of N-terminal pronatriuretic peptide (NT-proBNP) was 5950 pg/mL, which is abnormal with values higher than 450 pg/mL in the populations under 50-year-old (referrence value). The Electrocardiograms revealed sinus tachycardia.\nHemoperfusion was performed to remove circulating toxins. The patients refused other treatments in Department of Emergency. After 44 h later, gastrointestinal hemorrhage, acute liver injury, acute kidney injury and acute cardiac damage were reported, along with prolonged coagulation. She was then admitted to the intensive care unit. Adequate fluid and electrolyte replacement, oxygenation and other supportive cares was initiated. Anti-inflammatory ceftriaxone sodium was used. Since the unobstructed drainage tube revealed brown fluid, gastric lavage and charcoal were not recommended.\nDuring two days after admission, she presented with high fever, subcutaneous hemorrhage and anuria. Arterial blood gas analysis suggested hyperlactinemia. Uric convention and occult stool were positive for blood. The level of Creatine Kinase-MB had sharply increased to 182 U/L and HGB level and PLT count rapidly plunged to 49 g/L and 11 × 109 /L, respectively. APTT had increased to 72.4 s. At that time, renal function deteriorated and anuria was observed, and the levels of serum creatinine (Cr) and blood urea urea (BUN) were elevated. CRRT was used to remove metabolic wastes and poisons and promoted recovery of renal function. RBC, PLT and plasma were transfused to alleviate anemia and deficient coagulation.\nDue to the high dosage of colchicine ingestion, the patient progressed to exhibit shortness of breath, high fever, and subsequent coma. The vital signs at this point were: a heart rate of 87, respiration rate of 21, and the blood pressure was 103/52 mmHg. Blood lactic acid levels were slightly increased. Hyperleukocytosis, low hemoglobin and thrombocytopenia were present. Emergency treatment with tracheal intubation via oral cavity was initiated.\nOn 2018-02-01, the level of BUN and CK were elevated and anuria was noted. Maintenance therapy with CRRT was initiated to clear metabolic toxins. The arterial blood gas results were generally normal, and she was extubated and provide with supplemental oxygen through a nasal tube. The WBC count returned normal levels, and blood coagulation and liver function were gradually normalized as well.\nFollowing a month of treatment, urine volume increased, but renal function indicators remained abnormal. In addition, HGB levels gradually increased but remained low. Intermittent CRRT and diuretics were administered.\nOn 2018-03-06, her urine volume reached 3000 ml. Renal ultrasound showed the kidneys were full and diffusely changed (Fig. ). Urinary albumin-to-creatinine ratio (reference range of 0–200 mg/g) was also abnormal as displayed in Fig. . Intermittent hemodialysis was performed and renal function improved. Three days later, the levels of Cr and BUN were also normal, and the patient was discharged. (Blood and urine specimens, and blood biochemistry were reviewed one week later. These values and the time of CRRT treatment are shown in Table . Changes of Cr level and BUN level are presented in Figs. and . On 2018.05.28, the renal ultrasound urinary albumin-to-creatinine ratio were normal (Fig. and ). The treatment timeline is shown in Additional file : Figure S1.
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A rare case report of heavy dose colchicine induced acute kidney injury
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Your task is to provide a clear and precise title of this case report
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A 90-year-old man was referred to us with a mass in his right eye that had first been noticed three months earlier and had been growing progressively since then. VA was 20/200 in the right eye and hand movement in the left eye. Slit-lamp examination revealed a gelatinous temporal conjunctival mass (7 mm long, 10 mm wide) with dilated superficial vessels (Figure 4A ). Fundus examination showed age-related macular degeneration (AMD) in both eyes. Ocular movements were affected in the form of abduction limitation in the right eye (Figure 4B ). An incisional biopsy was performed and a moderately differentiated SCC was confirmed (Figure 5 ). Magnetic resonance imaging (MRI) showed malignant infiltration of the lateral rectus muscle (Figure 6A ). Anterior segment optical coherence tomography (AS-OCT) displayed a hyperreflective lesion which involved the conjunctival tissue and spread over the corneal surface (Figure 6B). Due to the advanced stage of the tumor, an exenteration or radiotherapy treatment was offered, but the patient rejected both. After five months, the tumor had progressed and involved ocular globe tissues and soft periorbital structures (Figure 7 ). The patient died due to metastatic disease nine months after the initial diagnosis.
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Epithelial conjunctival neoplasias – the importance of an early diagnosis and optimal treatment
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Your objective is to distill this medical case report into a succinct title
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A 26-year-old man visited the hospital on August 21, 2016, with a 6-month history of pain in his right leg. The pain had a radiating quality and had not been relieved by medication. On examination, the patient exhibited monoparesis of the sacral (S) 1-innervated gastrocnemius muscle, with difficulty in pushing the foot, revealing a lower right limb power of 4/5. Other neurological parameters were within normal limits. There was no related familial or past history. Results of MRI performed on August 23 showed a single fluid-containing lesion at the lumbar (L) 4–5 level measuring 8 × 6 mm (Fig. ); the nerve root traversing L5 could not be identified due to the mass effect of the lesion. The patient received ENLD on August 24, 2016. After confirming adequate positioning of the epiduroscope, multiple laser fenestrations (1.0 J, 10 Hz) were performed. Endoscopic visualization showed decompression of the cystic mass (Fig. ). The patient reported immediate improvement of his radiating pain following the procedure. The MR images acquired 2 weeks post-procedure showed that the lesion had significantly regressed, and post-operative MRI was now able to identify the nerve root traversing L5 (Fig. ).
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A novel technique for managing symptomatic spinal cysts using epiduroscopic neural laser decompression: technical note and preliminary results
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Your role is to extract the core information from this case report
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Approval was obtained from the Ethical Committees of the University of Medicine and Pharmacy “Iuliu Hatieganu” Cluj-Napoca (345/16 November 2020) and informed consent from the patient and her mother were taken for the publication of this case report.\nA female patient aged 9 (born 1995) was referred to the Maxillofacial Department in 2014 because of rapid onset of pain, swelling of the jaw and difficulty with eating. Clinical examination revealed no pus, abscess or fistulae. Further investigation reported a severe enlargement of the body, ramus and mandibular arch and associated pain. No sensitivity alteration was noted at the inferior alveolar nerve innervation territory.\nUpon examining the cone beam computer tomograph (CBCT) () and panoramic X-ray (), multiple poorly differentiated radiolucencies with diffuse radiopacities were observed spanning the entire length of the mandible body from one angle to the other. A sclerotic or sclerotic-permeative pattern, as well as a periosteal reaction, was also seen. The lesions did not seem to affect the teeth and the mandibular canal.\nAs a first empirical treatment, large doses of wide spectrum antibiotics were used, and bone biopsy was taken from the mandible. The Trichrome Masson, hematoxylin-eosin and the immunohistochemistry staining revealed chronic sclerosing osteomyelitis (a,b).\nAlthough no suppurative process was clinically evident, microbiological samples were collected, with no conclusive result. Under wide spectrum antibiotic therapy slowly favorable evolution was noted, but the thickening of the periosteum was still present with the relapse of the symptoms several weeks after the treatment ended.\nIn 2016, local surgical implantation of gentamicin-PMMA (Polymethyl methacrylate) beads (Septopal; Merck GmbH, Darmstadt, Germany; Biomet GmbH, Berlin, Germany) to the right and left body of the mandible was decided in an attempt to stop the evolving osteomyelitis.\nDue to loss of several deciduous teeth in the lateral region and pain reported by the patient in the temporomandibular joints (TMJs) bilaterally, the patient was referred for orthodontic assessment. Digital photographs and dental impressions were taken at her first visit and, moreover, the bite was registered in centric relation. In addition, the patient received indications for radiographs, CBCT and Magnetic resonance imaging (MRI) for the TMJs.\nThe initial extraoral facial examination revealed an increased lower face height and a straight profile, reduced static and dynamic upper frontal teeth exposure, lip incompetence (3 mm). The midline of the mandible and maxilla corresponded with the midline of the face ().\nIntraoral examination revealed partial destruction on the lateral deciduous supporting areas resulting in a loss of the leeway space bilaterally and bimaxillary shortening of the dental arches, accentuated Spee curve and poor oral hygiene.\nThe occlusal exam found a half a cusp distalization of the secondary right mandibular canine, due to the leeway space loss, a class I relationship on the left canine and a molar class I relationship on both sides ( and ). Tongue thrust and a habit of nail biting (onychophagia) were also noted at the functional exam.\nThe dental exam also revealed extensive carious lesions in the temporary maxillary second right molar and on both temporary left maxillary molars. The secondary inferior first molar had an incipient carious lesion on the occlusal surface (the tooth is vital for the vitality test).\nThe initial cephalometric analysis revealed a decreased articular angle, increased gonial-jaw angle and reduced corpus length, which signify a normal growth pattern. The anteroposterior relationship of the mandible and the maxilla was normal.\nFrom a dental point of view, the lower incisors were retrusive, due to the premature loss of deciduous teeth. The following were also noted: a tendency of inversion of the normal lordosis of the vertebrae and posterior rotation of the cranium ().\nCBCT and MRI analyses showed atrophic disks bilaterally and perforation on the right disk with antero-lateral displacement. On the left TMJ, an anterior-lateral displacement was noted. Bilateral condylar resorption and active erosions, without any inflammatory signs, were also seen ( and ).\nCast models were mounted in centric relation du jour using a face bow and articulator. A premature contact at 1.6–4.6 and the lateral shift of the mandible were noted. This reveals a Centric Occlusion—Centric Relation discrepancy, which might have determined the TMJ symptomatology. Upon analysis, an overjet of 1–2 mm and an overbite of 1–2 mm was found with an accentuated Curve of Spee.\nOne of the causes of the premature contact might be the premature loss of the deciduous teeth (1st and 4th quadrant), with a consecutive migration of the adjacent teeth.\nRelieve the TMJ pain, stabilize the mandible and muscle relaxation (physiotherapy and splint therapy);\nOrthopedic treatment to ensure a normal growth and development of the maxilla and the mandible, and the correct eruption of the permanent teeth (class I for canine and molar);\nDiminishing the growth of the inferior lower third of the face;\nLimiting the evolution of the osteomyelitis process by preventing further invasive treatment of the patient (braces, skeletal anchorage, any other forces that are beyond physiological which might increase the osteomyelitis process);\nDeconditioning of the tongue trust and nail biting and improving oral hygiene.\nCare was taken to avoid the usage of a fixed appliance after the mixed dentition phase, or any skeletal anchorage. To this end, the treatment had to use appliances to direct the growth pattern, in order to utilize only low physiologic forces (biting and tongue forces). These were intended to slowly close the open bite, to autorotate the mandible, to obtain a class I occlusion for the molars and canines bilaterally. Caution was also taken to prevent any potential resorption of the roots. All this was done to avoid any osteo-periosteal reaction and the possibility of aggravating the disease. Another very important objective, while planning the orthodontic treatment, was to adjourn unnecessary surgery including teeth extractions or wisdom teeth removal. Special consideration was taken not to use an unphysiological high pull force from a head-gear device to intrude the lateral teeth to close the open bite.\nUsually, in cases with loss of leeway space, an alternative would be to regain lost space with the help of fixed orthodontic appliances (braces) and space opening mechanics, but this treatment alternative was not advisable for the patient since it might produce exacerbation of the osteomyelitis.\nThe prognosis of this disease is unfavorable with severe pain of the jaw, TMJ discomfort and pain, difficulty with eating and with hygiene. The osteomyelitis will accentuate and fistulae can appear. Orthodontic-wise, due to the leeway space loss, crowding will appear in the permanent dentition with the development of open-bite and a hyperdivergent growth pattern. The orthodontic treatment, then, will have to include teeth extractions, which are a risk factor of aggravating the osteomyelitis. Additionally, extensive fixed appliances will have to be used alongside skeletal anchorage. All this determines the accentuation of the symptomatology of the underlying disease.\nDue to the symptomatic TMJs and the modifications revealed on the MRI and CBCT, treatment began with full-time wearing of an acrylic splint and physiotherapy, to deprogram the muscles and the TMJs and to establish the centric relation. A full coverage maxillary splint divided into three sections (one frontal and two lateral) was manufactured according to a centric bite registration ( and ).\nAfter 13 months of physiotherapy and splint therapy (, , and ), centric relation was established with a premature contact on teeth 2.6–3.6 and an anterior open bite of 3–5 mm, a lateral open bite of 3 mm and still a small lateral shift of the mandible to the right. As seen on the panoramic X-ray () the gentamicin-PMMA beads were applied in the left and right body of the mandible.\nThe cephalometric analysis () revealed an articular angle in the normal range, while all the other parameters remaining the same. Additionally, the natural curvature of the cervical spine was re-established and the space between C0, C1 and C2 was restored.\nA mandibular removable arch with bite-blocks (worn 24/7, even when eating) manufactured in centric relationship was used to inhibit the overeruption of the lateral mandibular teeth and a transpalatal arch (TPA) with an acrylic button on the permanent upper first molars was used to intrude the permanent upper molars by means of the physiological forces of the tongue when swallowing (, and ).\nDue to good local response and decreasing osteoclastic lesions, the gentamicin-PMMA beads (Septopal) were surgically removed in 2017. The biteblocks were used until the permanent dentition fully erupted.
