Inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease: a systematic review and meta-analysis.
Inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease: a systematic review and meta-analysis.
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DOI：
10.1001/jama.2008.717
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发表时间：
2008-11-26
期刊：
影响因子：
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通讯作者：
Fan E
中科院分区：
文献类型：
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作者：
Drummond MB;Dasenbrook EC;Pitz MW;Murphy DJ;Fan E
最近关于吸入皮质类固醇（ICS）治疗稳定期慢性阻塞性肺疾病（COPD）的研究在生存和不良事件风险方面产生了相互矛盾的结果。系统回顾和定量综合ICS治疗对稳定期COPD患者死亡率和不良事件的影响。搜索MEDLINE， CENTRAL， EMBASE， CINAHL， Web of Science和psychino至2008年2月9日。符合条件的研究是双盲、随机对照试验，比较ICS治疗6个月或更长时间与非类固醇吸入治疗COPD患者。两位作者独立提取了包括研究特征、全因死亡率、肺炎和骨折在内的数据。I2统计量用于评估异质性。采用随机效应模型（I2≥50%）或固定效应模型（I2<50%）汇总研究水平的数据。对于1年全因死亡率的主要结局，我们的荟萃分析发现，假设双侧α为，死亡率的绝对差异为1.0%。0.05，幂为0.80。纳入11项符合条件的随机对照试验（14426名受试者）。在有死亡率数据的试验中，1年全因死亡率无差异（治疗组4636例患者中有128例死亡，对照组4597例患者中有148例死亡；相对危险度[RR]为0.86；95%可信区间[CI]为0.68-1.09；P= 0.20; I2=0%）。在有肺炎数据的试验中，ICS治疗与肺炎发生率显著升高相关（治疗组5405例患者中有777例，对照组5371例患者中有561例；RR为1.34；95% CI为1.03-1.75；P= 0.03; I2=72%）。亚组分析显示，以下亚组的肺炎风险增加：ICS剂量最高（RR, 1.46; 95% CI, 1.10-1.92； P= 0.008; I2=78%）， ICS使用时间较短（RR, 2.12; 95% CI, 1.47-3.05； P< 0.001; I2=0%），呼气第一秒最低基线强制呼气量（RR, 1.90; 95% CI, 1.26-2.85； P= 0.002; I2=0%）， ICS和支气管扩张剂联合治疗（RR, 1.57; 95% CI, 1.35-1.82； P< 0.001; I2=24%）。在COPD患者中，ICS治疗对1年全因死亡率没有影响。ICS治疗与较高的肺炎风险相关。未来的研究应该确定特定的COPD患者亚群是否从ICS治疗中获益。
Recent studies of inhaled corticosteroid (ICS) therapy for managing stable chronic obstructive pulmonary disease (COPD) have yielded conflicting results regarding survival and risk of adverse events. To systematically review and quantitatively synthesize the effects of ICS therapy on mortality and adverse events in patients with stable COPD. Search of MEDLINE, CENTRAL, EMBASE, CINAHL, Web of Science, and PsychInfo through February 9, 2008. Eligible studies were double-blind, randomized controlled trials comparing ICS therapy for 6 or more months with nonsteroid inhaled therapy in patients with COPD. Two authors independently abstracted data including study characteristics, all-cause mortality, pneumonia, and bone fractures. The I2 statistic was used to assess heterogeneity. Study-level data were pooled using a random-effects model (when I2≥50%) or a fixed-effects model (when I2<50%). For the primary outcome of all-cause mortality at 1 year, our meta-analysis was powered to detect a 1.0% absolute difference in mortality, assuming a 2-sided α of .05 and power of 0.80. Eleven eligible randomized controlled trials (14 426 participants) were included. In trials with mortality data, no difference was observed in 1-year all-cause mortality (128 deaths among 4636 patients in the treatment group and 148 deaths among 4597 patients in the control group; relative risk [RR], 0.86; 95% confidence interval [CI], 0.68–1.09; P=.20; I2=0%). In the trials with data on pneumonia, ICS therapy was associated with a significantly higher incidence of pneumonia (777 cases among 5405 patients in the treatment group and 561 cases among 5371 patients in the control group; RR, 1.34; 95% CI, 1.03–1.75; P=.03; I2=72%). Subgroup analyses indicated an increased risk of pneumonia in the following subgroups: highest ICS dose (RR, 1.46; 95% CI, 1.10–1.92; P=.008; I2=78%), shorter duration of ICS use (RR, 2.12; 95% CI, 1.47–3.05; P<.001; I2=0%), lowest baseline forced expiratory volume in the first second of expiration (RR, 1.90; 95% CI, 1.26–2.85; P=.002; I2=0%), and combined ICS and bronchodilator therapy (RR, 1.57; 95% CI, 1.35–1.82; P<.001; I2=24%). Among patients with COPD, ICS therapy does not affect 1-year all-cause mortality. ICS therapy is associated with a higher risk of pneumonia. Future studies should determine whether specific subsets of patients with COPD benefit from ICS therapy.