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药物诱导的红斑狼疮,重点介绍皮肤表现和抗 TNFα 药物的作用。

Drug-induced lupus erythematosus with emphasis on skin manifestations and the role of anti-TNFα agents.

机构信息

Section of Dermatology and Venereology, Department of Medicine, University of Verona, Verona, Italy.

出版信息

J Dtsch Dermatol Ges. 2012 Dec;10(12):889-97. doi: 10.1111/j.1610-0387.2012.08000.x. Epub 2012 Sep 3.

Abstract

Drug-induced lupus erythematosus (DILE) is a lupus-like syndrome temporally related to continuous drug exposure which resolves upon drug discontinuation. There are currently no standard diagnostic criteria for DILE. Findings include skin manifestations, arthritis, serositis, anti-nuclear and anti-histone antibodies positivity. Similarly to idiopathic lupus erythematosus, DILE can be divided into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous lupus (CCLE). Systemic DILE presents as a milder version of idiopathic SLE, and the drugs most frequently implicated are hydralazine, procainamide and quinidine. Anti-TNFα therapies are the latest class of medications found to be associated, although rarely, with a "lupus-like" syndrome, which is however clinically distinct from classical DILE. Drug-induced SCLE is the most common form of DILE. It is very similar to idiopathic SCLE in terms of clinical and serologic characteristics. The most commonly implicated drugs are antihypertensive drugs and terbinafine, but in recent years also proton pump inhibitors and chemotherapeutic agents have been associated. Drug-induced CCLE is very rare and usually caused by fluorouracil agents and NSAIDS, but some cases have induced by pantoprazole and anti-TNFα agents.

摘要

药物诱导性狼疮(DILE)是一种与持续药物暴露时间相关的狼疮样综合征,停药后即可缓解。目前尚无 DILE 的标准诊断标准。其表现包括皮肤表现、关节炎、浆膜炎、抗核抗体和抗组蛋白抗体阳性。与特发性红斑狼疮一样,DILE 可分为系统性(SLE)、亚急性皮肤性(SCLE)和慢性皮肤性狼疮(CCLE)。系统性 DILE 表现为特发性 SLE 的较轻版本,最常涉及的药物是肼屈嗪、普鲁卡因胺和奎尼丁。抗 TNF-α 疗法是最新发现与“狼疮样”综合征相关的一类药物,尽管很少见,但与经典 DILE 在临床上不同。药物诱导性 SCLE 是最常见的 DILE 形式。它在临床和血清学特征方面与特发性 SCLE 非常相似。最常涉及的药物是降压药和特比萘芬,但近年来质子泵抑制剂和化疗药物也与之相关。药物诱导性 CCLE 非常罕见,通常由氟尿嘧啶类药物和 NSAIDs 引起,但也有一些病例由泮托拉唑和抗 TNF-α 药物引起。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7efe/3561694/c6e63ae091cf/ddg0010-0889-f1.jpg

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