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An Orthodontic Approach for Garre’s Sclerosing Osteomyelitis of the Mandible
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You are to provide a brief yet comprehensive title of this case report
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A 65-year-old man presenting with chest pain and back pain was transferred to our hospital for further evaluation of aortic arch aneurysm on chest radiograph. He had been taking anti-hypertensive for 2 years. On admission, his heart rate was 76 beats per minute in sinus rhythm and blood pressure was 110/70 mmHg.\nChest computed tomography (CT) was performed and revealed a thrombosed aneurysm of the aortic arch. Maximal diameter was 62 mm. The aneurysm extended from immediately distal to the left common carotid artery (LCA) up to the distal aortic arch, and the aberrant left vertebral artery originated from just proximal aortic arch segment with aneurysmal change. Neck and brain CT was performed to evaluate the neck vessels and the intracranial arteries. There was no occlusive lesion of the neck vessels, including both vertebral arteries, and the continuity of the circle of Willis was intact. However, there was hypoplasia on the left vertebral artery at T1 level (Fig. ).\nThe patient underwent arch vessel debranching surgery through a supraclavicular approach. The left supraclavicular incision was performed and the LSA and the LCA were isolated. A 7 mm ringed vascular graft (GORE-TEX® vascular graft FEP removable ring 7 mm-70 cm, W.L. Gore & Associates Inc., USA) was used to anastomose the LSA to the LCA. The aberrant left vertebral artery was transposed to the LCA (Fig. ). The proximal LSA was ligated to prevent endoleak. Next, endovascular stent-graft placement was performed after 2 days later. Using a right femoral artery cut-down and percutaneous left femoral artery access, the stent-graft (VALIANT THORACIC® stent graft 40–150, Medtronic., USA) was implanted, extending from zone 2 to the upper descending thoracic aorta, 5 cm distal to the aneurysm.\nThe patient was discharged without complications. Follow-up CT revealed patent arch vessels, including the transposed left vertebral artery (Fig. ).\nThere is increasing evidence pointing to the need for the LSA revascularization in order to prevent cerebral, spinal cord, and left arm ischemia; on the other hand, opposing opinion argues that the evidence is low-quality and the actual incidence of ischemia is rare [, ]. Nevertheless, in selected patients, specifically those who have a patent left internal thoracic artery to coronary artery bypass graft, a functioning arteriovenous shunt in the left arm, or presence of vertebral artery variations like hypoplasia or discontinuity of the vertebrobasilar collaterals, the LSA revascularization is strongly recommended []. The vertebral arteries converge into the basilar artery and it supplies blood to the brainstem, cerebellum and occipital lobes. In addition, the segmental arteries that supply the spinal cord arise from the vertebral arteries. Therefore, the LSA revascularization is important in order to prevent cerebrospinal ischemia in patients with normal left vertebral arteries originating from the LSA. At present, there is no clear recommendation on whether an aberrant left vertebral artery should be revascularized or not. While the LSA should ideally be revascularized to prevent arm ischemia, revascularization of an aberrant left vertebral artery may be omitted if the right vertebral artery is normal []. Vertebral artery variations are common in thoracic aortic patients, with the right vertebral artery being particularly more variable than the left, having a prevalence of up to 30% []. Although the patient’s right vertebral artery was patent in the brain and neck CT scan, we decided to transpose the left vertebral artery from the arch to the LCA because hypoplasia of the right vertebral artery was suspected. At the same time, he suffers from hypertension, which can increase the risk of stroke in the future. Furthermore, the neck CT scan revealed that the left vertebral artery did not enter the transverse foramen at the level of C6, but instead at a higher level at C4, coursing posterior to the LCA. Melia et al. demonstrated this course of the extracranial vertebral artery in patients with abnormal left vertebral arteries [].\nThe left supraclavicular incision is the most commonly used approach when performing an LSA bypass. This approach has long been used for the treatment of arch vessel diseases by neurosurgeons []. The LSA is easily manageable by this approach and the aberrant left vertebral artery originating from the aortic arch is readily accessible because of its parallel course to the LCA (Fig. ). In a recent study, although the LSA transposition to LCA showed longer patency than the LSA bypass using artificial graft, there was no difference between two methods [, ]. Furthermore, to obtain an adequate length for LCA transposition, the LCA should be transected to as proximal a location as possible. Since this can affect the weakened disease-aortic arch, we prefer the LCA bypass.\nMore complex arch reconstruction requires a sternotomy, especially zone 0 procedures. This approach is familiar to thoracic surgeons, but is more invasive than the supraclavicular approach. Few reports on aberrant left vertebral artery transpositions exist, and to our knowledge, this is the only report of hybrid TEVAR with transposition of an aberrant left vertebral artery through a supraclavicular approach [, ].
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Supraclavicular transposition of aberrant left vertebral artery for hybrid treatment of aortic arch aneurysm: a case report
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You are to provide a brief yet comprehensive title of this case report
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A 37-year-old woman went to the clinic of a local hospital because of abdominal pain and hematochezia for one week. Colonoscopy examination showed a polypoid mass protruding into the rectum cavity, measuring approximately 5 cm in maximum diameter, with a rough and uneven surface (Fig. ). Then the patient underwent a partial rectectomy. The lesion was considered as a myogenic sarcoma, preferring pleomorphic leimyosarcoma by the referring pathologists. The postoperativ adjunctive therapy was not administrated . There was no evidence of recurrence or metastasis 8 months after surgery.
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Epithelioid inflammatory myofibroblastic sarcoma: a clinicopathological, immunohistochemical and molecular cytogenetic analysis of five additional cases and review of the literature
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You are tasked with extracting and summarizing the essential information from this case report
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A 50-year-old woman presented to our hospital with hematochezia and anemia. 1 year earlier, she experienced severe anemia (hemoglobin 4.0 g/dL) that was treated with a blood transfusion at another hospital. The diagnosis at that time was a hemorrhagic gastric ulcer, and she was treated with a proton pump inhibitor. Contrast-enhanced abdominal computed tomography (CT) done just before the first administration to our hospital showed multiple liver lesions of arterioportal and portal venous shunts, hemangiomas, and a large focal nodular hyperplasia. She had hematochezia and anemia (hemoglobin 7.0 g/dL) again and was referred to our hospital for further examination. Upper and lower gastrointestinal endoscopies including double-balloon enteroscopy did not reveal any bleeding lesions in her esophagus, stomach, duodenum, proximal jejunum, colon, or rectum, although she had grade 1 esophageal varices. Angiographic examination revealed an AVM, with signs of extravasation, at the jejunal branch of the superior mesenteric artery (SMA; Fig. a). Three vasa recta branches of the jejunum at the AVM lesion were embolized with metallic coils to stop the bleeding (Fig. b). The patient was then discharged from the hospital without any complications. Three months after the embolization, she experienced hematochezia and anemia again and was admitted to our hospital. Repeat angiography showed rebleeding from the same AVM, and an additional 3 vasa recta branches were treated with metallic coil embolization (Fig. ). The coil embolization was temporarily successful again. However, because of the risk of another rebleeding from the same AVM in addition to the risk of necrosis of the coil-embolized jejunum, we considered resection of the affected jejunum to be the optimal treatment and recommended this to the patient.\nElective laparoscopic surgery was performed under general anesthesia. Although initial investigation under laparoscopy alone failed to localize the lesion, X-ray fluoroscopy showed a clear image of the metallic coils embolizing the AVM (Fig. a). Subsequently, the small bowel was taken out through the umbilical incision, and the metallic coils were confirmed by palpation under direct vision. Partial resection of the jejunum was performed, followed by functional end-to-end anastomosis using linear staplers (Fig. b). Pathological examination revealed fibrous thickening of the vessels and infiltration of inflammatory cells in the mesentery, suggesting a focal inflammation in response to the coil embolization (Fig. ). There was no necrotic intestine caused by the embolization (Fig. ). She had no complications after surgery and was discharged within 1 week. She did not have any hematochezia after resection of the AVM during 8 months of follow-up.
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Laparoscopic resection of idiopathic jejunal arteriovenous malformation after metallic coil embolization
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Your objective is to distill this medical case report into a succinct title
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A 55-year-old male patient had reported to our hospital with history of injury to right eye following fall from a height with complains of pain and a FB has entered into his right eye. As stated, the patient had climbed a tree to collect woods and while he was chopping a branch of the tree, he suddenly fell from the tree over a wooden [bamboo] fence below and a twig had got broken and entered into his right eye. There was no history of unconsciousness following the injury. No history of any other illness or injury was present except he was diabetic and hypertensive. He had come to our hospital about 13 h after the injury had occurred. On examination, the patient was fully conscious and well oriented. A wooden [bamboo] FB was seen projecting from right palpebral aperture and firmly impacted in an upward direction towards the upper part of the orbit []. Sight was conserved in right eye. There was no apparent distortion or injury in right globe with clear cornea, well-formed anterior chamber, normal iris details, and pupillary reaction. Left eye was within normal limit. Upon movement, dribbling of clear fluid from the projected end of the FB had raised suspicion of intracranial extension. The patient was admitted, given prophylactic Tetanus Toxoid injection, and started on prophylactic broad spectrum intravenous antibiotic Cefotaxime and intramuscular nonsteroidal anti-inflammatory medication Diclofenac. An urgent computed tomography (CT) scan of brain and orbit was advised, which revealed a linear FB piercing the superior aspect of right orbit through superior muscle complex and right frontal sinus and into right frontal lobe of brain by fracturing roof of right orbit. There was laceration in right frontal lobe without any intracranial hemorrhage (ICH) or pneumocephalus. The globe integrity was preserved except mild indentation by the FB []. An urgent neurosurgical intervention was sought and he was shifted to neurosurgery department. But due to uncontrolled hypertension, he could not be taken up for immediate surgery. As observed by the attendant, while he was kept admitted in the intensive care unit, he himself had pulled out the FB in his agony due to pain. Soon after, he was relieved from pain to some extent. He was examined immediately and found to be stable with fully conscious and oriented. The wound was examined meticulously for any remnant of FB. The FB track was clean with no remnant of FB with no cerebrospinal fluid (CSF) leak was found. Hemostasis was achieved using absorbable gelatin sponge and the wound was closed by suturing in layers. He was kept admitted under close monitoring with bed rest and strict maintenance of precautions to reduce or eliminate increases in intracranial pressure with prophylactic medications for 72 h. Postoperative recovery was uneventful, no signs of CSF leak were found. Postoperative magnetic resonance imaging (MRI) scan was performed after 24 h, which revealed no residual foreign body, no evidence of CSF leak inside the wound, no ICH or pneumocephalus, with the globe was normal in position and integrity. Later, he was discharged from the hospital with normal sensorium. He was on regular follow-up for 5 years since then and was found to be leading his daily life happily without any sequel of the injury [].
