Weinstein A
Prog Clin Immunol. 1980;4:1-21.
Despite some confusion in the literature, drug-induced SLE is a well defined reversible clinical entity. The lupus syndromes induced by procainamide, hydralazine, and isoniazid have been well studied and the data obtained have been convincing. Other drugs may also induce a lupus syndrome, but adequate prospective studies have not been done. Furthermore, many other drugs previously incriminated appear to activate spontaneous SLE rather than induce the de novo lupus syndrome. The mechanism by which procainamide, hydralazine, and isoniazid exert their effect is not known, and animal studies have been unrewarding. However, hydralazine and procainamide are capable of complexing with nuclear antigens in vitro and possibly in vivo and may evoke antinuclear antibody responses in this way. A number of defined factors influence the development of the clinical syndrome, including the cumulative drug dosage, the acetylator phenotype of the individual, and the biochemical nature of the drug. Studies to date have not revealed how these drugs induce the clinical disease. While these agents may induce antinuclear antibodies in many individuals, genetic influences may be important in determining which patients will develop clinical symptoms. Further study of drug-induced systemic lupus erythematosus is necessary in order to resolve these problems regarding pathogenesis. The resolution of these problems may shed light on the pathogenesis of spontaneous SLE.
尽管文献中存在一些混淆，但药物性系统性红斑狼疮是一种定义明确的可逆性临床实体。由普鲁卡因胺、肼屈嗪和异烟肼诱发的狼疮综合征已得到充分研究，所获得的数据令人信服。其他药物也可能诱发狼疮综合征，但尚未进行充分的前瞻性研究。此外，许多先前被认为有嫌疑的其他药物似乎是激活自发性系统性红斑狼疮，而非诱发新发狼疮综合征。普鲁卡因胺、肼屈嗪和异烟肼发挥作用的机制尚不清楚，动物研究也未取得成果。然而，肼屈嗪和普鲁卡因胺在体外甚至可能在体内能够与核抗原结合，并可能以此引发抗核抗体反应。一些明确的因素会影响临床综合征的发生，包括药物累积剂量、个体的乙酰化表型以及药物的生化性质。迄今为止的研究尚未揭示这些药物如何诱发临床疾病。虽然这些药物可能在许多个体中诱发抗核抗体，但遗传因素在决定哪些患者会出现临床症状方面可能很重要。有必要对药物性系统性红斑狼疮进行进一步研究，以解决这些关于发病机制的问题。解决这些问题可能会为自发性系统性红斑狼疮的发病机制提供线索。
