Division of Allergy, Asthma and Immunology, Nemours A.I. Dupont Childrens Hospital, Thomas Jefferson University, Wilmington, Delaware, USA.
Drug Saf. 2011 May 1;34(5):357-74. doi: 10.2165/11588500-000000000-00000.
The generation of autoantibodies and autoimmune diseases such as systemic lupus erythematosus has been associated with the use of certain drugs in humans. Early reports suggested that procainamide and hydralazine were associated with the highest risk of developing lupus, quinidine with a moderate risk and all other drugs were considered low or very low risk. More recently, drug-induced lupus has been associated with the use of the newer biological modulators such as tumour necrosis factor (TNF)-α inhibitors and interferons. The clinical features and laboratory findings of TNFα inhibitor-induced lupus are different from that of traditional drug-induced lupus or idiopathic lupus, and standardized criteria for the diagnosis of drug-induced lupus have not been established. The mechanism(s) responsible for the development of drug-induced lupus may vary depending on the drug or even on the patient. Besides lupus, other autoimmune diseases have been associated with drugs or toxins. Diagnosis of drug-induced lupus requires identification of a temporal relationship between drug administration and symptom development, and in traditional drug-induced lupus there must be no pre-existing lupus. Resolution of symptoms generally occurs after cessation of the drug. In this review, we will discuss those drugs that are more commonly associated with drug-induced lupus, with an emphasis on the new biologicals and the difficulty of making the diagnosis of drug-induced lupus against a backdrop of the autoimmune diseases that these drugs are used to treat. Stimulation of the immune system by these drugs to cause autoimmunity may in fact be associated with an increased effectiveness in treating the pathology for which they are prescribed, leading to the dilemma of deciding which is worse, the original disease or the adverse effect of the drug. Optimistically, one must hope that ongoing research in drug development and in pharmacogenetics will help to treat patients with the maximum effectiveness while minimizing side effects. Vigilance and early diagnosis are critical. The purpose of this review is to summarize the most recent developments in our understanding of the incidence, pathogenesis, diagnosis and treatment of drug-induced lupus.
自身抗体和自身免疫性疾病（如系统性红斑狼疮）的产生与人类使用某些药物有关。早期报告表明，普鲁卡因胺和肼屈嗪与狼疮发病风险最高相关，奎尼丁为中度风险，其他所有药物均被认为风险较低或非常低。最近，药物性狼疮与新型生物调节剂的使用有关，如肿瘤坏死因子（TNF）-α抑制剂和干扰素。TNFα 抑制剂诱导的狼疮的临床特征和实验室发现与传统药物诱导的狼疮或特发性狼疮不同，并且尚未建立药物性狼疮的诊断标准。导致药物性狼疮的机制可能因药物甚至患者而异。除狼疮外，其他自身免疫性疾病也与药物或毒素有关。药物性狼疮的诊断需要确定药物给药和症状发展之间的时间关系，并且在传统药物性狼疮中，必须没有预先存在的狼疮。一般来说，停止使用药物后症状会缓解。在这篇综述中，我们将讨论与药物性狼疮更相关的那些药物，重点介绍新型生物制剂以及在这些药物用于治疗的自身免疫性疾病背景下诊断药物性狼疮的困难。这些药物刺激免疫系统引起自身免疫，实际上可能与它们治疗疾病的疗效增加有关，从而导致了一个两难的境地，即哪一种情况更糟，是原发病还是药物的不良反应。乐观地说，人们必须希望药物开发和药物遗传学方面的持续研究将有助于以最小的副作用为患者提供最大的治疗效果。保持警惕和早期诊断至关重要。本综述的目的是总结我们对药物性狼疮的发病率、发病机制、诊断和治疗的最新认识。
