Musculoskeletal and systemic reactions to biological therapeutic agents.
Autoimmune disease, in particular systemic lupus erythematosus (SLE), can be induced by drugs. Over the past couple of years biologic agents have become available for the treatment of inflammatory disease; simultaneously, researchers have realized that these drugs can not only suppress autoimmune disease but may also potentiate it. Interferon-alpha and interferon-beta both may induce autoimmune disease, but this is more frequent with interferon-alpha. Therapy to block tumor necrosis factor-alpha, either with monoclonal antibodies or fusion proteins, has been associated with the development of antinuclear antibodies, but only rarely with clinical development of SLE. None of the three reported cases of SLE occuring after anti-tumor necrosis factor-alpha therapy has developed major organ involvement. The continued use of biologic agents will provide interesting insights into the pathogenesis of autoimmune disease.
Watts
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D000911:Antibodies, Monoclonal / Q000009:adverse effects; D001327:Autoimmune Diseases / Q000139:chemically induced*; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects; D007155:Immunologic Factors / Q000009:adverse effects*; D000069285:Infliximab; D016898:Interferon-alpha / Q000009:adverse effects; D016899:Interferon-beta / Q000009:adverse effects; D009140:Musculoskeletal Diseases / Q000139:chemically induced; D018124:Receptors, Tumor Necrosis Factor
D000911:Antibodies, Monoclonal; D007074:Immunoglobulin G; D007155:Immunologic Factors; D016898:Interferon-alpha; D018124:Receptors, Tumor Necrosis Factor; D016899:Interferon-beta; D000069285:Infliximab; D000068800:Etanercept