2065 A Rare Case of IgA Vasculitis Secondary to Infliximab Use in Crohn’s Disease

Abstract

INTRODUCTION: The advent of Infliximab (IFX) has revolutionized the treatment for inflammatory bowel disease. Although the most common adverse effects include infusion site reactions and loss of response due to antibody formation, there have been some reports of secondary autoimmune conditions. Herein, we report a rare case of IgA vasculitis likely as a result of IFX therapy. CASE DESCRIPTION/METHODS: A 53-year-old female with known fistulizing ileocolonic Crohn's disease (CD) on IFX since 2002, multiple bowel surgeries for her CD, rheumatoid arthritis, and postoperative deep vein thrombosis, presented with a 2-week history of progressive petechial rash on her bilateral lower extremities (Figures 1 and 2). Skin biopsy of one of the lesions was notable for granular deposition of IgA consistent with IgA vasculitis. She was initiated on oral Prednisone 1 mg/kg/day. Three weeks later, she was transitioned to oral Dapsone with a slow prednisone taper. The next day, the patient developed abdominal pain with nausea and vomiting. CAT scan of the abdomen was notable for a large thrombus in the descending thoracic aorta. A thorough workup for small vessel vasculitis was undertaken which was negative with pertinent negative tests including ANCA, Cryoglobulin levels, Rheumatoid Factor, serum electrophoresis, protein C & S, Anti-thrombin 4 level, Anticardiolipin antibody, and Beta-2 glycoprotein level. She was treated with anticoagulation for the aortic thrombus with IV heparin and then later transitioned to oral Rivaroxaban. Repeat CAT scan a month later showed resolution of the clot in the aorta. Regarding the Crohn’s disease, a decision was made to switch her therapy from IFX to Ustekinumab for maintenance of remission. DISCUSSION: IgA mediated vasculitis is a rare adverse reaction which can be caused by anti-tumor necrosis factor (TNF) agents and remains poorly understood. It has been described with all the commonly used anti-TNF agents and usually occurs after several months of use. In our patient, this occurred after several years of use. None of the other medications on her list were noted to have an association with IgA mediated vasculitis. Clinical symptoms can range from local cutaneous manifestations to multi-system involvement. In our patient, skin and large vessel (aorta) were involved. The resolution of symptoms may be achieved by discontinuing use of the culprit anti-TNF agent and initiating adjuvant treatment. Alternative non-anti-TNF therapies should be pursued for definitive treatment.