S3964 A Hidden Danger: Unmasking Colonic Amyloidosis Through Anticoagulation-Induced Massive GI Bleed in a Patient With Renal AL Amyloidosis and Multiple Myeloma

Introduction: Amyloidosis is a systemic disease characterized by the extracellular deposition of misfolded protein fibrils, leading to progressive organ dysfunction. AL amyloidosis is frequently associated with plasma cell dyscrasias, particularly multiple myeloma. Gastrointestinal (GI) involvement in AL amyloidosis is uncommon, and symptoms can vary; isolated colonic hemorrhage is exceedingly rare. Amyloid infiltration weakens the mucosa, and anticoagulation may increase the risk of severe GI bleeding. Case Description/Methods: A 78-year-old woman with a history of multiple myeloma, stage 4 chronic kidney disease due to renal AL amyloidosis, and recent lower extremity deep vein thrombosis was started on rivaroxaban. Three days later, she presented with acute rectal bleeding and generalized weakness. Hemoglobin was 5.5 g/dL (baseline 8.8), requiring transfusion of 3 units of packed red blood cells. A tagged red blood cell scan showed no active hemorrhage, suggesting intermittent bleeding. Colonoscopy with random biopsies was performed. Histopathology of the left colon revealed Congo red-positive deposits in the lamina propria, consistent with AL-type amyloidosis. Anticoagulation was discontinued, and an inferior vena cava (IVC) filter was placed. The patient improved with supportive care. Discussion: GI bleeding due to colonic involvement in AL amyloidosis is rare and underrecognized. AL-type amyloidosis tends to produce bulky mucosal deposits, in contrast to the ulceration and friability more typical of AA-type disease. While spontaneous GI bleeding has been described in amyloidosis, anticoagulant therapy may precipitate or unmask significant hemorrhage. Prior case reports include upper and lower GI bleeding in a patient with AL amyloidosis and myeloma on rivaroxaban and jejunal hemorrhagic polyps in an anticoagulated patient with AL amyloidosis. Our case adds to the limited literature by demonstrating isolated colonic AL amyloidosis unmasked by anticoagulation as the bleeding source. Given the risk of life-threatening hemorrhage, clinicians should maintain a high index of suspicion for GI amyloidosis in patients with unexplained bleeding and underlying plasma cell disorders. Additionally, consideration of pre-anticoagulation endoscopic screening in select high-risk patients may help identify those at increased risk of GI complications, though further studies are needed to validate such an approach.