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An unusual case of orbitocranial wooden foreign body with amazing outcome: A case report
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Your role is to provide a brief, accurate title of this medical case report
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A 33 year old female presented with vague epigastric discomfort, weakness and breathlessness on exertion, 3-4 episodes of melena and intermittent non-bilious vomiting episodes since 45 days. Her general physical examination revealed pallor. Abdomen showed mild epigastric fullness. Hemoglobin was 6.7 g/dl. Leucocyte count, liver and kidney function tests were within normal limits. Ultrasonography of the abdomen and pelvis revealed a 4.4x3.0x2.7 cm well defined isoechoeic solid mass within bowel lumen possibly in the second part of the duodenum. A contrasted tomography of the abdomen and pelvis (A) revealed an intraluminal polypoidal lesion in the second part of duodenum with mild thickening of duodenal wall with few subcentimetric lymph nodes.\nUpper gastrointestinal endoscopy with endoscopic ultrasound (EUS, B) showed a mixed echogenic submucosal lesion measuring 4.0x2.8 cm with a 2 cm thick, long pedicle and a feeding artery on color Doppler leading to duodenal intussusception and obstruction extending beyond the second part of duodenum. It was diagnosed as GIST based on endoscopic and EUS findings. EUS fine needle cytology or biopsy was not deemed necessary. The patient was planned for pancreas preserving duodenectomy with a pancreaticoduodenectomy if ampulla was involved. The patient was transfused two packed cells preoperatively.\nIntraoperatively (), an approximately 4x3 cm lesion in duodenal bulb and second part of duodenum with a 5 cm long stalk was arising from the posterior wall of first part of duodenum with ampulla at 3 cm distal to the root. Intraoperative frozen section confirmed the lesion as brunneroma. A supra-ampullary pyloroduodenectomy with Roux-en-y gastrojejunostomy was done. The specimen showed a lobulated, polypoid mass of 4×3×3 cm projecting into the duodenum. The stalk was 5.5x2.0 cm. The tumor was completely enveloped by duodenal mucosa. The surface was smooth and consistency was firm. Histopathology () revealed a lobular proliferation of benign Brunner's glands, accompanied by few ducts and scattered stromal elements, ulcerated surface duodenal epithelium and granulation tissue at places. Few foam cell aggregates were seen and center of the stalk was fibrovascular with normal overlying epithelium. No dysplasia or malignancy was seen. The patient recovered uneventfully and is symptom free at follow up.
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BRUNNER GLAND ADENOMA MASQUERADING AS DUODENAL GASTROINTESTINAL STROMAL TUMOR WITH INTUSSUSCEPTION: CASE REPORT
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Your role is to extract the core information from this case report
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This case describes a 25-year-old female with a family history of HAE, who was diagnosed with type 1 HAE when she was 4 years old and for whom the onset of HAE symptoms occurred at 12 years of age. She had previously received IV-C1-INH (Cinryze) for long-term prophylaxis, before switching to biweekly lanadelumab monotherapy, which she received for 15 months prior to her enrollment in the APeX-S study in 2020. In the 6 months leading up to study enrollment, the patient experienced an average of 2 HAE attacks per month with lanadelumab prophylaxis.\nAfter starting oral berotralstat, the patient continued self-administration of biweekly lanadelumab for one month before it was discontinued (Fig. ). The patient experienced two HAE attacks during this 4-week dual therapy phase, both requiring icatibant treatment. In the first 2.5 months of berotralstat monotherapy, the patient did not experience any HAE attacks, but 3 attacks occurred in the subsequent 2 weeks, two of which were self-assessed as mild and the other as moderate in severity. Two of these attacks were triggered by physical activity, and no identifiable trigger was reported for the third. All three attacks required icatibant treatment. Regardless, the patient’s attack rate during the 3 months of treatment with berotralstat monotherapy was lower than during the 6 months of lanadelumab monotherapy prior to study entry. No treatment-related adverse events were identified while she received berotralstat. Her level of satisfaction with this treatment was excellent at all time points; however, she is no longer enrolled in the study for personal reasons.
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Considerations for transition from subcutaneous to oral prophylaxis in the treatment of hereditary angioedema
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You are to provide a brief yet comprehensive title of this case report
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A 43-year-old woman was admitted to our hospital complaining of continuous frontal and occipital headaches for 4 months, and a left hearing loss for 2 months. One week before admission, she began vomiting for about 5 times a day. She had no significant medical background or family history. No lymphadenopathy or organomegaly were found upon general physical examination. Skull, bone, cardiac, chest, and per rectal examinations revealed no abnormalities. She was oriented and conscious. Visual fields and acuity was normal. Neurological examinations revealed normal motor function and sensation in all four limbs. No obvious changes in superficial or deep tendon reflexes were detected. Ataxia and pathological signs were absent. Routine hematological test results were all normal and the serological HIV test was negative. However, a brain magnetic resonance imaging (MRI) showed a homogeneously enhancing mass in the left CPA, measuring 5 cm × 5 cm × 3.5 cm; neuritis or a CPA tumor was suspected (Fig. ). The tumor showed relatively equal signal intensities on T2-weighted imaging (T2WI) and T1-weighted imaging (T1WI), extending slightly to the left temporal pole meninges. The mass also mildly compressed the cerebellum, the adjacent brain stem, the aqueduct of Sylvius, and the fourth ventricle. The MRI revealed cerebellar swelling, dilation of supratentorial ventricles system, and interstitial edema. Along with her clinical history, these findings implied an acoustic neuroma in the left side.\nThe patient underwent a left retromastoid craniectomy and a tumor resection. During surgery, a well-defined left CPA lesion extending to the left internal auditory canal was seen. It was against the petrous bone and tentorium cerebelli, with abundant vascularization and relatively clear boundaries. The tumor was extirpated as multiple pieces of friable, gray, and firm tissues, which were fixed in 10% paraformaldehyde and embedded in paraffin. Microscopically, the tissues were a mixture of cancerous lymphocytes and plasma cells. Immunohistochemical tests showed the tissues to be positive for CD38, CD20, CD38, and CD79α, and negative for AE1/AE3, Bcl-6, CD3, CD10, glial fibrillary acidic protein, neuron-specific enolase, and Syn. The positive rate for Ki-67 was 10%.\nPathological examination confirmed the diagnosis of LPL (Fig. ). The patient then underwent a bone marrow biopsy and a computed tomography (CT) scan of the entire chest, abdomen, and pelvis. No abnormalities were found. According to the Ann Arbor–Cotswald staging system for lymphomas, this case of CPA LPL was classified as Stage I, indicating that the cancer was located in a single region.\nOne week after the surgery, the patient's headache and hearing loss were much relieved. Postoperative MRI showed that the CPA tumor was totally removed, and adjacent structures were thoroughly decompressed. She was then transferred to the hematology department for chemotherapy. The chemotherapy protocol was the cyclophosphamide, vincristine, and prednisone regimen along with rituximab. After 6 cycles of chemotherapy, her Karnofsky Performance Scale score was 95. An MRI performed half a year after the surgery showed no recurrence (Fig. ).
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An uncommon case of lymphoplasmacytic lymphoma in cerebellopontine angle region
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Your objective is to distill this medical case report into a succinct title
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A 38-year-old British male presented to a South African hospital in August 2004 after 2 years of travelling in South Africa, Malawi, Mozambique and Namibia. He presented with a 4-month history of progressive fatigue, fever, headache and sleeplessness.\nOn arrival he was found to be febrile with mild hepatomegaly and lymphadenopathy. Bloods showed raised inflammatory markers with a CRP of 54 mg l−1 and an of 120. CSF showed a raised protein at 1.2 g l−1 with a glucose level of 2.1 mmol l−1, the WCC was 82 (100% mononuclear). CT head was unremarkable.\nAn HIV test was negative. A blood film was positive for trypanosomes and a diagnosis of Stage 2 EAT was made. He was treated with suramin and melarsoprol with prednisolone cover. He made a full recovery and 2 weeks post-treatment his CSF had normalised.\nIn June 2005 he reported a 2-month history of headache, night sweats, somnolence and fever. Repeat LP showed a WCC of 58 (100% mononuclear), a protein of 0.79 g l−1 and a glucose of 2.9 mmol l−1. Blood and CSF showed no trypanosomes. He was treated as a relapsed trypanosomiasis and was commenced on a 2-week course of eflornithine from which he made a rapid recovery. His CSF WCC count fell to normal levels by August 2005.\nIn December 2005 he presented with a 2-week history of headache, fever, vertigo, diplopia and somnolence. He had a left sixth nerve palsy on examination. LP showed trypanosomes in his CSF with a WCC of 125 (100% mononuclear), a protein of 0.8 g l−1 and a glucose of 3.1 mmol l−1. His blood was positive for trypanosomes. He was treated with a repeat course of suramin and melarsoprol with prednisolone cover for relapsed Stage 2 EAT.\nOn day 16 of his treatment he became confused and suffered a generalised tonic-clonic seizure. LP showed an opening pressure of 34cmH2O with no cells and a protein of 1.06 g l−1. An MRI at this time demonstrated T2W hyperintense signal in the supratentorial white matter extending into the posterior limbs of the internal capsules and splenium of the corpus callosum (), both of which showed corresponding restricted diffusion (). Post-contrast sequences revealed mild ependymal enhancement of the occipital horns of the lateral ventricles with no parenchymal enhancement (). Focal signal loss on T\n2-star (T\n2*) imaging was also present in the splenium of the corpus callosum and basal ganglia () in keeping with microhaemorrhages and he was transferred to ITU where he was sedated and intubated.\nFollow-up imaging 6 months later showed residual but reduced T2W FLAIR signal hyperintensity in the deep white matter, resolution of the restricted diffusion abnormalities and mild supratentorial atrophy when compared to his admission MRI ().
