P114 - SYSTEMIC STEROIDS IN ANTI-PD1-INDUCED COLLAGENOUS COLITIS
(Room Poster Hall)
19 Jan 18
5:30 PM
-
7:00 PM
Tracks:
Clinical and Research Challenges
Background: Immune dysregulation is thought to be a contributing factor to the development of microscopic colitis (MC), which encompasses lymphocytic and collagenous colitis. MC pattern has been observed in colitis resulting from immunotherapy, newer agents that work on the immune system to augment its response against tumor cells. We describe a case of collagenous colitis that developed after the use of anti-PD1 antibody. Case: A 63-year-old man with metastatic hemangiopericytoma who developed non-bloody grade 3 diarrhea 10 days after the 4th dose of anti-PD1, PDR001. He received empiric budesonide 6mg daily for 14 days then 9mg daily without clinical improvement and was subsequently hospitalized. Stool infectious studies were negative. Colonoscopy showed diffuse mildly erythematous colonic mucosa with biopsies significant for increased intraepithelial lymphocytes and subepithelial collagen deposition consistent with collagenous colitis. He received prednisone 40mg daily, loperamide and cholestyramine with improved diarrhea frequency to 2 semi-formed stools daily. He was discharged on budesonide 9mg daily with complete symptom resolution 4 weeks later. Conclusion: Lymphocytic colitis pattern has been observed in anti-PD1-induced colitis. Collagenous colitis after the use of anti-PD1 is rare with only one case described in the literature. The case describes anti-PD1-induced collagenous colitis treated with budesonide 9mg daily followed by cholestyramine leading to symptom resolution. While acknowledging collagenous colitis can be seen with the use of anti-PD1, our case is unique in that our patient did not initially improve on budesonide 9mg daily and required a short course of systemic steroids. Our case highlights the need to consider the use of a short course of oral prednisone in patients with anti-PD1-induced collagenous colitis who do not respond to budesonide.