Williams Emma L, Gadola Stephan, Edwards Christopher J
Department of Rheumatology, Southampton General Hospital, Southampton, UK.
Rheumatology (Oxford). 2009 Jul;48(7):716-20. doi: 10.1093/rheumatology/kep080. Epub 2009 May 4.
The use of protein-based anti-TNF-alpha therapies such as antibodies and soluble TNF-alpha receptors is commonly associated with the induction of autoantibodies, whereas anti-TNF-induced lupus (ATIL) is rare. ATIL can occur with any of the available TNF inhibitors, but the frequency and clinical characteristics of ATIL vary between different drugs. Cutaneous, renal and cerebral involvement as well as dsDNA antibodies are more common in ATIL compared to classical drug-induced lupus (DIL), suggesting different pathogenic mechanisms of ATIL and DIL. True ATIL must be clinically differentiated from mixed CTD, SLE or overlap syndromes unmasked, but not induced, by anti-TNF-alpha treatment of unclassified polyarthritis. The pathogenesis of ATIL is still unknown. Concomitant immunosuppression can reduce autoantibody formation in ATIL, and withdrawal of anti-TNF-alpha therapy usually leads to resolution of symptoms. Steroids and/or immunosuppressive therapy may be required in severe cases.
使用基于蛋白质的抗TNF-α疗法，如抗体和可溶性TNF-α受体，通常与自身抗体的诱导有关，而抗TNF诱导的狼疮（ATIL）则很少见。任何一种可用的TNF抑制剂都可能引发ATIL，但不同药物引发ATIL的频率和临床特征有所不同。与经典药物性狼疮（DIL）相比，皮肤、肾脏和脑部受累以及双链DNA抗体在ATIL中更为常见，这表明ATIL和DIL的致病机制不同。真正的ATIL必须在临床上与混合性结缔组织病、系统性红斑狼疮或未分类多关节炎经抗TNF-α治疗后未被诱发而是被揭示出的重叠综合征相鉴别。ATIL的发病机制仍然未知。联合免疫抑制可减少ATIL中自身抗体的形成，停用抗TNF-α疗法通常会使症状缓解。严重病例可能需要使用类固醇和/或免疫抑制疗法。