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MRI findings of the brain in human African trypanosomiasis: a case series and review of the literature
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 77-year-old female experienced repeated TIAs of motor aphasia and dysarthria. On admission, she was alert and well oriented. She had no cranial nerve deficits or focal neurological signs. Magnetic resonance (MR) imaging revealed no evidence of acute cerebral infarction []. MR angiography showed an occlusion of the left internal carotid artery (ICA) and stenosis of the right MCA [Figure and ]. Some anomalous arteries were also identified faintly on MR angiography and ordinary angiography, but the detailed anatomy was not clear. Fusion images of three-dimensional digital subtraction angiography (3D-DSA) demonstrated an occlusion of the cervical portion of the left ICA and stenosis of both the proximal segments (M1) of the MCA []. In addition, a left AMCA, originating from near the anterior communicating artery (ACoA), was identified [Figures and ].\nThree-dimensional DSA revealed the characteristic cerebral blood flow (CBF) supply pattern. The AMCA supplied CBF to the frontal lobe alone. The AMCA was perfused by the right ICA via the ACoA. In addition, the left MCA, which was perfused by the left posterior cerebral artery via the left posterior communicating artery, supplied CBF to the temporal and parietal lobes [Figures -]. Because the proximal segment (A1) of the left ACA was occluded, the flows of the AMCA and MCA were clearly separate []. Single-photon emission computed tomography (SPECT) showed a marked decline in the CBF to the left fronto-temporo-parietal lesion at rest, while cerebral vascular reactivity was impaired by acetazolamide loading []. After diagnosis, we started antiplatelet medication (ASA 100 mg/day) and it continued until bypass surgery.\nIt was concluded that bypass surgery was needed for the territory of both the AMCA and MCA. A double anastomosis was performed that consisted of: (1) the frontal branch of the left superficial temporal artery (STA) to the cortical artery of the left AMCA; and (2) the parietal branch of the STA to the cortical branch of the left MCA. Prior to anastomosis, intraoperative indocyanine green video angiography was performed and demonstrated bidirectional flow in the left frontal cortical artery []. After anastomosis, the flow in the frontal cortical artery improved. A remarkable improvement in CBF in all lesions was confirmed postoperatively. The patient was discharged with no neurological deficits and remained free from ischemic attacks without antiplatelet medication for at least 1 year.
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Unusual hemodynamic stroke related to an accessory middle cerebral artery: The usefulness of fusion images from three-dimensional angiography
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Your objective is to distill this medical case report into a succinct title
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A 58-year-old woman presented with a mass found incidentally on a chest radiograph. She had been treated for hypertension and hypercholesterolemia for the past 10 years.\nLaboratory tests revealed no abnormality. The posteroanterior chest radiograph showed a well-defined mass with a smooth margin in the right paratracheal area (). Precontrast computed tomography (CT) showed a 4 cm mass in the subcarinal area (), but on the postcontrast CT obtained 2 minutes later, the mass was observed in the right paravertebral area (). The attenuation value of the mass was 42-44 Hounsfield units on precontrast CT, and the mass did not show contrast enhancement. In a follow-up posteroanterior chest radiograph, the mass had migrated to the subcarinal area (). The impression based on the imaging studies was a pedunculated solitary fibrous tumor of the pleura, and the differential diagnosis included a benign neurogenic tumor. Cystic mass types, such as the bronchogenic cyst, were not included in the differential diagnosis due to the mass' mobile nature.\nThe patient underwent video-assisted thoracoscopic surgery. A 3 × 4 cm "soap-like" white hard mass was found floating freely in the pleural cavity. The mass did not have a stalk connecting it to the parietal pleura (). Histopathologically, the mass consisted of hypocellular hyalinized collagen and the surface of the tumor showed some scattered chronic inflammatory cells and the characteristic "basket-weave" configuration of laminated hypocellular mature collagen (). The final diagnosis was a fibrin body in the pleural cavity.
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A Pleural Loose Body Mimicking a Pleural Tumor: A Case Report
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You are required to condense this medical case report into a title
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A 47-year-old female with no significant past medical history, including RF in childhood, presented to the emergency department (ED) with the chief complaint of acute onset respirophasic chest pain for two days. The pain was described as sharp in quality, 7/10 in intensity, unrelated to rest or activity, and non-radiating. She also complained of generalized fatigue, bilateral shoulder and knee pain, bilateral leg swelling, and dark frothy urine, all of which started a few days prior to the onset of chest pain. Other review of systems was negative. She reported a sore throat which started three weeks prior to admission and lasted approximately one week before spontaneously resolving. The patient was originally from Honduras; however, she had no history of travel outside of the United States in the past 14 years. She was living in Florida during the same period. Of note, her children were sick with pharyngitis a month prior to her presentation, however, they did not seek medical treatment.\nOn physical examination, her temperature was 98.2°F, blood pressure was 160/90 mmHg, heart rate was 84 beats/min, respiratory rate was 12 breaths/min, and oxygen saturation was 99% on ambient air. Cardiopulmonary examination revealed bilateral diffuse lung crackles, normal S1 and S2, a holosystolic 3/6 murmur at the cardiac apex which radiated to her axilla. She also had bilateral 2+ pitting pedal edema. Examination of the skin was normal without any evidence of pyoderma or cutaneous abscess. Labs were significant for creatinine of 1.57 mg/dL, mildly elevated troponin of 0.14 ng/mL, elevated brain natriuretic peptide (BNP) of 16667 pg/mL, and erythrocyte sedimentation rate (ESR) of 69 mm/h (Table ) . The chest X-ray showed bilateral interstitial edema (Figure ) and the echocardiogram showed severe mitral regurgitation (Figure ), grade 1 diastolic dysfunction, and ejection fraction of 55%-60%.\nGroup A Streptococcal antigen was negative, but antistreptolysin O (ASO) antibody was positive at 900 IU/mL (Table ).\nBased on her history, physical examination and laboratory, there was a concern for acute RF. We utilized the revised Jones criteria: evidence of Streptococcal infection with positive ASO antibody, one major criterion with carditis, and two minor criteria with elevated ESR and arthralgia. The diagnosis of acute RF was confirmed.\nIn the setting of elevated creatinine, frothy urine and pitting pedal edema, there was also a concern for a nephrogenic process. The urinalysis was positive for 3+ proteinuria and red blood cells (RBC) of 50-100/hpf, urine protein to creatinine ratio was 8000 mg/g. Serum albumin was 2.9 g/dL, total cholesterol and low-density lipoprotein (LDL) were 174 and 107 mg/dL respectively. She was screened for HIV, Hepatitis B and C, all of which were negative. Rheumatoid factor, Anti-nuclear antibody (ANA), anti neutrophilic cytoplasmic antibodies (ANCA), double-stranded DNA antibody, and anti-glomerular basement membrane were negative. C4 was normal at 19.30 mg/dL, however, C3 was low at <40 mg/dL (Table ).\nRenal biopsy reported diffuse immune complex mediated proliferative and exudative glomerulonephritis. Specifically, the light microscopy showed enlarged glomeruli with diffuse global mesangial and endocapillary hypercellularity (Figure ).\nThere were also focal glomeruli showing subsegmental subendothelial periodic acid-Schiff (PAS)-positive deposits forming ‘wire loop’ like lesions (Figure ).\nThere was moderate interstitial fibrosis and tubular atrophy, with a mononuclear infiltrate predominately limited to the areas of fibrosis. Immunofluorescence microscopy showed glomeruli with global mesangial and capillary loop granular staining by immunoglobulin G (IgG) (3+) (Figure ), C3 (3+) (Figure ), and C1q (1+).\nElectron microscopy showed frequent capillary loop hypercellularity. The mesangial region was expanded, hypercellular and showed frequent electron-dense deposits (Figures -).\nThere was also moderate to severe epithelial foot process effacement.\nGiven the multiple findings above, the patient was diagnosed to have APSGN concurrently with acute RF. She was started treatment with furosemide and lisinopril. She was also given amoxicillin for the GABHS infection. She was recommended to continue amoxicillin for secondary prophylaxis of GABHS for lifelong.
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Concomitant Acute Rheumatic Fever and Acute Post Streptococcal Glomerulonephritis
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Your objective is to distill this medical case report into a succinct title
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A 68-year-old woman with a history of diabetes mellitus, living-donor renal transplant on current immunosuppression, and compensated cirrhosis secondary to hepatitis C genotype 1a presented for esophageal variceal surveillance. The patient had no history of variceal bleeding, encephalopathy, or ascites. Liver function indices were unremarkable. Upon her first endoscopy [], large columns of varices were found with high-risk stigmata of a red wale sign, and 5 bands were applied successfully. She presented to us for her third session of surveillance and 3 additional variceal bands were applied (, ; before and after banding). Immediately after the procedure the patient could not swallow any liquids or secretions, with persistent spitting up of saliva admixed with small streaks of blood. Viscous lidocaine mixed with water failed to provide any relief. The patient was admitted for observation with nothing by mouth. Sucralfate was started along with proton-pump inhibitor therapy. By the second day, the patient was still unable to swallow any liquids including her own saliva. A barium esophagram showed complete obstruction of the distal esophagus (). Repeat esophagogastroduodenoscopy (EGD) the following day showed pooling of saliva in the distal esophagus, which was suctioned, along with necrotic and ulcerated esophageal mucosa at the base of the banded varices causing complete luminal obstruction (, ). We grasped the 3 bands with the hook of an endoloop cutter (Olympus America, Melville, NY, USA) (, ), and the bands were removed intact from the base of necrotic varices one-by-one without any bleeding. This restored the esophageal lumen () and led to resolution of symptoms. The patient was discharged home the following day tolerating a regular diet. Upon follow-up endoscopy, scars were seen in the area without any varices.
