There is currently considerable interest in the increasing number of pharmaceutical agents, including newer biologic agents, which have been associated with the development of autoantibodies and drug-related SLE. Two recent epidemics of scleroderma-like illness, one in Spain to a contaminant of rapeseed oil and one in the United States to a contaminant of l-tryptophan, have raised interest in potential environmental triggers of autoimmunity. Many patients receiving procainamide (PA) develop autoantibodies that may persist after discontinuation of the drug; most of these patients do not develop drug-induced SLE. Slow acetylator status correlated with IgG antibodies to H2A-2B but was not a risk factor for developing PA-related lupus. Case reports increasingly note drug-induced SLE as an adverse event after therapy with TNF inhibitors, interferon, and other biologics employed as therapeutic agents.
Curr Opin Rheumatol. 2003;15(2) © 2003 Lippincott Williams & Wilkins
Cite this: Environmental Epidemiology and Risk Factors for Autoimmune Disease - Medscape - Mar 01, 2003.