Levo Y, Pick A I, Avidor I, Ben-Bassat M
Ann Rheum Dis. 1976 Apr;35(2):181-5. doi: 10.1136/ard.35.2.181.
A patient who developed a multisystem involvement of systemic lupus erythematosus (SLE) after 9 years of procainamide therapy, during which time he ingested enormous amounts of the drug, is described. The patient first suffered from recurrent episodes of pleuritis and arthritis, after which he developed a characteristic SLE nephritis associated with a high level of antinative DNA antibodies and a low level of complement. He finally died from a complication of a nonbacterial endocarditis. Autopsy showed polyserositis and typical deposits of electron-dense material on the glomerular basement membrane, and confirmed the clinical diagnosis of Libman-Sacks endocarditis. The possibility that procainamide-induced SLE might have all the clinical, immunological, and pathological features of spontaneous SLE, especially in patients exposed to large doses of the drug for many years, is discussed.
本文描述了一名患者，在接受普鲁卡因胺治疗9年后出现系统性红斑狼疮（SLE）的多系统受累，在此期间他摄入了大量该药物。患者最初反复出现胸膜炎和关节炎发作，之后发展为典型的SLE肾炎，伴有高水平的抗天然DNA抗体和低水平的补体。他最终死于非细菌性心内膜炎的并发症。尸检显示多浆膜炎以及肾小球基底膜上有典型的电子致密物质沉积，并证实了临床诊断为Libman-Sacks心内膜炎。本文还讨论了普鲁卡因胺诱发的SLE可能具有自发性SLE的所有临床、免疫学和病理学特征的可能性，尤其是在长期接触大剂量该药物的患者中。
