Sarecka-Hujar Beata, Łoboda Danuta, Paradowska-Nowakowska Elżbieta, Gołba Krzysztof S
Department of Basic Biomedical Science, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, 41-200 Sosnowiec, Poland.
Department of Electrocardiology and Heart Failure, Faculty of Health Sciences in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.
J Clin Med. 2022 Jun 15;11(12):3454. doi: 10.3390/jcm11123454.
Polymorphisms within the gene that encodes for coagulation factor XIII (FXIII) have been suggested to be involved in the pathogeneses of ischemic stroke (IS) and myocardial infarction (MI). The Val34Leu polymorphism is one of the most commonly analysed polymorphisms. However, studies on the role of the Val34Leu polymorphism in the aetiology of vascular diseases often show contradictory results. In the present meta-analysis, we aimed to pool data from available articles to assess the relationship between the Val34Leu polymorphism and the susceptibilities to IS of undetermined source and premature MI in patients aged below 55 years.
We searched databases (PubMed, Embase, Google Scholar, SciELO, and Medline) using specific keywords (the last search was in January 2022). Eventually, 18 studies (627 cases and 1639 controls for IS; 2595 cases and 4255 controls for MI) met the inclusion criteria. Data were analysed using RevMan 5.4 and StatsDirect 3 link software. The relation between Val34Leu polymorphism and disease was analysed in five genetic models, i.e., dominant, recessive, additive, heterozygous, and allelic.
No relation between Val34Leu polymorphism and IS in young adults was observed in all analysed genetic models. For premature MI, significant pooled OR was found between the carrier state of the Leu allele (Val/Leu + Leu/Leu vs. Val/Val) and a lack of MI, suggesting its protective role (OR = 0.80 95%CI 0.64-0.99, = 0.04). A similar finding was observed for the heterozygous model in MI (Val/Leu vs. Val/Val) (OR = 0.77 95%CI 0.61-0.98, = 0.03). No relation was found for the recessive, additive, and allelic models in MI.
In the population of young adults, no positive correlation was found between the Val34Leu polymorphism and IS of undetermined source in any of the analysed genetic models. In turn, the carrier state of the 34Leu allele as well as heterozygotes themselves were found to play a protective role in relation to premature MI.
编码凝血因子 XIII（FXIII）的基因中的多态性被认为与缺血性中风（IS）和心肌梗死（MI）的发病机制有关。Val34Leu 多态性是最常分析的多态性之一。然而，关于 Val34Leu 多态性在血管疾病病因学中的作用的研究往往显示出相互矛盾的结果。在本荟萃分析中，我们旨在汇总现有文章的数据，以评估 Val34Leu 多态性与 55 岁以下患者不明来源的 IS 和早发性 MI 的易感性之间的关系。
我们使用特定关键词搜索数据库（PubMed、Embase、谷歌学术、SciELO 和 Medline）（最后一次搜索于 2022 年 1 月进行）。最终，18 项研究（IS 患者 627 例，对照 1639 例；MI 患者 2595 例，对照 4255 例）符合纳入标准。使用 RevMan 5.4 和 StatsDirect 3 链接软件进行数据分析。在五种遗传模型中分析了 Val34Leu 多态性与疾病之间的关系，即显性、隐性、加性、杂合子和等位基因模型。
在所有分析的遗传模型中，未观察到 Val34Leu 多态性与年轻人 IS 之间的关系。对于早发性 MI，在 Leu 等位基因的携带者状态（Val/Leu + Leu/Leu 与 Val/Val）与无 MI 之间发现了显著的合并 OR，表明其具有保护作用（OR = 0.80，95%CI 0.64 - 0.99，P = 0.04）。在 MI 的杂合子模型中（Val/Leu 与 Val/Val）也观察到了类似的结果（OR = 0.77，95%CI 0.61 - 0.98，P = 0.03）。在 MI 的隐性、加性和等位基因模型中未发现相关性。
在年轻人中，在任何分析的遗传模型中，均未发现 Val34Leu 多态性与不明来源的 IS 之间存在正相关。相反，发现 34Leu 等位基因的携带者状态以及杂合子本身对早发性 MI 具有保护作用。
