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.

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http://dx.doi.org/10.1016/j.intimp.2012.08.018DOI Listing

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