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Author: Stephanie E. Dreifuss, University of Pittsburgh School of Medicine, Class of 2014
We present a 64-year-old male with a past medical history of hypertension who presented with diarrhea and 12 kilogram weight loss over the preceding three months. He reported 3-10 daily episodes of fatty, non-bloody diarrhea with associated abdominal pain, bloating, and distention. He denied any changes in his diet or medications (olmesartan 40mg daily and omeprazole 40mg daily) within the last few years. He had a recent hospitalization for prerenal acute kidney injury (AKI) secondary to intractable diarrhea.
Stool cultures, Clostridium difficile toxin, and stool ova and parasites were negative. Stool osmolality, stool electrolytes, serum gastrin, serum VIP, and urine 5-HIAA were within normal limits. Fecal fat was elevated. A colonoscopy revealed no abnormalities. Small intestinal biopsy revealed villous blunting and intraepithelial lymphocyte infiltration. Based on the biopsy results and fecal fat elevation, celiac sprue was suspected. Therefore, the patient was instructed to begin a gluten-free diet, and serologic studies were ordered. IgA, anti-endomysial, and anti-tissue transglutaminase antibodies returned within normal limits, while the patient reported no improvement in his diarrhea.
He was admitted to the hospital three weeks later with dehydration, AKI, and orthostatic hypotension. Given his blood pressure of 83/48, olmesartan was discontinued. At a two week follow-up, he reported complete resolution of his diarrhea. He was gaining weight, having only one formed bowel movement daily, and beginning to reintroduce gluten into his diet. Amlodipine was started in place of olmesartan. Two months later, he reports having no diarrhea.
We report this case for two important reasons. First, we aim to alert clinicians of an unusual entity to include in the differential diagnosis of chronic diarrhea. The clinical features of this enteropathy include gastrointestinal symptoms (chronic diarrhea, weight loss, steatorrhea), negative serology (IgA tissue transglutaminase or endomysial antibodies), histologic evidence of enteropathy (villous atrophy and intraepithelial lymphocytosis), lack of improvement in symptoms with a gluten-free diet, exclusion of other causes of enteropathy, and evidence of improvement after discontinuing olmesartan. The findings in this case are similar to another case series in the literature (Mayo Clin Proc 2012;87:732). Our second objective is to emphasize the potentially dramatic consequences of drugs we prescribe. In this case, our patient endured three months of repeat hospitalizations, invasive tests, and weight loss before the offending drug was discontinued.
Further investigation is needed to elucidate the specific mechanism of olmesartan-associated enteropathy and to determine whether other ARBs elicit similar adverse reactions. Until these questions are answered, it is important for clinicians to maintain a high index of suspicion for olmesartan, and potentially other ARBs, as precipitants of a celiac sprue-like picture.
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