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Removal of Esophageal Variceal Bands to Salvage Complete Esophageal Obstruction
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Your job is to distill the important information into a title from this case report
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A 65-year-old male patient with atrial fibrillation prior HTx 1 year ago for end-stage ischaemic cardiomyopathy, presented with a sensation of feeling his ‘heart sink’. There was no prior history of autoimmune disease or thyroid dysfunction and Type 2 diabetes was diagnosed ages prior HTx. The level of patient’s thyroid-stimulating hormone (TSH) prior HTx was 1.35 mIU/L (normal values: 0.35–4.94 mU/L). Before HTx recipient was managed with antiarrhythmic treatment with amiodarone (200 mg/day) for atrial arrhythmias. But there were no indications to continue antiarrhythmic treatment after HTx. Recipient was treated with triple-drug therapy (steroids, tacrolimus, and mycophenolic acid), and basiliximab was used as an induction. Through the months we slowly tapered the dose of steroids that was at 8 mg/day. In fact, there were no associations between changes of doses of immunosuppressive agents and development of patient’s complaints.\nOn cardiac examination, patient’s heart rate (HR) and rhythm (108 b.p.m.) were regular with frequent extrasystoles. During auscultation heart sounds were clear and no cardiac murmurs have been heard. His 24-h Holter demonstrated sinus rhythm with a HR of 107 b.p.m. (from 93 to 131 b.p.m.), monomorphic ventricular extrasystoles (VES) (total amount: 27 472/day) were diagnosed (Figure ). There was no evidence of atrial fibrillation and no other specific features have been found. According to trans-thoracic echocardiogram (TTE) results, the left ventricle function was normal and left ventricular ejection fraction (LVEF) was above 60%. There were no signs of diastolic dysfunction. N-terminal prohormone of brain natriuretic peptide, D-dimer, and troponin levels were fine.\nPatient had no history of thyroid disorders but due to a development of VES we performed an extra investigation. Thyroid function tests (TFTs) were as follows: free thyroxine (FT4)—34 (normal values: 9.0–19.0 pmol/L); free triiodothyronine (FT3)—6.99 (normal values: 2.63–5.69 pmol/L); and TSH <0.003 mIU/L. The level of anti-TSH-receptor antibodies was 0.67 ME/L (normal values: <1.00 ME/L) and antithyroid peroxidase (antithyroperoxidase)—0.0 ME/mL (normal values: 0.0–5.6 ME/mL). Erythrocyte sedimentation rate, C-reactive protein, and cell blood count were normal. Thyroid ultrasonography evidenced a diffusive enlargement of the gland and with no nodules; colour flow Doppler sonography showed a pattern 0 (absent hypervascularity). Our investigation revealed that patient had thyrotoxicosis. The diagnosis of destructive thyroiditis was based on the absence of hypervascularity in spite of high levels of serum thyroid hormones and antithyroid antibodies negativity. He was consulted with an endocrinologist. Prednisolone (30 mg/day) treatment was initiated. Moreover, endomyocardial biopsy was performed. There were no histological signs of cellular and/or antibody-mediated rejection.\nA timeline of the patient’s outpatient and inpatient follow-up was outlined: blood tests every 2 weeks to estimate levels of thyroid hormones and to fix doses of antithyroid treatment and 24-h Holter monitoring every 2–3 months. Two months after initiated treatment recipient was studied with an ambulatory 24-h Holter electrocardiogram and results were the same: sinus rhythm with HR: 117 b.p.m. (from 104 to 138 b.p.m.), total amount of VES were 26 768/24 h. On the other side, the level of FT4 increased and mixed type AIT was hypothesized. According to blood results thiamazole was added to treatment (10 mg/three times a day). Furthermore, he had the same complaints, the same as exercise intolerance.\nGiven the presence of persistent VES, despite therapy for thyroid disease, we decided to consider a VE ablation. However, this was deferred as it was felt appropriate to achieve a euthyroid state in the first instance.\nIn fact, 5 months after antithyroid treatment was started, the number of VES per day was significantly decreased to 9901. At the same time, there was positive outcome of combined antithyroid treatment: serum free thyroid hormone concentrations (FT3: 2.35 pmol/L and FT4: 10.8 pmol/L, respectively) normalized in 4.5 months after initiated treatment and remained normal forward. After that recipient had been maintained by oral prednisolone (from 30 to 15 mg/day in <2 months) given in association with thiamazole (from 15 to 10 mg/day). In a month after doses had been reduced TSH became 5889 mIU/L, FT3 and FT4 were normal (3.88 and 11.5 pmol/L, respectively).\nIn addition, TTE remained normal during the whole post-transplant follow-up, LVEF: 61–65%.\nApproximately 9 months after commencing antithyroid therapy (3 months post-normalization of TFTs), the patient had no recurrence of frequent VES on Holter monitoring. Also there was no dyspnoea and exercise tolerance increased. The antithyroid treatment (prednisolone plus thiamazole) had to be discontinued after 9 months. Moreover, the 24-h Holter monitoring was performed and results were unremarkable, no monomorphic VES and only two polymorphic VES were found (Figure). His last follow-up visit confirmed an euthyroid state 3 months after the antithyroid treatment had been stopped. Thyroid function tests remained normal off prednisolone plus thiamazole and the total amount of VES significantly decreased. Furthermore, patient admitted that his well-being improved. So there were no indications for any antiarrhythmic treatment or ablation.,
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Frequent ventricular extrasystoles after heart transplantation: a late presentation of amiodarone-induced thyrotoxicosis: a case report
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Your task is to provide an accurate and brief title of this case report
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Case 1 is a male, 65 years old, having squamous cell carcinoma of upper gingiva.\nThe emergency situation in flap harvesting was the perforator vessel variation. When seeking perforator, we found that the perforator was not from the peroneal artery. It resulted in the unavailability of the skin paddle. The patient had both bone defect and soft tissue defect. We had to abandon the unavailable skin paddle and seek substitution to replace it. The operator flexibly used the FHL to close the intraoral defect (Fig. ). The FFF was without skin paddle. To accelerate the intraoral mucosa forming, we used an artificial biological membrane to cover the myofascial surface of FHL and used an iodoform cotton wrapping for pressing. The skin paddle was sutured in situ. One week later, when we removed the iodoform cotton wrapping, the intraoral mucosa recovered well. (Fig. a–d) And the fibular flap survived and had no infection and necrosis. The patient was satisfied with the appearance and oral functional recovery.
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The application of fibular free flap with flexor hallucis longus in maxilla or mandible extensive defect: a comparison study with conventional flap
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Your role is to extract the core information from this case report
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A 21-year-old man with a 4-year history of end-stage renal disease, on hemodialysis (three 4-h sessions/week), secondary to untreated bilateral vesico-ureteral reflux and neurogenic reactive bladder.\nThe patient was referred for a bone scan because of osteoarticular complaints, especially at the elbows with limited mobility, and he reported mild and nonspecific symptoms, especially no significant dyspnea.\nPatient had high creatinine (428 μmol/l); serum phosphorus (4.51 mmol/l); total alkaline phosphatase, 108 U/L and serum parathyroid hormone level was 1700 pg/mL.\nWhole body bone scintigraphy images [], showed a diffuse uptake in both lungs, more intense in the right one, suggesting an extra-osseous pulmonary calcification and an increased radiotracer uptake in the soft tissues of the left arm and in the periarticular soft tissues surrounding the elbows. The chest X-ray was normal [].\nParathyroidectomy was declined by the patient. The medical therapeutic was chosen with dietary phosphorus restriction, noncalcium phosphate binders, calcimimetics, optimal control of secondary hyperparathyroidism, and intensive hemodialysis with a low-calcium dialysate.\nSecond bone scan was done 3 months later [] revealed a significant decrease, without disappearance, in the lung's uptake.
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Pulmonary calcification in renal failure patient incidentally revealed by bone scintigraphy
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Summarize this medical case report, ensuring to cover the initial presentation
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We report the case of a 9-year-old Caucasian female affected by suprasellar non-germinomatous germ cell tumor (NGGCT) associated with multiple pituitary deficit, who tested positive for SARS-CoV-2 an April 1, 2020.\nHer problem began 2 years earlier, with polyuria, polydipsia (she drank almost 8 liters of water/day) and growth delay. In October 2019, she came to Verona’s Paediatric Emergency Department in a state of confusion. Brain magnetic resonance imaging revealed a suprasellar mass, compatible with germinoma (). This hypothesis was confirmed by high levels of alfa-fetoprotein and human chorionic gonadotropin (hCG) in plasma and cerebrospinal fluid (CFS). Based on alfa-fetoprotein and hCG levels the tumor was classified as a non germinomatous germ cell tumor (NGGCT). Ophthalmologic evaluation and a study of visual fields were normal. At the time of diagnosis, blood exams tests confirmed a multiple pituitary deficit with diabetes insipidus, central hypothyroidism, hypocortisolism, growth hormone deficiency and mild hyperprolactinemia. The patient’s laboratory test results at time of diagnosis are shown in . The girl started therapy with levothyroxine (initially at dosage 25 mcg/day) and desmopressin (initially intranasal, then sublingual). She was given dexamethasone after the MRI to reduce tumoral edema. Over the next few days the patient was found to have “cerebral salt wasting” with hyponatremia, high urinary sodium excretion (129 mmol/L) and persistent polyuria, so we started fludrocortisone. It was stopped after four days when laboratory tests normalized. She continued therapy with desmopressin, levothyroxine and hydrocortisone and the patient had periodical laboratory tests and therapeutic adjustments.\nIn October 2019 chemotherapy according to SIOP CNS GCT II standard risk protocol for non-germinomatous germ cell tumor (NGGCT) was started. The first cycle was complicated by hydrocephalus that required ventricular-peritoneal derivation. At the end of the third cycle, the MRI showed a partial response to chemotherapy. Therefore, in January 2020, the patient underwent neurosurgery. The histopathological examination was conclusive for immature teratoma. Follow-up MRI one month after surgery showed a suspected small residual lesion. Chemotherapy with high-dose etoposide was started.\nFrom the 8 March, the “lockdown” for all Italy was adopted together with the use of surgical mask, hand hygiene, and social distancing, to prevent the massive spread of SARS-CoV-2; moreover, a screening program by nasopharyngeal swab (NPS) for any patient and caregiver parent accessing the Pediatric Hematology Oncology Unit was started (). On March 12, the patient (and her mother) underwent the NPS and both resulted negative for SARS-CoV-2. She was taking desmopressin (sublingual tablets 60 mcg, 2 + 1+2, 300 mcg/day), levothyroxine at 75 mcg/day and hydrocortisone at 8,92 mg/m2.day divided into 2 doses. Therapy with recombinant GH was not yet started. Since her neurosurgical operation, she suffered from hypothalamic obesity (incontrollable hyperphagia, decreased satiety and decreased physical activity) with massive weight gain.\nOn March 5 she was admitted to the Pediatric Oncology Unit for mobilization chemotherapy with high-dose etoposide and granulocyte colony-stimulating factor (G-CSF) followed by peripheral stem cell collection for autologous stem-cell transplantation (ASCT). On April 1 she was admitted to the Pediatric Oncology Unit for ASCT. Her weight was 40,9 kg (93,21 percentiles based on Cacciari’s charts) and her height was 120,2 cm (6,08 percentiles based on Cacciari’s charts), with a BMI of 28,31 kg/m2 (99,06° centiles based on Cacciari’s charts).\nWhen she came for screening, a second NPS for SARS-CoV-2 was performed on the patient and parent caregiver (the father) and both resulted positive. The pre-transplant conditioning regimen (HD PEI cycle - cisplatin, etoposide and ifosfamide- according to SIOP CNS GCT II protocol) was already started on April 2 in the morning, and was therefore withdrawn as soon as the result of NPS was communicated in the evening of the same day (administration of day 1 of conditioning regimen). Both patient and father were quarantined in a pediatric COVID19 section of the department to monitor the patient’s symptoms or signs of SARS-CoV-2 infection. During observation, blood count, urine tests. inflammatory markers, chest X-ray were unremarkable. In particular, her blood exams showed leukocytes 6,87x10^9/L, neutrophils 5,77x10^9/L and lymphocytes 0,40x10^9/L. No respiratory, cutaneous signs, or fever appeared during recovery and the patient continued her previous therapies. The most significant laboratory tests before, during and after Sars-Cov2 infection are summarized in . Her diuresis remained in the range of 2-2,9 ml/kg/h. The patient was discharged 3 days later, in good general conditions. Her weight at discharge was stable. Another two nasal and pharyngeal swabs were both negative after 28 days (). The ASCT was performed on April 30 after a conditioning regimen with high dose ifosfamide, etoposide and cisplatin. She received 4.38 x 106/kg CD34+. The patient engrafted on day + 9 for neutrophil and on day + 12 for platelets and was discharge home in good clinical conditions. In accordance with Verona University and University of Verona Institutional review Board (IRB) policies, case reports are not considered to be research subject to IRB review and are thus except from formal IRB approval for publication. Written informed consent was obtained from the patient’s legal guardians for the publication of any potentially identifiable images or data included in this article.
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Case Report: SARS-CoV-2 Infection in a Child With Suprasellar Tumor and Hypothalamic-Pituitary Failure
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You are tasked with extracting and summarizing the essential information from this case report
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A 51-year-old male (UNC-0852 2-V) was investigated for possible PCD after undergoing double lung transplantation at age 43. Sweat chloride testing, CFTR genotyping, and immunology labs were normal. Ciliary electron microscopy was not performed in this case, and the patient had a normal nasal nitric oxide level at 234 nL/min. Prior to transplantation, he had year-round productive cough since early infancy, two hospitalizations annually for acute respiratory exacerbations, and diffuse bronchiectasis that was first discovered at 26 years of age. His sputum cultures routinely grew Staphylococcus aureus and Aspergillus species but were eventually colonized with Pseudomonas aeruginosa, and lung function pre-transplantation was quite impaired, with an FEV1 of 0.84L (23% predicted).\nDespite a term birth, the patient had neonatal respiratory distress as well as recurrent otitis media with speech delay in childhood, though he never required tympanostomy tubes. He endorsed year-round (non-seasonal) nasal congestion from the first year of life, with chronic sinusitis and nasal polyposis evident on the CT scan of the sinuses. There were no identified organ laterality defects upon CT or ultrasound imaging of the heart, thorax, or abdomen. His physical examination was notable for diffuse, low-pitched wheezing and digital clubbing. Further surgical history was remarkable for ventriculoperotineal shunt placement for hydrocephalus discovered shortly after birth (with multiple subsequent revisions), left lower lobectomy at 4 years old, and scoliosis correction in adolescence. Family history revealed the patient was unmarried and never had children. He was of mixed Irish (father) and Irish/Native American (mother) heritage, and there were no similarly affected siblings or extended family members. Mutation profiling of the full coding region revealed a frameshift, heterozygous pathogenic variant at c.929_932delACTG (p.Asp310Glyfs*22) in exon 3 of the FOXJ1 gene (NM_001454.4). The proband's father and four unaffected siblings did not carry this variant. Unfortunately, genetic material for maternal testing was not available (Figure ).
