Schwarz J A
Arzneimittelforschung. 1977;27(96):1856-64.
Drug induced Lupus erythematosus (LE)-like syndromes are generally observed after long-term and/or high-dose therapy with so called "principal inducers" procainamide, hydralazine, isoniazide, chlorpromazine, anticonvulsives and possibly with D-penicillamine, too, and even so in some cases after some additional 26 drugs. The rare pseudo LE syndrome appears after combined drugs which usually contain pyrazolone derivatives used especially against venous diseases. The mechanism of induction of autoimmune reactions in these disorders varies and is after all still unknown. There are individual differences in drug metabolism, genetic disposition for increased autoantibody formation and sometimes humoral and cellular immune reactions against the drug itself. Essentially involved in the indication of autoimmune reactions is often the production of hapten carrier complexes between drugs and body constituents and drug induced changes of autoantigen elimination as well as drug mediated immunologic imbalance.
药物性红斑狼疮(LE)样综合征通常在长期和/或高剂量使用所谓的“主要诱导剂”普鲁卡因胺、肼屈嗪、异烟肼、氯丙嗪、抗惊厥药,可能还有D-青霉胺,甚至在某些情况下使用另外26种药物后出现。罕见的假性LE综合征出现在通常含有吡唑酮衍生物的复方药物之后,这些药物尤其用于治疗静脉疾病。这些疾病中自身免疫反应的诱导机制各不相同,毕竟仍然未知。药物代谢存在个体差异,自身抗体形成增加存在遗传倾向,有时还会出现针对药物本身的体液和细胞免疫反应。自身免疫反应的发生通常涉及药物与身体成分之间半抗原载体复合物的产生、药物诱导的自身抗原清除变化以及药物介导的免疫失衡。