Angiotensin-converting enzyme inhibitor-induced cough - ACCP evidence-based clinical practice guidelines

Angiotensin-converting enzyme inhibitor-induced cough - ACCP evidence-based clinical practice guidelines
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DOI:
10.1378/chest.129.1_suppl.169s
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发表时间:
2006-01-01
期刊:
影响因子:
9.6
通讯作者:
Dicpinigaitis, PV
Dicpinigaitis, PV
中科院分区:
医学1区
文献类型:
--
作者:
Dicpinigaitis, PV

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背景:持续性干咳是血管紧张素转换酶(ACE)抑制剂类药物的一种已被充分描述的类效应。ACE介导的咳嗽的机制尚不清楚,但可能涉及促咳介质缓激肽和P物质,这些介质被ACE降解,因此当酶被抑制时在上呼吸道或肺中积聚,以及缓激肽刺激产生的异甘草素。方法:本综述的数据来自于2004年5月进行的国家医学图书馆(PubMed)检索,检索了1985年至2004年以英语发表的文献,使用检索词“血管紧张素转换酶”、“血管紧张素转换酶抑制剂”和“咳嗽”。“结果:据报道,在接受这些药物治疗的患者中,ACE药物诱导的咳嗽发生率在5%至35%之间。然而,在对评估慢性咳嗽的患者进行的研究中,描述了低得多的发生率。ACE底物诱导的咳嗽的发作范围从首次给药后数小时内到开始治疗后数月。通常,在停止治疗后1至4周内消退,但咳嗽可能持续长达3个月。唯一一致有效的治疗血管紧张素转换酶抑制剂引起的咳嗽是停止治疗与得罪代理。与血管紧张素受体阻滞剂治疗相关的咳嗽发生率似乎与对照药物相似。在少数患者中,咳嗽不会复发后重新引入ACE抑制剂therapeutic.Conclusions:在慢性咳嗽患者中,ACE抑制剂应被视为全部或部分病因,无论ACE抑制剂治疗的开始和咳嗽发作之间的时间关系。虽然停止治疗是唯一一致有效的治疗ACE介导的咳嗽,一些药物已被证明可以减轻咳嗽。
Background: A dry, persistent cough is a well-described class effect of the angiotensin-converting enzyme (ACE) inhibitor medications. The mechanism of ACE inhibitor-induced cough remains unresolved, but likely involves the protussive mediators bradykinin and substance P, agents that are degraded by ACE and therefore accumulate in the upper respiratory tract or lung when the enzyme is inhibited, and prostaglandins, the production of which may be stimulated by bradykinin.Methods: Data for this review were obtained from a National Library of Medicine (PubMed) search, which was performed in May 2004, of the literature published in the English language from 1985 to 2004, using the search terms "angiotensin-converting enzyme'" "angiotensin converting enzyme inhibitors," and "cough."Results: The incidence of ACE inhibitor-induced cough has been reported to be in the range of 5 to 35% among patients treated with these agents. However, a much lower incidence has been described in studies of patients presenting for the evaluation of chronic cough. The onset of ACE inhibitor-induced cough ranges from within hours of the first dose to months after the initiation of therapy. Resolution typically, occurs within I to 4 weeks after the cessation of therapy, but cough may linger for up to 3 months. The only uniformly effective treatment for ACE inhibitor-induced cough is the cessation of treatment with the offending agent. The incidence of cough associated with therapy with angiotensin-receptor blockers appears to be similar to that of the control drug. In a minority of patients, cough will not recur after the reintroduction of ACE inhibitor therapy.Conclusions: In a patient with chronic cough, ACE inhibitors should be considered as wholly, or partially causative, regardless of the temporal relation between the initiation of ACE inhibitor therapy and the onset of cough. Although the cessation of therapy is the only uniformly effective treatment for ACE inhibitor-induced cough, some pharmacologic agents have been shown to attenuate the cough.