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Autosomal dominant variants in FOXJ1 causing primary ciliary dyskinesia in two patients with obstructive hydrocephalus
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Summarize this medical case report, ensuring to cover the initial presentation
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A 23-year-old female, known case of chronic kidney disease due to IgA nephropathy (diagnosed 6 months back) and resultant malignant hypertension, presented with complaints of sudden painless decrease in vision in her right eye since last 1 day. The blood pressure at presentation to us was 210/140 mm Hg while mean arterial blood pressure (MABP) was 136 mm Hg. The patient had been started on systemic corticosteroids 1 month back. The best-corrected visual acuity (BCVA) was 3/60 in the right eye and 6/18 in the left eye. Detailed fundus evaluation revealed severe HTR[] leading to disc edema, macular edema, hard exudates, and retinal hemorrhages in both the eyes [Fig. and ]. Swept source optical coherence tomography (SS-OCT) showed presence of disc edema, intraretinal and subretinal fluid, and intraretinal hyperreflective lesions corresponding to hard exudates in both the eyes [Fig. and ]. In view of poor visual acuity, the patient was advised intravitreal injection of Bevacizumab (1.25 mg in 0.05 mL) in the right eye after informed consent. At 1 month after intravitreal injection, BCVA in the right and left eyes improved to 6/18 and 6/12, respectively. The blood pressure was 160/96 mm Hg while MABP was 101.3 mm Hg. Fundus showed marked improvement in disc edema, macular edema, and retinal hemorrhages in both the eyes [Fig. and ]. SS-OCT showed complete resolution of intra- and subretinal fluid at the macula [Fig. and ] along with disruption of outer retinal layers in the papillomacular bundle. The patient was advised regular follow-up and good control of blood pressures.
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Dramatic response to intravitreal Bevacizumab in hypertensive retinopathy
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Summarize this medical case report, ensuring to cover the initial presentation
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The patient is a 39-year-old female with past medical history of tobacco use (7.5 pack-years), anxiety, and depression. She was not on any home medications. The patient presented with three months of anorexia, malaise, weakness, and fatigue, associated with unintentional weight loss (20-30 lbs). The patient also reported several weeks of diarrhea followed by constipation, and a dull but intermittently sharp pain in her left lower and upper abdominal quadrants. The pain was aggravated by pressure and with any oral intake; alleviating factors included heat and bowel rest. The patient was also recently admitted (two months prior) for similar symptoms, but left against medical advice after she was unable to tolerate bowel preparation for colonoscopy.\nOn initial presentation to the emergency department, the patient was hemodynamically stable. Blood pressure was 108/84 mmHg, oxygen saturation was 98% on room air, and heart rate was 103 beats per minute. The patient was cachectic and appeared much older than her stated age. Physical examination was significant for angular cheilitis and white plaques on an erythematous oral mucosa. Significant dental decay was noted with numerous dental caries and a maxillary denture. Her abdomen was tender to palpation in the left abdominal quadrants, left flank, and left anterolateral chest wall. Mottled skin, consistent with a heating pad burn, was observed along the left lateral abdomen.\nInitial serologic evaluation was significant for leukocytosis (white cell count 15.8 K/uL), anemia (hemoglobin 11.7 g/dL), thrombocytosis (platelets 453 K/uL), hypokalemia (potassium 2.5 mmol/L), hypoalbuminemia (albumin 2.7 g/dL), elevated C-reactive protein (9.4 mg/L), and an elevated erythrocyte sedimentation rate (37 mm/h). Urinalysis was positive for hyaline casts (10-20/lpf) and a small amount of bilirubin. CT of the abdomen and pelvis revealed colonic wall thickening at the splenic flexure and proximal descending colon with some adjacent small volume fluid.\nAt this point in time, the patient was started on piperacillin-tazobactam (Zosyn) 3.375 mg intravenously three times daily for suspected bacterial colitis and admitted for further gastroenterologic evaluation. Colonoscopy revealed a descending colon and splenic flexure stricture approximately 45 cm from the rectum without mass lesions. Dilation to 13.5 mm via a through-the-scope colonic balloon dilator was performed. Retained partially obstructing fecal matter was removed, and the scope was advanced into the transverse colon. During the colonoscopy, the patient's abdomen became progressively more distended and then developed crepitus in the chest wall and neck. Colonoscopy was aborted after subcutaneous air was noted in the abdominal wall. Upon arrival to the intensive care unit, the patient was noted to have diffuse crepitus above the diaphragm, throughout the chest wall, neck, and right eye. The patient was intubated, sedated and mechanically ventilated for respiratory distress. Care was assumed by the pulmonary medicine and critical care team.\nAbdominal radiograph revealed significant intraperitoneal air and was positive for Rigler's sign, consistent with pneumoperitoneum (Figure ).\nChest radiograph revealed extensive subcutaneous emphysema, bilateral pneumothorax, and pneumomediastinum, and was positive for diaphragm sign (Figure ).\nCT of the abdomen and pelvis showed significant pneumoperitoneum and ascites, consistent with the suspected colonic perforation (Figure ).\nCT of the chest again confirmed pneumomediastinum, subcutaneous emphysema, and bilateral pneumothorax (Figure ).\nThe patient underwent bilateral chest tube placement and was emergently taken to the operating room for exploratory laparotomy. A perforation at the proximal transverse colon with stool in the peritoneum was identified, along with a splenic flexure mass and a serosal tear at the cecum without perforation. A left hemicolectomy with mobilization of the colon at the splenic flexure was performed. The abdomen was temporarily closed with a surgical wound vacuum. On postoperative day 2, the patient returned to the operating room for a right hemicolectomy with ileocolic anastomosis, diverting loop ileostomy, Jackson-Pratt (JP) drain placement, and fascial closure. The patient was extubated, and chest tubes were removed on postoperative day 3. Pathology was suggestive of atypical Crohn’s disease without small intestine involvement.\nThe patient was started on TPN via peripherally inserted central catheter from postoperative days 3-6 while awaiting initiation of oral intake. After tolerating enteral nutrition, the patient had sufficient ostomy output and was discharged in stable condition to an extended care facility with a midline abdominal wound vacuum and right lower quadrant JP drain, both of which were removed in office one week after discharge. After the 15-day admission, the patient was discharged with no new medications. Plans were made to begin anti-tumor necrosis factor therapy six to eight weeks after surgery, with repeat endoscopic evaluation in six to twelve months after ileostomy reversal. Unfortunately, the patient was readmitted four days later for suspected small bowel obstruction, which was treated medically with bowel rest and small bowel decompression (nasogastric tube placement to low intermittent wall suction). The patient was advised to follow up with primary care and gastroenterology prior to discussion of ileostomy reversal with general surgery.
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Intraperitoneal and Extraperitoneal Colonic Perforation Following Diagnostic and Therapeutic Colonoscopy with Crohn’s-related Stricture Dilation
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A fifty-year-old Caucasian woman presented with fever, malaise, and pancytopenia. Her surgical history was significant for a splenectomy following a motor vehicle accident several years ago, and her vaccination status was up to date. Bone marrow biopsy revealed a diagnosis of Hairy Cell Leukemia. Immunophenotyping by flow cytometry was positive for CD11c, CD25, CD103, CD19, and CD20. The patient was started on Cladribine (2-chlorodeoxyadenosine), a purine analog, 0.14 mg/kg/day, for a five-day course. Chemotherapy was administered through a central venous catheter. While receiving Cladribine, the patient was noted to have persistent fevers with stable hemodynamics. After carefully excluding infectious etiologies of her persistent fever intravenous Cefepime was changed to oral ciprofloxacin and prophylactic fluconazole. Upon discharge, blood and sputum cultures were negative for bacteria.\nOne week later, she presented with persistent fevers and dyspnea. She was intubated and transferred to the Intensive Care Unit. Chest X-ray showed a left lower lobe infiltrate. She was started on vancomycin, piperacillin/tazobactam, and levofloxacin for healthcare associated pneumonia in the setting of neutropenic fever. Liposomal amphotericin-B was also added for broad-spectrum antifungal coverage as she was at high risk for developing fungal infection.\nBronchoscopy, performed at bedside, revealed diffuse petechial lesions in the airway. Bronchoalveolar lavage (BAL) culture grew greater than 10,000 colonies of a gram-positive organism that grew in clusters but was neither Staphylococcus aureus nor coagulase negative Staphylococcus when tested by fluorescent in situ hybridization using peptide nucleic acid probes (PNA FISH). The patient's blood cultures were also positive for the same nonstaphylococcal gram-positive bacteria in two separate aerobic culture tubes. Because the bacterium was unidentified, the patient remained on vancomycin. However, despite aggressive treatment, the patient deteriorated and expired four days after hospitalization. Our facility could not identify the bacteria and the sample was sent to the Department of Community Health of Michigan. The isolate was identified via sequencing of the 16S rDNA segment as Kytococcus schroeteri. Because the bacterium was detected posthumously, no susceptibility testing was performed by our facility and no samples were available to perform testing after the bacterium was identified.
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Kytococcus schroeteri Bacteremia in a Patient with Hairy Cell Leukemia: A Case Report and Review of the Literature
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A 14-month-old female with a history of gross motor delay and iron deficiency anemia presented to an urgent care with right hip pain. On evaluation, she had cervical and inguinal lymphadenopathy, an elevated ESR (109), CRP (10.19), anemia (Hgb 7.6) and WBC of 10 with 14% bands. Bilateral hip X-ray showed persistent undertubulation without fracture. After having several similar presentations for fever and inconsolability with significantly elevated inflammatory markers and concerning x-rays, she was admitted to the hospital for further evaluation. Intake exam was notable for hepatosplenomegaly, central hypotonia and erythematous maculopapular rash. The differential diagnosis included storage disorders, metabolic disorders, and infiltrative processes, such as leukemia.\nBrain MRI was unrevealing, only noting cervical lymphadenopathy. Echocardiogram was unremarkable. Blood smear did not show leukemic blasts. Her rash was consistent with scabies and treated with permethrin. Her extensive metabolic work-up was normal (including urine mucopolysaccharides, creatine kinase, acylcarnitine profile, and plasma amino acids), except for elevated urine mevalonic acid. Repeat urine organic acids performed during another febrile episode again showed elevation of urine mevalonic acid. Genetic testing revealed two mutations in her mevalonate kinase gene with one allele having deletion of exons 10–11, while the other allele having a variant of p.Asn166Lys of unknown significance. Given mutations on both alleles for her mevalonate kinase enzyme, she was diagnosed with MKD.\nOur patient is now 23 months old and thriving. Since her diagnosis of MKD, she was started on Anakinra with an excellent response, but she developed diarrhea and was transitioned to Canakinumab. To date, she has had no recurrence of fevers, rash, hepatosplenomegaly, or arthralgias. She is receiving physical and occupational therapy for her gross motor delay, and her skills have improved significantly. She is now walking without difficulty.
