McCrory D C, Brown C D
Pulmonary and Critical Care Medicine, Duke University Medical Center, Box 3221, 350 Bell Building, Durham, North Carolina, 27710, USA.
Cochrane Database Syst Rev. 2001;2001(2):CD002984. doi: 10.1002/14651858.CD002984.
BACKGROUND: Inhaled short acting beta2 adrenergic agonists and ipratropium bromide are both used in the treatment of acute exacerbations of chronic obstructive pulmonary disease. OBJECTIVES: In patients with acute exacerbations of COPD to: 1. To assess the efficacy of short-acting beta-2 agonists against placebo; 2. Compare the efficacy of short-acting beta-2 agonists and ipratropium. SEARCH STRATEGY: A comprehensive search of the literature was carried out of EMBASE, MEDLINE, CINAHL and the Cochrane COPD trials register was carried out using the terms: bronchodilator* OR albuterol OR metaproterenol OR terbutaline OR isoetharine OR pirbuterol OR salbutamol OR beta-2 agonist. SELECTION CRITERIA: All trials that appeared to be relevant were assessed by two reviewers who independently selected trials for inclusion. Differences were resolved by consensus. DATA COLLECTION AND ANALYSIS: All trials that appeared to be relevant were assessed by two reviewers who independently selected trials for inclusion. Differences were resolved by consensus. References listed in each included trial were searched for additional trial reports. Trials were combined using Review Manager using a fixed effects model. The size of the treatment effects were tested for heterogeneity. MAIN RESULTS: We identified no placebo-controlled comparisons of beta-2 agonists. Three studies permitted comparison of ipratropium to an inhaled beta-2 agonist. These studies included a total of 103 patients. The beta2-agonists used were: fenoterol and metaproterenol. One study was a parallel group trial of regular therapy for seven days. The other two were cross over studies of single dose treatments, with efficacy measured 90 min post dose. There was no washout period between treatments. Both treatments produced an improvement in forced expiratory volume (FEV1) after 90 min in the range 150-250 ml. The was no difference between treatments, mean difference in FEV1 10 ml; 95% CI -220, 230 ml. In one small crossover study (n=10) there was a significant improvement in arterial PaO2 after 30 minutes with ipratropium (+5.8 mm Hg +/- 3.0 (SEM)) compared to metaproterenol (-6.2 +/- 1.2 mm Hg), but this was not significant at 90 min. There were no data concerning respiratory symptoms. The crossover studies showed no evidence of an additive effect of the two treatments, although they were not designed specifically to test this. REVIEWER'S CONCLUSIONS: There are few controlled trial data concerning the use of inhaled beta2-agonist agents in acute exacerbations of COPD and none that have compared these agents directly with placebo. None of the studies used the more modern beta2-agonists used most widely in this setting (salbutamol and terbutaline). Beta2-agonists and ipratropium both produce small improvements in FEV1, but beta2-agonists may worsen PaO2 for a period. We could not draw conclusions concerning possible additive effects.
背景:吸入性短效β2肾上腺素能激动剂和异丙托溴铵均用于治疗慢性阻塞性肺疾病急性加重期。 目的:在慢性阻塞性肺疾病急性加重期患者中:1. 评估短效β2激动剂与安慰剂相比的疗效;2. 比较短效β2激动剂和异丙托溴铵的疗效。 检索策略:使用以下检索词对EMBASE、MEDLINE、CINAHL和Cochrane慢性阻塞性肺疾病试验注册库进行了全面的文献检索:支气管扩张剂*或沙丁胺醇或间羟异丙肾上腺素或特布他林或异他林或吡布特罗或沙丁胺醇或β2激动剂。 选择标准:所有似乎相关的试验均由两名评审员评估,他们独立选择纳入试验。分歧通过协商解决。 数据收集与分析:所有似乎相关的试验均由两名评审员评估,他们独立选择纳入试验。分歧通过协商解决。对每个纳入试验中列出的参考文献进行检索以获取其他试验报告。使用Review Manager软件采用固定效应模型对试验进行合并。对治疗效果的大小进行异质性检验。 主要结果:我们未找到β2激动剂与安慰剂对照的比较研究。三项研究允许将异丙托溴铵与吸入性β2激动剂进行比较。这些研究共纳入103例患者。所使用的β2激动剂为:非诺特罗和间羟异丙肾上腺素。一项研究是为期7天的常规治疗平行组试验。另外两项是单剂量治疗的交叉研究,给药后90分钟测量疗效。治疗之间没有洗脱期。两种治疗在90分钟后均使用力呼气量(FEV1)改善了150 - 250 ml。两种治疗之间没有差异,FEV1的平均差异为10 ml;95%可信区间为 - 220, 230 ml。在一项小型交叉研究(n = 10)中,与间羟异丙肾上腺素(-6.2 ± 1.2 mmHg)相比,异丙托溴铵给药30分钟后动脉血氧分压有显著改善(+5.8 mmHg ± 3.0(标准误)),但在90分钟时不显著。没有关于呼吸道症状的数据。交叉研究未显示两种治疗有相加作用的证据,尽管它们并非专门设计用于测试这一点。 评审员结论:关于吸入性β2激动剂在慢性阻塞性肺疾病急性加重期使用的对照试验数据很少,且没有将这些药物直接与安慰剂进行比较的研究。没有一项研究使用在这种情况下最广泛使用的更现代的β2激动剂(沙丁胺醇和特布他林)。β2激动剂和异丙托溴铵均使FEV1有小幅改善,但β2激动剂可能在一段时间内使动脉血氧分压恶化。我们无法得出关于可能的相加作用的结论。
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