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使用血管紧张素转换酶抑制剂会加重遗传性血管性水肿吗?

Does angiotensin-converting enzyme inhibitor use exacerbate hereditary angioedema?

作者信息

Hassen Getaw Worku, Tu Ting Jia, Wei Daniel Hsiang, Hwang Albert, Lamothe Romus, Costea Ana, Liu Lydia Liyun, Smith Tennyson, Mualim Felicia, Johnston Paul, Ng Jennifer Ming Wai, Usmani Shakeel, Kalantari Hossein

机构信息

Department of Emergency Medicine, NYMC, Metropolitan Hospital Center, New York, New York; Department of Emergency Medicine, Lutheran Medical Center, Brooklyn, York; Department of Emergency Medicine, St. George's University School of Medicine, St. George, Grenada.

出版信息

J Emerg Med. 2013 Oct;45(4):602-8. doi: 10.1016/j.jemermed.2013.05.045. Epub 2013 Jul 25.

DOI:10.1016/j.jemermed.2013.05.045
PMID:23890533
Abstract

BACKGROUND

Approximately 2% of angioedema (AE) patients have a hereditary or an acquired deficiency of the complement 1 (C1) esterase inhibitor (C1 INH) gene. Some case reports indicate an association between angiotensin-converting enzyme inhibitor (ACEI) use and exacerbation of hereditary AE (HAE).

OBJECTIVE

The aim of this retrospective study is to investigate the association between HAE and ACEI use in a larger patient population.

METHODS

A retrospective chart review of patients who presented with AE and patients with diagnostic serum assays for functional C1 INH, C1 INH antigenic protein, C1q, C1q immune complex (C1q IC), and complement 4 (C4) regardless of medical complaint. Descriptive statistics were used to analyze the data.

RESULTS

A total of 1594 patients had complement levels measured (136 C1 INH, 55 C1q, 10 C1q IC, and 1500 C4), of which 156 (9.7%) patients presented with AE. Angiotensin-converting enzyme inhibitor use was documented in 747 (47%) patients. Low C1 INH was detected in one patient with recurrent AE who was not taking ACEI. Another patient who presented with recurrent AE was found to have systemic lupus erythematosus with abnormal C4, C1q, and C1q IC, but normal C1 INH. A low C4 level was present in 94 patients, 4 of which had AE.

CONCLUSIONS

The risk of exacerbating HAE by ACEI might be present, but we did not find any association in this retrospective study. Further studies are needed to determine the existence of this association.

摘要

背景

约2%的血管性水肿(AE)患者存在补体1(C1)酯酶抑制剂(C1 INH)基因的遗传性或后天性缺乏。一些病例报告表明血管紧张素转换酶抑制剂(ACEI)的使用与遗传性血管性水肿(HAE)的加重之间存在关联。

目的

这项回顾性研究的目的是在更大的患者群体中调查HAE与ACEI使用之间的关联。

方法

对出现AE的患者以及进行了功能性C1 INH、C1 INH抗原蛋白、C1q、C1q免疫复合物(C1q IC)和补体4(C4)诊断性血清检测的患者进行回顾性病历审查,无论其医疗主诉如何。采用描述性统计分析数据。

结果

共有1594名患者进行了补体水平检测(136名检测C1 INH,55名检测C1q,10名检测C1q IC,1500名检测C4),其中156名(9.7%)患者出现AE。747名(47%)患者有使用ACEI的记录。在一名未服用ACEI的复发性AE患者中检测到低C1 INH。另一名出现复发性AE的患者被发现患有系统性红斑狼疮,C4、C1q和C1q IC异常,但C1 INH正常。94名患者C4水平低,其中4名患有AE。

结论

ACEI加重HAE的风险可能存在,但在这项回顾性研究中我们未发现任何关联。需要进一步研究来确定这种关联是否存在。

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