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A case report of mevalonate kinase deficiency in a 14-month-old female with fevers and lower extremity weakness
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Please create a concise title of this case report, focusing on critical details
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A 38-year-old lady presented with frequent attacks of right hypochondrial pain for the last 4 months, the pain was mainly at the night time and was associated with nausea, no vomiting, and no fever.\nThe patient had no history of any medical diseases, and the past surgical history was negative.\nUltrasound of the abdomen showed distended gall bladder with 1.3 cm gall bladder polyp at the region of the fundus.\nAdvices given to the patient to reduce the fatty meals and antispasmodic medications prescribed with little improvement. Decision done for laparoscopic cholecystectomy. During surgery a duplicated gall bladder found with single cystic duct. Successful surgery done and the gall bladder sent for the histopathological examination which showed a benign gall bladder polyp (, , ).\nThere were no post-operative complications and the patient discharged on the third day.
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Duplicated gall bladder with gall bladder polyp presenting with cholecystitis: Case report with literature review
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Your role is to provide a brief, accurate title of this medical case report
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A 19-year-old man was referred to our clinic with the chief complaint of dyspnea. Physical examinations revealed cyanosis and clubbing with oxygen saturation of 82% at room temperature. ECG showed sinus rhythms without significant ST-T changes. Based on the echocardiographic data, the size and function of the left ventricle were normal, while the right ventricle was small with apical hypoplasia and moderate dysfunction. Assessments of the tricuspid valve revealed moderate tricuspid regurgitation and normal pulmonary artery pressure. There was also a large atrial septal defect with a bidirectional shunt. Angiographic and catheterization data showed increased right atrium pressure and right ventricle end diastolic pressure (). On the basis of the information gathered, the patient underwent the Glenn surgery and the incomplete closure of the atrial septal defect. The surgery conferred significant alleviation in the patient’s symptoms.
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Best management in isolated right ventricular hypoplasia with septal defects in adults
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You need to condense this case report into a succinct title
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Our institution follows a 1-year-old male child with tetralogy of Fallot, born to a 35-year-old woman after an uncomplicated pregnancy. He is the only child of unrelated parents. The family history was negative for CHD. Furthermore he had mild developmental delay and soft dysmorphic features, consisting in hypertelorism, low set ears, broad nasal bridge, and receding chin, while limbs and fingers were normal. Cytogenetic analysis of the proband and his parents was performed on cultured lymphocytes, using a validated oligonucleotide array comparative genomic hybridization Human Genome CGH 180 K Oligo Microarray kit (AMADID 22060, Agilent Technology) with a mean 13 Kb resolution.\nA male karyotype with a terminal 118 Kb deletion in the long arm of chromosome 4 (46,XY,del4q34.3) was demonstrated in the proband. Paternal chromosomes were normal. On the other hand his phenotypically and intellectually normal mother was found to carry the same imbalance. She underwent a cardiac examination in order to rule out a subclinical congenital malformation. Cardiac auscultation revealed a systolic murmur in the mitral area. The ECG was normal. Transthoracic echocardiography showed a thin perforated membrane dividing the left atrium into two chambers (Figures and ). Color-Doppler examination showed a mild mitral insufficiency and a nonturbulent flow through the diaphragm, while the pulsed-wave Doppler ruled out a significant obstruction between the two atrial chambers. Diagnosis of nonobstructive cor triatriatum sinister was established. Since the patient was asymptomatic surgical treatment was deemed unnecessary and only periodical examinations were recommended.
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Different Cardiac Anomalies in Mother and Son with 4q-Syndrome
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 48-year-old woman was admitted to our hospital with pain in the upper abdomen,\nsubstantial weight loss, and hematemesis. Laboratory examination showed a serum\ncarcinoembryonic antigen (CEA) level of 41.53 ng/ml. All other laboratory tests\nwere within the normal range. An auxiliary examination using a gastroscope\nrevealed a lesion in the body of the stomach with a depressed shape (. Abdominal\ncomputed tomography (CT) revealed lymph node invasion of the surrounding gastric\ntissue. There were no signs of metastasis to the liver, spleen, or lungs.\nPreoperative staging was cT3N1M0, and a\nlaparoscopic partial gastrectomy and Roux-en-Y gastrogastrostomy were performed\nafter the preoperative assessment. Histological examination of the resected\nspecimens showed tumor cells invasion of the serosa layer and lymph node\nmetastasis in Stage II. Staging was updated to\npT4aN2M0 Stage III B. The postoperative\ncourse was uneventful until day 5, when the patient abruptly developed a\nhigh-grade fever of 38.5°C without other specific symptoms. Laboratory\nexamination showed an elevated C-reactive protein level (60.7 mg/L) and white\nblood cell count (11.34 × 109/L). An abdominal plane scan showed a\nslight anastomotic fistula in the lesser curvature of the stomach (. A diagnosis of\nabdominal cavity infection was made and antibiotic treatment was initiated\n(cefoperazone and sodium sulbactam; 3 g b.i.d intravenous infusion). The fever\ngradually subsided and the laboratory parameters slowly returned to normal\nwithout the patient developing further complications. The patient was discharged\non postoperative day 15. In accordance with the Japanese Gastric Cancer\nTreatment Guidelines 2014 for SOX (S-1 plus oxaliplatin) regimens, oxaliplatin\nwas administered by intravenous infusion at a dose of 130 mg/day for 1 day and\nS-1 was administered orally at a dose of 100 mg/day on day 2 to 14, followed by\na 7-day drug-free period. After one course of chemotherapy, the patient abruptly\ndeveloped a high-grade fever of 39.5°C along with chills, fatigue, and loss of\nappetite. The laboratory data showed elevated procalcitonin (93.17 ng/ml), white\nblood cell count (13.34 × 109/L), C-reactive protein (60.7 mg/L),\nD-dimer (1.17 μg/ml), and aspartate transaminase (46 IU/L), and a reduction in\nalbumin (22.3 mg/L). Other laboratory data were normal. A contrast-enhanced CT\nshowed a clot embolism along the main portal vein and the right hepatic vein\n(.\nCefoperazone and sodium sulbactam (3 g, b.i.d, intravenous infusion) and\nlow-molecular-weight heparin calcium (0.6 ml, b.i.d, s.c.) were immediately\nadministered, and chemotherapy was discontinued. Two weeks later, the fever\ndiminished and the laboratory data returned to normal. An imaging examination\nshowed the appearance of a smaller clot and a cavernous transformation of the\nportal vein. The patient was discharged on oral rivaroxaban. During 6 months of\nfollow up, no hepatic decompensation or liver cirrhosis was observed.
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Portal vein thrombosis secondary to postoperative gastric cancer:\nReport of two cases
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You are to provide a brief yet comprehensive title of this case report
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A 58-year-old male patient underwent aortic valve replacement surgery (On-X mechanical prosthesis, ring size 23 mm) due to severe aortic valve stenosis with preserved LV function and normal coronary arteries. The postoperative period was complicated by third-degree AV block and sustained ventricular tachycardias and a DDD-ICD implantation was implanted. After 3 months of surgery, the patient presented with symptoms of progressive fatigue, dyspnoea on exertion and generalised peripheral oedema. No chest pain was reported. The patient had gained 30 kg in weight in 3 months. Physical examination revealed a raised jugular venous pressure with prominent vein pulsations, normal cardiac sounds with normal artificial valve clicks and no murmurs. Auscultation of the lungs was normal. The patient had a palpable liver of 4 cm, noticeable ascites, and extensive pitting oedema from ankle to hip. Laboratory results revealed elevated liver enzymes and moderately raised NT-proBNP (328 pmol/l) without other abnormalities. Electrocardiogram revealed a sinus rhythm with ventricular pacing. Chest X-ray demonstrated an enlarged heart but no pulmonary congestion. The echocardiogram was limited by severely impaired image quality. Left ventricular function was normal, right heart function was mildly impaired and LV diastolic function was normal with E/A ratio 2.7 (E 0.82; A 0.30; deceleration time 153 ms), with normal E/E’ ratio 7.4 (E’ = 11.1) (Fig. ). The mechanical aortic valve was sufficient. Respiratory variation of transmitral flow velocity signal appeared >25 % but not conclusive because of limited interpretability due to low echo quality. During echocardiography, an echodense layer or mass was seen at the LV apex outside the myocardium, which could be pericardial fluid (blood or thrombus), thickened pericardium or epicardial fat. A chest CT proved the layer to be a thickened pericardium (6 mm) (Fig. ). Although unlikely so soon after surgery, the signs of previously absent right-sided heart failure and the thick pericardium suggested the diagnosis of constrictive pericarditis without any signs of calcification yet. Other causes such as inflammatory (normal CRP) or autoimmune disorders (M-protein negative) were ruled out. Differential diagnostics now included constrictive pericarditis and restrictive cardiomyopathy. The normal E’ of 11.1 makes restrictive cardiomyopathy unlikely (in which the myocardium itself is diseased). To confirm the diagnosis of constrictive pericarditis (which would have severe consequences for the patient as a re-thoracotomy would be necessary), we performed a right heart catheterisation. The right heart catheterisation revealed a diastolic dip plateau phase (Fig. ) and right atrial Y wave further confirming our diagnosis of constrictive pericarditis (Fig. ). We did not perform simultaneous left-sided pressure measurements with the mechanoprothesis in situ. At that stage, we discussed re-operation with the cardiothoracic surgeon and decided to perform pericardiectomy. Surgery revealed a thickened pericardium and an extensive fibrous net/rind of the thickened pericardium was found and removed (Fig. ). Histological examination of the removed material confirmed the diagnosis with signs of chronic fibrotic inflammation. After pericardiectomy, the patient recovered slowly with a regimen of intravenous diuretics and positive inotropes (enoximone) for the first postoperative days. He was discharged in a good condition on oral diuretics.
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Early rapidly developing constrictive pericarditis after aortic valve surgery
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Please create a concise title of this case report, focusing on critical details
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A 76-year-old female, known to be hypertensive on treatment, presented with a 2-day history of colicky abdominal pain, bilious vomiting, and abdominal distension. On examination, she was sick looking and afebrile.\nOn physical examination, she had a moderately distended abdomen, with a moderately tender swelling in the left anterior abdominal region which according to the patient had been there for over 20 years. The rest of the abdomen was mildly tender but no rebound tenderness, and bowel sounds were of increased frequency and pitch. A digital rectal exam revealed an empty rectum. Notably from the cardiovascular system exam, she was in hypertensive urgency with a blood pressure of 200/100 mmHg.\nInvestigation results show the following data: full blood count: total white cell count 13.9 g/L, hemoglobin 11.9 g/dL, and platelets 563 g/L; serum electrolytes: chloride 99.9 mmol/L, sodium 134.9 mmol/L, and potassium 5.40 mmol/L generally normal; and abdominal ultrasound scan: bowel loops were distended () with contents showing back and forth peristaltic motion. There was also an abdominal wall defect measuring 4.45 cm in diameter with herniated bowel loops in the anterior abdominal region with mild fluid collection in the hernia sac. An erect abdominal X-ray revealed uneven bowel gas distribution mainly in the upper abdomen with dilated bowel loops and significant air fluid levels ().\nCT scan was requested but not done due to financial constraints. Working impression was intestinal obstruction due to sigmoid volvulus, also querying an obstructed hernia in the left anterior abdominal wall and hypertensive urgency.\nConservative management for intestinal obstruction which included nil per os, nasogastric tube decompression of the stomach, soapy enema, maintenance intravenous fluids, and antibiotic cover was started plus blood pressure management, and 24 hours later, she had improved as the abdominal pain, distension, and vomiting had stopped. She was able to pass stool normally. The blood pressure had also normalized. Decision was made to repair the hernia; and an explanation was given to the patient, and informed consent was obtained.\nIntraoperatively, using a Rutherford-Morrison incision in the left anterior abdominal region, the abdomen was opened in layers; a large defect was found (6 × 5 cm) at the Spigelian aponeurosis (), with a huge, thick, inflamed sac protruding; the sac was opened; and an inflamed jejunum was found, obstructed with adhesions (). The Spigelian hernia was repaired with a mesh under layers (of the rectus sheath), fixing it with Nylon 0, from the lower part of the inguinal ligament and up to the sheath of the muscles; the mesh was covered with the sheath of the rectus and transversus muscle (). The mesh was subcutaneously apposed with Vicryl 2/0, and the skin was closed with Vicryl 2/0 (). The patient recovered uneventfully and was discharged on the tenth postoperative day. The follow-up was done at 2 months and 6 months, and no sign of recurrence was identified.
