Glatiramer acetate-induced acute hepatotoxicity in an adolescent with MS

Abstract

Glatiramer acetate (GA), a synthetic copolymer, is a frequently used first-line treatment for relapsing-remitting multiple sclerosis (RRMS). Probable autoimmune hepatotoxicity during GA treatment has been reported,(1-4) but GA hepatotoxicity in the absence of positive autoimmune markers has not previously been described. Here, we report GA-induced hepatotoxicity in a pediatric patient with multiple sclerosis (MS).

Figure 1. Liver transaminases over time and liver pathology in a 15-year-old patient with multiple sclerosis

(A) Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in our patient. Arrows indicate time of initiation of interferon-β-1a (IFN) and glatiramer acetate (GA). Pathology shows (B) isolated single hepatocyte cell death at earliest phase (blue arrow) and (C) late phase hepatocyte death triggering an inflammatory response. (D) Immunostain for CD8+ cytotoxic T cells shows that these are the principal cells of the inflammatory response.