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Gastric volvulus is a rare and life-threatening condition that involves the abnormal rotation of the stomach around its axis by more than 180°. The association between acute gastric volvulus and atrial fibrillation with rapid ventricular response is rare with only few cases that have been reported. Our patient was an 86-year-old female who presented with upper abdominal pain, distension, nausea, and shortness of breath. Clinical and laboratory workup revealed acute gastric volvulus with diaphragmatic hernia. On presentation, she was also in atrial fibrillation with rapid ventricular response. She was successfully treated by laparotomy with reduction of the gastric volvulus and repair of the diaphragmatic hernia, with significant improvement.

case presentation A 52-year-old African American man with untreated AIDS and active intravenous drug abuse presented with a three-day history of bilateral upper abdominal pain radiating to the back, which was associated with loss of appetite and generalized weakness. There was no fever or night sweats, and no vomiting, diarrhea, dysuria or hematuria. He denied cough, shortness of breath or chest pain. He also denied nasal congestion or headache. Physical examination showed a cachectic middle-age man. Vital signs included temperature of 98.4°F (36.9°C), blood pressure 123/76 mmHg, heart rate 83 beats/min and a respiratory rate of 18 breaths/min. His lungs were clear to auscultation and his heart examination revealed normal heart sounds with no murmurs or gallops. Abdominal palpation revealed tenderness in the right upper quadrant and right costovertebral angle. He exhibited no rashes or lymphadenopathy. Laboratory results revealed a white blood cell count of 3.3×109/L with absolute neutrophil count of 2×109/L and hemoglobin level of 96 g/L. The patient’s CD4 cell count was 20 cells/μL and HIV viral load was >105 copies/mL. Urine showed pyuria and a high leukocyte esterase level, but no hematuria. His serum creatinine level was 106.08 μmol/L. The patient was started empirically on meropenem, but his symptoms persisted. A transthoracic echocardiogram showed normal ejection fraction and no valvular abnormalities or vegetations. Urine and blood cultures were negative. A computed tomography (CT) scan (Figure 1) and CT-guided biopsy were performed (Figure 2). What is your diagnosis?

The immunosuppression required after solid organ or hematopoietic transplantation leaves some patients vulnerable to lymphoprol iferative disorders that are difficult to treat. Several factors may play a role in the development of these malignancies, some of which may initially be nonspecific and have overlapping manifestations, but are, nevertheless, associated with exceedingly high mortality rates. This article describes a case of post-transplant lymphoproliferative disorder in a patient who underwent a stem cell transplant for chronic lymphocytic leukemia.

Case presentation A 19-year-old woman with a medical history significant for poorly controlled diabetes mellitus (DM) (hemoglobin A1C 11.2%) presented with a 12-day history of right-sided pleuritic chest pain. One month earlier, she had developed sudden-onset fever, dry cough and shortness of breath. At the time, she did not have any gastrointestinal symptoms including epigastric pain, heartburn, vomiting or retching. She denied sick contacts and had no preceding symptoms of an upper respiratory tract infection. She was seen at a local emergency department and was released home on a 10-day course of oral doxycycline (100 mg every 12 h) to treat a community-acquired pneumonia (CAP). After an initial two-week improvement, her complaints relapsed, with fevers, dry cough, poor appetite and the above-described chest pain. The patient did not smoke and she denied alcohol abuse or illicit drug use. On presentation to the hospital, she was febrile (temperature 38.2°C), her oxygen saturation was 86% on room air and she was thin. She was awake and oriented but in obvious pain. She had no jugular venous distention. Her heart sounds were regular without murmurs or gallops. The lung examination revealed reduced air entry over the right lung base with bronchial breath sounds and egophony. The abdomen was soft without tenderness or distension and she had no evidence of subcutaneous emphysema or lymphadenopathy. There were no lower limb edema and no joint swelling or deformities. The laboratory tests revealed a white blood cell count of 26.0×109/L and a hemoglobin level of 119 g/L. Blood chemistry showed normal kidney and liver function. Tests for HIV and pregnancy were negative. Chest imaging included a chest x-ray and a contrasted chest computed tomography scan (Figures 1 and 2). The patient was admitted to hospital with severe sepsis due to CAP complicated by an empyema and was started on intravenous broad-spectrum antibiotics, vancomycin (15 mg/kg every 12 h) and piperacillin/tazobactam (3.375 g every 6 h). She underwent computed tomography-guided drainage 48 h afterwards. An interventional radiologist performed the procedure under strict sterile techniques. Cytopathology (Figure 3) and cultures were ordered on the drained fluid. What is your diagnosis?

Given the number of similar-appearing conditions among a widely heterogeneous group of pulmonary diseases, pneumonia is a commonly overdiagnosed entity, which makes establishing a diagnosis for a specific disease particularly challenging. This article describes the presentation, history, work-up and eventual diagnosis of a 28-year-old woman who was diagnosed with a variety conditions over a span of five months.

Case presentation A 68-year-old Hispanic woman presented with a third episode of cystitis. She complained of multiple episodes of dysuria, frequency and suprapubic discomfort for the past six months. She denied fevers, chills, hematuria and flank pain. There was no history of nephrolithiasis and she had no other complaints. Her symptoms responded to oral levofloxacin, administered for 14 days after each episode of infection; however, they recurred a few weeks thereafter. Her medical history was significant for diabetes mellitus that was well controlled on oral hypoglycemic agents. She did not smoke, had immigrated to the United States 45 years previously and had a negative purified protein derivative test on intake. She was married with three healthy children, was a homemaker and had no contact with animals. On examination, the patient was afebrile, with a temperature of 37.6°C. Her blood pressure was 126/78 mmHg, heart rate was 82 beats/min and her oxygen saturation was 97% on room air. She was awake, alert and not in acute distress. Her skin was intact with no rashes or lymphadenopathy. She had clear lung fields, regular heart sounds without murmurs and soft nontender abdomen with no organomegaly. She had no renal angle tenderness and no lymphadenopathy. Her neurological examination was nonfocal. Blood tests revealed a hemoglobin level of 97 g/L and white blood cell count of 8.4×109 cells/L. She had chronic kidney disease with a creatinine level of 133 μmol/L. Her liver function tests were normal. Urinalysis revealed a white blood cell count of >100 cells per highpower field, with hematuria and proteinuria. Routine urine culture was negative. A computed tomography scan of the abdomen and pelvis showed normal kidney size with no stones, and a thickened urinary bladder wall with no ascites or lymphadenopathy. The patient underwent cystoscopy and biopsy (Figures 1 and 2). What is your diagnosis?

Prolonged survival in HIV infection is accompanied by an increased frequency of non-HIV-related comorbidities. It is suggested that cardiovascular diseases (CVD) occur earlier among HIV-positive patients compared with HIV-negative patients, and at a higher rate. Several factors have been proposed which can be categorized into traditional and nontraditional risk factors. Immune dysfunction is a nontraditional risk factor that contributes significantly to cardiovascular pathology. Markers of inflammation are elevated in HIV-infected patients, and elevations in markers such as high-sensitivity C-reactive protein, D-dimer, and interleukin-6 (IL-6) have been associated with increased risk for cardiovascular disease. However, the data currently suggest the most practical advice is to start antiretroviral therapy early and to manage traditional risk factors for CVD aggressively. A better understanding of the mechanisms of CVD in this population and further efforts to modify chronic inflammation remain an important research area.