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Large Strangulated Spigelian Hernia: Management of an Uncommon Presentation of Abdominal Hernias in Central Uganda
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Please create a concise title of this case report, focusing on critical details
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A 28-year-old female patient presented to the emergency department (ED) with a five-day history of high-grade fever, runny nose, severe persistent throbbing headache associated with nausea, vomiting (not projectile), and mild photophobia. Her vital signs showed 38.9 C temperature, 107/74 mm/Hg blood pressure, 115 beats/min pulse, soft, lax abdomen, and clear chest with equal air entry bilateral. On neurological examination, she was fully conscious, alert, oriented, with normal speech. Her neck was mildly stiff on flexion; however, Kerning and Brudzinski's signs were negative. There was tenderness of bilateral frontal sinus. The cranial nerves examination, including oculomotor nerves, visual acuity, and field, was normal. The fundus examination showed no papilledema. Other neurological examinations, including motor, sensory, and coordination, showed no abnormalities. A brain non-contrast computed tomography (CT) scan was done without any abnormalities detected (Figures -). Initial serum laboratory investigations, including complete blood count, liver function test, renal function test, international normalized ratio (INR), and lactic acid, were normal, except that C-reactive protein (CRP) was 7.6 mg/L.\nMoreover, rapid strep, dengue fever, and swine flu (H1N1) tests were negative, so a nasal swab and blood sample were sent for culture. A decision to perform LP to search for central nervous system (CNS) infection was made and written consent obtained from the patient. The procedure was done in the left lateral position by a senior anesthesiologist through dural puncture at the L3-4 vertebral level using a 22-gauge spinal needle. CSF opening pressure was 11 cmH2O. The fluid was clear, and three samples, each of 3 ml, were obtained and sent for the lab. CSF investigations were within normal ranges, including protein 0.19 gm/l, glucose 4.2 mmol/l, and white blood cell (WBC) count was 1/mm3. Moreover, gram staining showed no organism and culture pending. Over the 24 hours following the procedure, she was complaining of pain in the procedure site and post-LP positional headache, which responded to analgesics, caffeine, and proper hydration. On hospital day two, the nasal swab was positive for influenza B, so Tamiflu was started with an improvement of general condition. On day three, blood and CSF cultures were negative; the patient was afebrile and her headache improved, so she was discharged home with adequate pain killers and Tamiflu.\nTwo days later, the patient came back to the emergency department (ED) complaining of drowsiness, a worse bilateral front-temporal headache not responding to analgesics and exacerbated by lying down and movement; moreover, it was associated with blurred vision, nausea, and vomiting. A new CT brain was done that revealed an acute left temporal SDH, extending within the tentorium-cerebelli with little mass effect (Figure ).\nThe patient was admitted for close monitoring and symptomatic treatment. She denied any head trauma after discharge; extensive hematological workup for any bleeding tendency was negative. Magnetic resonance imaging (MRI) brain and magnetic resonance venography (MRV) with gadolinium (Figure ) was done and revealed the same hematoma and patent venous system without any signs of sinus thrombosis. Cerebral CT angiography (CTA) with contrast was done and didn't show any vascular malformation or aneurysmal dilatation (Figure ).\nNeurosurgical consultation recommended conservative medical treatment and observation. She remained neurologically stable and her headache and general condition mildly improved. Repeat CT brain (Figure ) showed no change in SDH size and decreased hemorrhage size of tentorium-cerebelli on day five (Figure ). The clinical course was good, and the patient's headache gradually improved during the hospital course. She was discharged home on hospital day eight with analgesics and antiemetics with a diagnosis of post-LP SDH complication. She asked to follow up at the outpatient clinic and repeated CT brain after three weeks revealed decreased SDH size and entirely resolved SDH after two months.
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Acute Subdural Haemorrhage as a Complication of Diagnostic Lumbar Puncture
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 57-year-old female was brought to the hospital because of new onset of confusion and apraxia. The patient had a past medical history significant for nonischemic cardiomyopathy for 2 years. The patient had a stroke several weeks prior during an admission to another facility. At that time, work-up for the etiology of the stroke was negative except for cardiomyopathy with an ejection fraction of 30%. The patient did not have any residual focal motor neurologic deficits, although she was cognitively impaired. Medications at discharge included aspirin, carvedilol, lisinopril and atorvastatin.\nOn admission, the patient was hemodynamically stable without any distress. Her speech was incoherent and tangential. She had difficulty identifying objects and could not use eating utensils appropriately. Pupils were equal and reactive without any nystagmus or gaze disturbance. No other neurologic deficits were present. On cardiac auscultation, first and second heart sounds were heard normally without any murmur. Lungs were clear. Carotid and other peripheral pulses were palpable and symmetric. Trace bilateral ankle edema was present.\nThe patient had a normal complete blood count, electrolytes, liver function and thyroid function tests. The cardiac BNP value was 340 pg/mL. Electrocardiogram revealed normal sinus rhythm with T wave inversions in the lateral leads. A chest X-ray was negative for active cardiopulmonary disease. Non-contrast CT scan of the head showed areas of low attenuation in the right posterior frontal and parietal regions consistent with subacute infarctions which were outlined with high attenuation representing hemorrhagic conversion. Subsequent MRI was consistent with these findings with additional tiny acute infarcts in the parietal lobes ().\nA transthoracic echocardiogram for an embolic source showed severe reduction of the left ventricular systolic function with ejection fraction of 10-15%. On close observation, there was a suspicious appearance of prominent trabeculations in the left ventricle (). Cardiac MRI showed signs of non-compaction cardiomyopathy with prominent trabeculations in the left ventricular myocardium (). A transesophageal echocardiogram with contrast showed more clearly the prominent trabeculations with contrast occupying recesses between the trabeculae (, ). A diagnosis of isolated LVNC syndrome was established which caused recurrent embolic stroke in the patient. Continuous telemetry revealed episodes of nonsustained ventricular tachycardia. An implantable cardiac defibrillator (ICD) was placed. The patient was started on systemic anticoagulation with warfarin to lower the risk of systemic embolism and recurrent stroke. Since non-compaction has a familial occurrence, the patient’s two sisters were recommended to undergo screening echocardiography. The patient was discharged home with resolution of her neurologic deficits.
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Left Ventricular Non-Compaction Syndrome Misdiagnosed as Dilated Cardiomyopathy on Several Occasions, Presenting With Recurrent Stroke
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You are required to deliver a compact title of this case report, outlining the significant findings
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A 3-year-old female child, first issue of a third-degree consanguineous union, presented to us with history of developmental delay and recent loss of achieved milestones. She had a normal birth history and history of two episodes of pneumonia, at 2 months and at 1 year of age, both requiring inpatient treatment. She achieved head holding at 5 months, sitting at 1 year, standing with support at nearly 18 months, transfer of objects at 1 year, and scribbling at 22 months. She also had social language delay with social smile at 4 months, stranger anxiety after 1 year, speaking bisyllables after 14 months, and two words with meaning at nearly 22 months of age. She stopped gaining new milestones after 22 months, and at 2 years she lost her ability to stand and became progressively unable to sit, speak meaningfully, scribble, or hold objects. She developed abnormal eye movements and auditory inattention. There were no seizures. There was no family history of neurological disease. On examination, her head circumference was normal and she did not have any dysmorphic features. Ophthalmological examination showed rotatory and horizontal nystagmus with optic disc atrophy in both eyes. She had hearing loss. She had titubations, and was hypotonic and hyporeflexic, with a normal plantar response.\nInvestigations showed normal basic metabolic tests, creatine kinase, blood ammonia, serum lactate, alpha fetoprotein, lipid profile, and vitamin E and B12 levels. Neuroimaging showed mild cerebellar atrophy []. Brainstem evoked response audiometry (BERA) showed sensorineural hearing loss. Nerve conduction velocity (NCV) was normal at this stage, but on electromyography (EMG), chronic partial denervation was seen in the tibialis anterior muscle bilaterally.\nThe child was started on physical therapy and nutritional supplementation and was followed up. She showed steady deterioration with loss of head control, vocalization, and hearing, and also developed ataxia and pyramidal signs. PLA2G6 sequencing was performed and a homozygous mutation was found for c2047A > T at p. K683X, which confirmed the diagnosis of INAD in the child. The patient was continued on physical therapy, baclofen, and nutritional support but has, by now, progressed to a vegetative state.
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Two unusual cases of PLA2G6-associated neurodegeneration from India
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Your task is to summarize this medical case report into a title
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The patient was a 66-year-old male with diffuse lymphadenopathy and B symptoms. The white cell count was 56,800/μL (WBC differential: Neutrophils: 70.0%; Eosinophils: 2.0%; Basophils: 2.0%; Metamyelocytes: 1.0%; Myelocytes: 7.0%; Monocytes: 11.0%; Lymphocytes: 3.0%), the hemoglobin was 9.9 g/dL, and the platelet count was 314,000/μL. As the differential demonstrated, his peripheral blood showed increased left-shifted granulocytes, mild basophilia, and absolute monocytosis. There are no circulating blasts. Bone marrow biopsy showed a hypercellular marrow (95–100% cellularity) with marked myeloid hyperplasia and left-shift, increased hypolobated megakaryocytes, and no increase in blasts (). Flow cytometry of bone marrow showed no increased myeloid cells (1% blasts) and no T lymphoblasts were present. The concurrent left inguinal lymph node biopsy revealed an effaced lymph node with diffuse infiltration of small to intermediate sized blasts (). These blasts were CD3+, CD1a+, and TdT+ () by immunohistochemistry. Flow cytometry of the lymph node revealed a population of T-lymphoblasts which were CD45+, CD1a+, CD2+, sCD3−, cy-CD3+, CD4−, CD5+, CD7+, CD8−, CD10−, CD19−, CD20−, CD38+, CD16−, CD57−, CD103−, CD13−, CD33+dim, CD34−, CD117+/−, and TdT+. Cytogenetic analysis showed an abnormal karyotype in the bone marrow: 46,XY,t(9;22)(q34.1;q11.2)[12]/47,idemdel(5)(q13q33),+MAR[CP8], and a complex karyotype in the lymph node: 46,XY,del(5)(q13q33),t(9;22)(q34;q11.2),add(12)(p11.2),+14,−22[11]/51,idem,+8,+10,+11,+13,+19[9]. FISH studies were positive for BCR-ABL1 in both peripheral blood and bone marrow (), but negative for rearrangements of the FIPIL1/PDGFRA. RT-PCR showed a BCR-ABL1 fusion transcript with minor breakpoint encoding the p190 protein.\nThe patient was diagnosed as CML-CP with monocytosis in the bone marrow and T-ALL BP of CML in the lymph node. His monocytosis (11%) in the peripheral blood was consistent with the minor BCR breakpoint []. After being treated with cyclophosphamide, daunorubicin, vincristine, and prednisone and imatinib, he was lost to follow up.
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Unusual T-Lymphoblastic Blast Phase of Chronic Myelogenous Leukemia
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