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Alcohol consumption and risk of subarachnoid hemorrhage: A meta-analysis of 14 observational studies

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 database...

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Detalles Bibliográficos
Autores principales: Yao, Xiyang, Zhang, Kai, Bian, Jieyong, Chen, Gang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5038345/
https://www.ncbi.nlm.nih.gov/pubmed/27699009
http://dx.doi.org/10.3892/br.2016.743
Descripción
Sumario: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.