Huadong Hospital Fudan University, Shanghai, China.
Clin Rev Allergy Immunol. 2011 Aug;41(1):67-75. doi: 10.1007/s12016-009-8195-1.
The objective of this study is to evaluate the effect of exhaled CO (eCO) on the development of asthma and allergic rhinitis (AR) by means of reviewing published literature. The literatures published between January 1997 and December 2008 from the US National Library of Medicine (NLM) Database were obtained according to inclusion criteria. Meta-analysis of randomized controlled trials (RCTs) was performed. CO levels of asthma and AR patients were compared with that of normal controls. HO-1(heme oxygenase-1) expression and effect of corticosteroids on eCO levels were also analyzed. Fifteen studies concerning asthma and four studies concerning AR were included in this analysis. Heterogeneity from different studies was evident (P < 0.0001), so a random-effects model was preferred. The meta-analysis revealed that asthmatic patients had significantly higher levels of eCO compared to normal controls. There was significant difference between asthma and control groups in terms of eCO (combined weighted mean difference (WMD) 1.33 (95% confidence interval 0.72 to 1.95), P < 0.0001), and no significant difference between AR and control (combined WMD 0.93 (95% confidence interval -0.54 to 2.40), P = 0.22). HO-1 expression were also reviewed, asthma group produced greater expression of HO-1 than control group with significant difference (combined standardized mean difference (SMD) 2.98 (95% confidence interval 1.13 to 4.84), P = 0.002). After corticosteroid therapy, significantly different levels of eCO were produced after corticosteroid therapy than did asthma group (combined WMD -1.23 (95% confidence interval -2.43 to -0.03), P = 0.04). The analysis reveals that eCO levels were significantly raised in asthma and it may attribute to high expression of HO-1, but there were no significantly high eCO levels between AR and control groups. Due to sensitivity to corticosteroid inhibition, eCO may be used as a practical marker to detect and monitor exacerbation of asthma.
本研究旨在通过回顾已发表文献评估呼出气一氧化碳（eCO）对哮喘和变应性鼻炎（AR）发展的影响。根据纳入标准，从美国国家医学图书馆（NLM）数据库中获取了 1997 年 1 月至 2008 年 12 月期间发表的文献。对随机对照试验（RCT）进行了荟萃分析。比较哮喘和 AR 患者的 CO 水平与正常对照组。还分析了 HO-1（血红素加氧酶-1）的表达和皮质类固醇对 eCO 水平的影响。本分析共纳入 15 项哮喘研究和 4 项 AR 研究。不同研究之间存在明显的异质性（P <0.0001），因此首选随机效应模型。荟萃分析显示，哮喘患者的 eCO 水平明显高于正常对照组。eCO 在哮喘组和对照组之间存在显著差异（合并加权均数差（WMD）1.33（95%置信区间 0.72 至 1.95），P <0.0001），而 AR 组和对照组之间无显著差异（合并 WMD 0.93（95%置信区间 -0.54 至 2.40），P = 0.22）。还回顾了 HO-1 的表达，哮喘组的 HO-1 表达高于对照组，差异有统计学意义（合并标准化均数差（SMD）2.98（95%置信区间 1.13 至 4.84），P = 0.002）。皮质类固醇治疗后，哮喘组患者 eCO 水平较治疗前明显降低（合并 WMD -1.23（95%置信区间 -2.43 至 -0.03），P = 0.04）。分析表明，哮喘患者的 eCO 水平明显升高，可能归因于 HO-1 的高表达，但 AR 组与对照组之间并无明显的 eCO 水平升高。由于对皮质类固醇抑制敏感，eCO 可作为一种实用的标志物来检测和监测哮喘的恶化。
