S6173 Beyond the Usual Suspects: Cracking the Case of AA Amyloidosis in the Gut

Introduction: Amyloidosis refers to a group of disorders characterized by the extracellular deposition of abnormally folded proteins in various tissues. Involvement of the gastrointestinal (GI) tract can lead to a wide range of symptoms. We present a case of chronic diarrhea secondary to gastric amyloidosis. Case Description/Methods: A 76-year-old woman with a history of Waldenström macroglobulinemia (MYD88 mutation), renal amyloidosis, prior pulmonary embolism (on rivaroxaban), and stage IV marginal zone lymphoma (treated with R-CHOP in 2013), was transferred from a care facility due to hypotension. She reported a 10-month history of chronic diarrhea, characterized by 2–3 episodes daily, which began after a course of amoxicillin. She denied any progression, changes in stool volume, bleeding, weight loss, or abdominal pain. She had tried antidiarrheals with mild improvement in stool consistency but no reduction in frequency. Her last chemotherapy treatment was several months prior to presentation. An esophagogastroduodenoscopy and colonoscopy with biopsies had previously been performed, though results were not available. During hospitalization, laboratory evaluation revealed elevated fecal calprotectin, gastrin, and 5-HIAA levels. Infectious workup was negative. A small bowel push enteroscopy demonstrated gastric mucosal atrophy, gastritis, multiple gastric and duodenal polyps, and erythematous duodenopathy. Biopsies revealed amyloid deposition extending from the stomach to the jejunum. Colonoscopy showed friable mucosa with spontaneous bleeding and 3 polyps (5–10 mm, including a tubular adenoma and a tubulovillous adenoma). Colon biopsies also confirmed amyloid deposition, later identified as type AA amyloid protein. Discussion: Gastrointestinal (GI) involvement in systemic amyloidosis is rare, reported in approximately 3% of cases. Amyloidosis subtypes include primary (AL amyloidosis, associated with monoclonal light chains and plasma cell dyscrasias) and secondary (AA amyloidosis, related to serum amyloid A protein and chronic inflammatory conditions). In this case, biopsy results were consistent with AA amyloidosis, which typically deposits in the propria mucosae, leading to mucosal friability, erosions, vascular proliferation, and clinical manifestations such as diarrhea and malabsorption. Management of GI amyloidosis is primarily supportive, focusing on symptom control and treatment of the underlying condition. This case highlights amyloidosis as an important differential for chronic diarrhea.