A 22-year-old Asian woman presented with respiratory distress, cough, and wheezing for 1 week. Prior history included asthma and Turner syndrome. On presentation to the emergency department, the patient was hypotensive, tachycardic, tachypneic, with an oxyhemoglobin saturation in the mid 80% range while breathing ambient air. Chest radiograph revealed pulmonary vascular congestion and a left lower lobe infiltrate. Endotracheal intubation, mechanical ventilation, and vasopressors were initiated. Empiric therapy for community-acquired pneumonia was administered utilizing broad-spectrum intravenous antibiotics. Routine sputum culture was negative for pathogens. Nasopharyngeal swab submitted for multiplex amplified nucleic acid testing yielded enterovirus-human rhinovirus (EV-HRV). Thus, the diagnosis of EV-HRV pneumonia complicated by acute respiratory distress syndrome (ARDS) was established. Multiple attempts to wean from the ventilator were unsuccessful, and a tracheostomy was performed. This report highlights EV-HRV as a cause of severe ARDS and prolonged respiratory failure in adults.
Glycosylated haemoglobin (HbA1c) is a measurement commonly performed in patients with diabetes. Factors causing a change in the life span of the red blood cell (RBC) can affect the measurement of HbA1c. Thus haemolysis is an important factor that may affect the HbA1c level determination. Haemolysis has been shown to cause a falsely low HbA1c. A 62-year-old man with a history of autoimmune haemolytic anaemia was admitted for severe haemolytic anaemia and an Hb of 2.9 g/dL. HbA1c tested during hospitalisation was unrecordable due to the extremely low Hb. The patient was treated with intravenous steroids, immunoglobulin, fluids and RBC transfusions but continued to haemolyse and eventually expired. We emphasise that an extremely low HbA1c level can serve as a marker of haemolysis and an unrecordable HbA1c level may point towards fatal haemolysis.
The incidence rate of chronic lymphocytic leukemia (CLL) in the United States is approximately 0.005%; men are at slightly higher risk than women. Bony involvement or pathological fracture rarely occurs in CLL, and it may be the initial presentation. An 85-year-old woman presented with acute respiratory failure secondary to pneumonia. Symptomatology included dyspnea. She was found to have pathological fracture of the femur caused by CLL. The diagnosis of CLL had been made 6 years previously, but the patient had refused therapy. On admission, the patient required endotracheal intubation, mechanical ventilation, and admission to the medical intensive care unit. Endotracheal intubation extubation was successful after 48 hours. The patient then complained of severe left knee pain. Bone radiograph and femoral computed tomography scan revealed acute pathological fracture of the left distal femur. There was no history of trauma. The fracture was stabilized with extension lock splint. Pathological fracture in patients with CLL is associated with hypercalcemia, Richter’s transformation, or multiple myeloma. This patient exemplifies the fact that pathological fracture can be caused by CLL in the absence of hypercalcemia, Richter’s transformation, or multiple myeloma and can be the initial presentation of CLL.
Medications have been known to cause adverse drug reactions that affect various organs; these are mostly reversible reactions that improve with the cessation of the culprit medication. Losartan is an angiotensin-one receptor blocker which has been approved by the Food and Drug Administration (FDA) for the treatment of arterial hypertension. Fatigue, anemia, weakness, and cough are some of the common adverse effects of losartan. Acute hepatic injury has rarely been reported as an adverse effect of losartan. We report a case of a 61-year-old female with severe hepatic injury secondary to losartan use. None of the cases reported so far had such a high elevation of liver enzymes as seen in our patient.
Infliximab therapy is associated with higher rates of active tuberculosis (TB), particularly extrapulmonary and disseminated forms with unusual symptoms. We report the case of a 66-year-old man with Crohn’s disease who developed TB mimicking lung cancer on imaging. He presented with cough and fever of 2 weeks’ duration shortly after starting infliximab. Computed tomography of the chest revealed a 7.0 × 3.2 cm2 pleural-based mass, highly suspicious for malignancy. Histopathological examination confirmed the diagnosis of TB. The mass disappeared after antitubercular treatment, and the patient recovered completely. A review of the literature suggests that TB masquerades as lung cancer clinically and radiologically. The classical lesions of TB are cavitatory with calcifications. Mass lesions without cavity or calcifications are rare and are mostly reported from regions endemic for TB. The majority of patients on infliximab therapy required biopsy for accurate diagnosis of TB because of its unusual presentation.
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