Yao Xiyang, Zhang Kai, Bian Jieyong, Chen Gang
Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Department of Neurosurgery, Suzhou Xiangcheng People's Hospital, Suzhou, Jiangsu 215131, P.R. China.
Biomed Rep. 2016 Oct;5(4):428-436. doi: 10.3892/br.2016.743. Epub 2016 Aug 23.
The association between alcohol consumption and the risk of subarachnoid hemorrhage (SAH) is inconsistent. Thus, meta- and a dose-response analyses are presented with the purpose of assessing their associations. A systematic literature search was performed using Pubmed and Embase electronic databases for pertinent observational studies. Random-effects or fixed-effect models were employed to combine the estimates of the relative risks (RRs) with corresponding 95% confidence intervals (CIs). A dose-response pattern was conducted for further analysis. The current meta-analysis includes 14 observational studies reporting data on 483,553 individuals and 2,556 patients. The combined RRs of light alcohol consumption (<15 g/day) and moderate alcohol consumption (15-30 g/day) compared with teetotal individuals were 1.27 (95% CI: 0.95, 1.68) and 1.33 (95% CI: 0.84, 2.09), respectively, which indicated no significant association between light-to-moderate alcohol consumption and SAH. An increased risk of SAH was noted in heavy alcohol consumption (>30 g/day) when compared with no alcohol consumption, as demonstrated by a result of 1.78 (95% CI: 1.46, 2.17). Dose-response analysis showed evidence of a linear association (P=0.0125) between alcohol consumption and SAH. The risk of SAH increased by 12.1% when alcohol consumption was increased by 10 g/day. Therefore, heavy alcohol consumption was found to be associated with an increased risk of SAH. Furthermore, the association between SAH and alcohol consumption has clinical relevance with regard to risk factor modification and the primary and secondary prevention of SAH.
饮酒与蛛网膜下腔出血（SAH）风险之间的关联并不一致。因此，本文进行了荟萃分析和剂量反应分析，以评估它们之间的关联。使用PubMed和Embase电子数据库对相关观察性研究进行了系统的文献检索。采用随机效应或固定效应模型来合并相对风险（RRs）估计值及其相应的95%置信区间（CIs）。进行剂量反应模式分析以作进一步分析。当前的荟萃分析纳入了14项观察性研究，报告了483,553名个体和2,556例患者的数据。与不饮酒者相比，轻度饮酒（<15克/天）和中度饮酒（15 - 30克/天）的合并RRs分别为1.27（95% CI：0.95，1.68）和1.33（95% CI：0.84，2.09），这表明轻度至中度饮酒与SAH之间无显著关联。与不饮酒相比，重度饮酒（>30克/天）时SAH风险增加，结果显示为1.78（95% CI：1.46，2.17）。剂量反应分析显示饮酒与SAH之间存在线性关联的证据（P = 0.0125）。当饮酒量每天增加10克时，SAH风险增加12.1%。因此，发现重度饮酒与SAH风险增加有关。此外，SAH与饮酒之间的关联在风险因素调整以及SAH的一级和二级预防方面具有临床相关性。
