Case reports in gastroenterology · 2026
Case Report: Olmesartan-Induced Enteropathy Mimicking Amyloidosis in the Setting of New Multiple Myeloma Diagnosis.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Osman Mohamad Mahdi, Salgado-de la Mora Moises, Sharma Rishaan, Ahmed Abdelwahab, Fansa Sima, Massad Talal, Kawas Hussam, El Hag Mohamed, Rotenberg Vitaliy
Аннотация
INTRODUCTION: Olmesartan-induced enteropathy is an uncommon but important cause of severe chronic diarrhea and weight loss that can mimic celiac disease and infiltrative gastrointestinal disorders.
CASE PRESENTATION: We report a 71-year-old man on long-term olmesartan who presented with months of diarrhea, nausea/vomiting, profound weakness, and ∼100 pounds of unintentional weight loss. Esophagogastroduodenoscopy demonstrated duodenal villous blunting with lamina propria lymphoplasmacytic inflammation and rare periodic acid-Schiff-positive macrophages. An empiric 3-week gluten-free diet trial was ineffective. Celiac serologies, infectious stool studies, and HIV testing were negative. Laboratory evaluation revealed anemia, elevated creatinine, hypercalcemia, and a gamma gap; serum and urine protein electrophoresis showed an M-protein, and bone marrow biopsy confirmed multiple myeloma. Repeat duodenal biopsies again showed villous blunting, while Congo red staining was negative, arguing against gastrointestinal amyloidosis. Olmesartan-induced enteropathy was favored; olmesartan was discontinued and budesonide was started. Within 1 month, gastrointestinal symptoms resolved and the patient gained 20 pounds.
CONCLUSION: Recognition of this drug effect is critical, particularly when concurrent hematologic disease raises concern for infiltrative etiologies.
CASE PRESENTATION: We report a 71-year-old man on long-term olmesartan who presented with months of diarrhea, nausea/vomiting, profound weakness, and ∼100 pounds of unintentional weight loss. Esophagogastroduodenoscopy demonstrated duodenal villous blunting with lamina propria lymphoplasmacytic inflammation and rare periodic acid-Schiff-positive macrophages. An empiric 3-week gluten-free diet trial was ineffective. Celiac serologies, infectious stool studies, and HIV testing were negative. Laboratory evaluation revealed anemia, elevated creatinine, hypercalcemia, and a gamma gap; serum and urine protein electrophoresis showed an M-protein, and bone marrow biopsy confirmed multiple myeloma. Repeat duodenal biopsies again showed villous blunting, while Congo red staining was negative, arguing against gastrointestinal amyloidosis. Olmesartan-induced enteropathy was favored; olmesartan was discontinued and budesonide was started. Within 1 month, gastrointestinal symptoms resolved and the patient gained 20 pounds.
CONCLUSION: Recognition of this drug effect is critical, particularly when concurrent hematologic disease raises concern for infiltrative etiologies.