de Duve Institute and Université catholique de Louvain, Brussels, Belgium.
Int Immunopharmacol. 2012 Dec;14(4):444-5. doi: 10.1016/j.intimp.2012.08.018. Epub 2012 Sep 3.
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.
血栓栓塞（TE）事件在约 4.5%接受 TNF 拮抗剂治疗的患者中观察到。有人认为可能与抗药物抗体有关。然而，另一种机制更符合现有免疫化学数据，并且可以在抗 TNF 治疗期间采取实际措施来预防 TE 事件。不良反应与拮抗剂的类型无关，而是与 TNF 的抑制和一些患者易发生狼疮样反应（包括抗磷脂综合征）的倾向有关。这些个体中 TNF 的抑制导致干扰素-α的过度产生，促进狼疮样综合征的发展。因此，在给予抗 TNF 之前寻找系统性红斑狼疮的常规标志物（例如抗 dsDNA、抗磷脂、抗 β(2)-糖蛋白抗体）可能是一项谨慎的措施。
