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普鲁卡因胺诱发的系统性红斑狼疮。肾脏受累伴免疫复合物沉积。

Procainamide-induced systemic lupus erythematosus. Renal involvement with deposition of immune complexes.

作者信息

Whittle T S, Ainsworth S K

出版信息

Arch Pathol Lab Med. 1976 Sep;100(9):469-74.

PMID:782399
Abstract

A 54-year-old man sustained an acute anterior myocardial infarction and was subsequently treated with procainamide hydrochloride for 5 1/2 months, resulting in development of a drug-induced systemic lupus erythematosus (SLE) syndrome with renal involvement. In over 60 reported cases of procainamide-induced SLE, clinical renal evaluation has led to the concept that renal involvement is a rarity in this disease. Direct immunofluorescence examination of necropsy kidney tissue revealed mesangial deposition of immunoproteins and C3 in a granular pattern characteristically seen in idiopathic SLE. Ultrastructural studies confirm mesangial deposition of immune complexes. The immunological and ultrastructural pattern of immune complex deposition in glomeruli suggests similar pathological mechanisms for glomerular injury in procainamide as seen in idiopathic SLE.

摘要

一名54岁男性发生急性前壁心肌梗死,随后接受盐酸普鲁卡因胺治疗5个半月,结果出现药物性系统性红斑狼疮(SLE)综合征并累及肾脏。在60多例已报道的普鲁卡因胺诱发的SLE病例中,临床肾脏评估得出这样的概念,即肾脏受累在该疾病中较为罕见。对尸检肾脏组织进行的直接免疫荧光检查显示,免疫蛋白和C3在系膜区呈颗粒状沉积,这是特发性SLE的典型表现。超微结构研究证实免疫复合物在系膜区沉积。肾小球中免疫复合物沉积的免疫学和超微结构模式表明,普鲁卡因胺诱发的肾小球损伤与特发性SLE具有相似的病理机制。

引用本文的文献

1
Acetylator phenotype and lupus erythematosus.
Clin Pharmacokinet. 1981 Mar-Apr;6(2):118-34. doi: 10.2165/00003088-198106020-00003.

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