PO158 Sarcoidosis following alemtuzumab treatment for multiple sclerosis. (1st December 2017)

• Record Type: Journal Article
• Authors: Willis, MD; May, K; Hope-Gill, B; Flood-Page, P; Jeffrey, D; Joseph, F; Robertson, NP
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 88(2017)Supplement 1
• Page Start: A54
• Page End: A55
• Publication Date: 2017-12-01
• Subjects: Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp-2017-ABN.187
• Languages: English
• ISSNs: 0022-3050

Abstract

Abstract : Alemtuzumab, a licensed treatment for relapsing multiple sclerosis (MS) has proven efficacy in reducing relapse rates and improving disability outcomes. However, despite these beneficial effects, approximately 50% of patients develop secondary autoimmune disease (AID). The constellation of AIDs reported thus far encompasses Th2, B cell/antibody-driven pathologies including thyroid autoimmunity, idiopathic thrombocytopenic purpura and Goodpasture's syndrome. In contrast to this, we present two patients with MS treated with alemtuzumab whom subsequently developed systemic sarcoidosis, a Th1 mediated disease. The first case presented with chest pain and shortness of breath 8 years after the initial infusion of alemtuzumab with computed tomography (CT) of the thorax demonstrating widespread lymphadenopathy and peri-bronchovascular nodularity. Biopsy of a cervical lymph node demonstrated non-caseating granulomas with the changes considered consistent with sarcoidosis. Four years after initial infusion, the second case was found to have incidental right-sided hilar lymphadenopathy following routine Xray with CT demonstrating widespread lymphadenopathy. Subsequent sub-carinal lymph node core biopsy demonstrated granulomatous inflammation in association with a raised serum ACE and a diagnosis of sarcoidosis was made. To our knowledge, these are the first reported cases of Th1-cell mediated secondary autoimmunity following alemtuzumab for MS and we speculate on the possible immunological mechanisms to account for this.