S2411 Secondary Amyloidosis Presenting as a Rare Complication of IBD

Introduction: 35% of patients with Inflammatory Bowel Disease (IBD) experience extraintestinal manifestations. However, amyloidosis is a rare complication of IBD;the incidence in the US is <1% for both Crohn's disease (CD) and Ulcerative Colitis (UC). We hope to shed some light in this underdiagnosed consequence with a clinical vignette. Case description/methods: A 75 year old man with recently diagnosed UC 6 weeks prior and history of thoracic laminectomy presented with bilateral lower extremity weakness that resulted in a fall in the shower and complaints of bloody diarrhea. Prior to his admission he was ambulating with a walker, he then developed loss of motor function of his lower extremities. He had been having several episodes of bloody diarrhea a day along with tenesmus and fecal incontinence for almost a year. He delayed getting medical aid until recently due to the COVID-19 pandemic. He had a colonoscopy which revealed pancolitis and he was started on aggressive steroids and mesalamine. CT and MRI imaging of the spine were inconclusive, but revealed swelling of the iliopsoas muscle with concern for polymyositis. However EMG, muscle enzymes and Immunological studies were all unremarkable. Muscle biopsy of the gastrocnemius revealed interstitial amyloid deposition. Mass spectrometry was indeterminate and could not isolate the type of amyloid protein. The patient's UC flare slowly improved after several weeks and he was transferred to acute rehab and later to a tertiary care center for further evaluation. Discussion: Primary amyloidosis is AL amyloid deposition associated with plasma cell dyscrasias such as multiple myeloma (MM). AA Amyloid can also build up as an acute phase reactant from chronic inflammatory conditions such as IBD and be deposited in extracellular tissue. Amyloidosis is more associated with CD than UC, more found in men and is often associated with renal involvement. One study found that only 15 out of 1709 (0.9%) patients with CD and 1 in 1341 (0.7%) patients with UC had amyloidosis. Our patient's long standing uncontrolled UC likely resulted in amyloid protein production and deposition. Although it is important to rule out MM in cases of amyloidosis, the timing of our patient's lower extremity weakness and diagnosis of amyloidosis in the setting of uncontrolled UC flare strongly suggests secondary amyloidosis. We hope this diagnostic walk through can guide clinicians to approach similar situations in the future.