Colitis and Pancreatitis in a Patient with Systemic Lupus Erythematosus: Due to Disease or to Drug?

Excerpt

A 37-year-old female with a history of developmental delay, left-sided focal epilepsy due to polymicrogyria, systemic lupus erythematosus (SLE), and stage 3 chronic kidney disease due to lupus nephritis was initially evaluated for diarrhea of 4 months duration. Due to the presence of cognitive issues, her history was obtained from her mother, her primary caregiver. She reported that her daughter had been having 5–6 loose bowel movements per day for 4 months, associated with a weight loss of 15 lbs over this time period, contrasting with the one formed bowel movement per day she had experienced prior to the onset of diarrhea. Moreover, she was stated to have had sharp epigastric pain and intermittent nausea and vomiting for 3 days prior to evaluation and was currently not able to tolerate any oral intake. The patient was hospitalized 1 month prior to the current admission and diagnosed with influenza B. At that time, she was neutropenic with a white blood cell count of 0.7 × 10⁹/dl (4.5–11.0 × 10⁹/dl) which on consultation with the hematology service was attributed to her acute viral infection. She was treated with oseltamivir and given one dose of filgrastim prior to hospital discharge. Other past medical history included hypertension, hypothyroidism, and avascular necrosis of the femur due to chronic steroid use. In her family history, her mother and father had diabetes. She denied any history of smoking, alcohol, or illicit drug use. Her lupus nephritis had been treated with mycophenolate mofetil (MMF) for over 2 years, but 2 months prior to admission this treatment was changed to mycophenolate sodium (MPS) by her rheumatologist who thought MMF might have caused her diarrhea. Since the medication switch did not relieve the diarrhea, she presented to the Emergency Department, where she was afebrile and tachycardic (115/min), with a blood pressure of 70/42 mm Hg and respiratory rate 18/min with oxygen saturation of 100% on room air per pulse oximetry. Physical examination revealed signs of marked intravascular volume depletion with a dry oral mucosa; abdominal examination revealed hyperactive bowel sounds and tenderness to palpation in the epigastric and periumbilical regions, but no rebound tenderness. Rectal examination was unremarkable. Laboratory tests on admission showed a blood hemoglobin of 10.1 g/dl (12-16 g/dl), a white blood cell count—3.4 × 10⁹ per liter (4.5–11.0 × 10⁹ per liter), a platelet count—150,000 mm³ (150,000–400,000/mm³), and serum concentrations of sodium—129 mmol/L (134-144 mmol/L), potassium—3.5 mmol/L (3.5–5 mmol/L), chloride—98 mmol/L (98–111 mmol/L), bicarbonate—10 mmol/L (20–30 mmol/L), BUN—52 mg/dl (7–31 mg/dl), creatinine-3.81 mg/dl (baseline 0.7–0.9 mg/dl), and lipase—479 mg/dl (10–73 mg/dl); liver function tests were normal. A computerized tomographic (CT) scan of the abdomen performed on admission showed findings suggestive of acute pancreatitis and a hydropic gall bladder. An ultrasound scan of the abdomen showed a dilated gall bladder but no evidence of the presence of cholelithiasis or choledocholithiasis. The patient was aggressively resuscitated with intravenous fluids followed by improvement in her blood pressure, heart rate, electrolyte abnormalities, and kidney function. Other tests included stool culture, examination for ova and parasites, fecal fat, Clostridium difficile testing of stool, and serum lipid concentrations, all of which were unremarkable. Her intermittent nausea and vomiting, epigastric and upper abdominal pain and tenderness, elevated serum lipase, and abnormal findings on CT scan, in the absence of other obvious risk factors, were attributed to acute pancreatitis. …