5-oxoprolinemia is caused by a defect in the gamma-glutamyl pathway which can present with severe anion gap metabolic acidosis not caused by ketoacidosis, lactic acidosis, methanol/ethylene glycol ingestion, renal failure, ethanol, iron/isoniazid or salicylate ingestion. This case will describe a 59-year-old female presenting with elevated anion gap metabolic acidosis with no discernible classical cause, chronic acetaminophen use, malnourishment, and severe hypothyroidism with 5-oxoprolinemia after extensive investigation of other causes. Treatment involved correcting the acidosis with bicarbonate, IV fluid administration, oral levothyroxine and avoiding further acetaminophen use. The patient’s acidosis resolved soon after and she was counseled on the avoidance of acetaminophen in the future. This case highlights the importance of pharmacologic vigilance with everyday over-the-counter medicines such as acetaminophen and metabolic states such as hypothyroidism which can lead to tumultuous cases of metabolic acidosis. This is the first case in which we know that 5-oxoprolinemia has presented with concomitant severe hypothyroidism. Due to this patient’s course, it may have been the preceding factor for the development of her oxoprolinemia alongside her acetaminophen consumption.
Haemophilus influenzae is a nonmotile gram-negative cocobacillus that is responsible for a broad spectrum of infections. Type b and nontypable strains are the most clinically relevant strains. Invasive disease is usually associated with type b strains because of the virulence conferred by its capsule. In recent years, the overall incidence of type b infection has decreased secondary to widespread vaccination. Nonencapsulated, nontypable strains can also cause invasive disease; however, this usually occurs in immunosuppressed patients or those with underlying medical conditions. We present a fatal case of severe gastroenteritis associated with biotype 3 H. influenzae. (Infect Dis Clin Pract 2010;18: 139Y140) CASE REPORTThe patient was a 51-year-old African American human immunodeficiency virusYnegative man with a history of chronic alcohol use who presented to Harlem Hospital Center for the first time with a 2-day history of profuse, nonbloody diarrhea after eating chicken soup. There was no history of nausea, vomiting, abdominal pain, sick contacts, or recent travel. On physical examination, he was a middle-aged man in no acute distress with very dry oral mucosa. His vital signs were significant for tachycardia. He was afebrile, and his blood pressure was normal. There was no orthostasis. There were no upper respiratory findings. His cardiac and respiratory examination results were unremarkable. There was no abdominal tenderness, and the rectal examination result was normal. Urine output was 50 mL in 3 hours. Initial laboratory results revealed a lactate level of 6 mmol/L, blood urea nitrogen level of 37 mg/dL, creatinine level of 6 mg/dL, and platelet count of 88,000/KL (Tables 1, 2). Transaminases were mildly elevated. The albumin level was 3 g/dL. The white blood cell count was 4400/KL, and the hemoglobin level was 13.5 g/dL. The stool guaiac test result was negative. The chest radiograph was normal. He was then hydrated with isotonic sodium chloride boluses for severe volume depletion secondary to acute gastroenteritis. However, despite aggressive fluid resuscitation and the maintenance of adequate blood pressure, the patient remained tachycardic and oliguric. The lactate levels also remained elevated. The patient's condition then rapidly deteriorated. Oxygen saturation had dropped to 80% in room air. Respiratory support was immediately administered; however, he became pulseless within minutes. The patient died on his 12th hour of hospitalization. Blood cultures drawn on admission later grew Haemophilus influenzae biotype 3 using the Vitek 2 system (bioMérieux, Inc., Durham, NC).
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