title: Thromboembolic events and anti-tumor necrosis factor therapies.
abstract: Thromboembolic (TE) events have been observed in about 4.5% of patients treated with TNF antagonists. It has been suggested that anti-drug antibodies could be involved. However, another mechanism fits more with the available immunochemical data and could lead to practical measures to prevent TE events during anti-TNF therapies. Adverse effects are not related to the type of antagonist, but well to the combination of the inhibition of TNF and the predisposition of some patients to lupus-like reactions, including antiphospholipid syndrome. The overproduction of interferon-α, caused by the inhibition of TNF in these individuals would foster the development of lupus-like syndrome. Therefore, seeking conventional markers of systemic lupus erythematosus (e.g. anti-dsDNA, anti-phospholipid, anti-β(2)-glycoprotein antibodies) before the administration of an anti-TNF could be a prudent measure.
authors.affiliation: de Duve Institute and Université catholique de Louvain, Brussels, Belgium. plmasson@skynet.be
authors.forename: P L
authors.initials: PL
authors.lastname: Masson
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000276:immunology; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects* / Q000276:immunology; D018501:Antirheumatic Agents / Q000009:adverse effects* / Q000276:immunology; D001323:Autoantibodies / Q000097:blood; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects* / Q000276:immunology; D000069285:Infliximab; D018124:Receptors, Tumor Necrosis Factor / Q000276:immunology; D013923:Thromboembolism / Q000139:chemically induced* / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D001323:Autoantibodies; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept