The Positive Association of Cough with Angiotensin‐Converting Enzyme Inhibitors
The Positive Association of Cough with Angiotensin‐Converting Enzyme Inhibitors
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咳嗽与血管紧张素转换酶抑制剂呈正相关
DOI：
10.1002/j.1875-9114.1989.tb04107.x
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
P. Just
中科院分区：
文献类型：
--
作者：
P. Just
已证实，卡托普利、依那普利、赖诺普利、雷米普利、西拉西坦和喹尼替尼均会诱发咳嗽，估计频率至少为15%的治疗患者。常见的描述包括发痒、干燥、非生产性和持续性。发作通常发生在治疗的第一周，持续时间与药物服用时间相同，停药后几天内缓解。替代血管生成素转换酶（ACE）抑制剂复制咳嗽。其机制可能与前列腺素E2刺激肺传入C纤维有关。这也可能与P物质分解减少有关，P物质是咳嗽反射的神经化学介质，响应于C纤维的刺激而释放，并由ACE代谢。两份关于接受非甾体类抗炎药的患者咳嗽消失的轶事报告支持了木兰素的可能作用。未来的试验应认识到咳嗽是ACE抑制剂治疗的副作用，并有必要前瞻性确定其真实频率和交叉发生率。
Captopril, enalapril, lisinopril, ramipril, cilazipril, and quinipril have all been documented to induce cough with an estimated frequency of at least 15% of treated patients. Common descriptors include tickling, dry, nonproductive, and persistent. Onset usually occurs during the first week of therapy and lasts as long as the drug is taken, remitting within a few days after the agent is discontinued. Alternative angiogensin‐converting enzyme (ACE) inhibitors replicate the cough. The mechanism seems related to stimulation of lung afferent C fibers, perhaps by prostaglandin E2. It may also be related to decreased breakdown of substance P, the neurochemical mediator of the cough reflex released in response to stimulation of C fibers and metabolized by ACE. The possible role of prostaglandins is supported by two anecdotal reports of cough disappearing in patients receiving nonsteroidal antiinflammatory agents. Future trials should recognize cough as a side effect of ACE inhibitor therapy, and prospective determination of its true frequency and cross‐occurrence are necessary.