Association between vitamin D receptor gene polymorphism and essential hypertension: a systematic review and meta-analysis

Abstract

Abstract Background and aim Recent publications reported that the association between Vitamin D Receptor (VDR) gene polymorphism of Fokl (rs228570 or rs10735810) and essential hypertension (EH) remains controversial. Thus, we conducted this study to investigate the relationship between Fokl and EH. Methods Major medical databases (EMBASE, PUBMED, Science Direct, Cochrane, Springer, Scopus, ProQuest, and Lilacs) were systematically searched for observational studies evaluating the impact of Fokl polymorphism on EH, published until January 2022 with predefined protocol and without language restriction regarding PRISMA guideline. Analysis was performed in RevMan 5.3 (fixed and random-effects model through heterogeneity test) to provide pooled measures for odds ratio (OR) under Hardy-Weinberg Equilibrium based-on allele contrast, additive, dominant, and recessive genetic models. Results Eight observational studies enrolled comprising 3,762 cases and 4,445 controls. Under the allele model, Fokl polymorphism (f vs F) significantly increased the odds of having EH (OR=1.27; 95% confidence interval: 1.05–1.53), p=0.01. Fokl polymorphism was not significantly associated with EH under additive model (ff vs FF) with OR=0.94 (0.57–1.54), p=0.79, dominant model (Ff + ff vs FF) with OR=0.97 (0.8–1.16), p=0.76 and recessive model (FF + Ff vs ff) with OR=0.96 (0.59–1.56), p=0.97 However, subgroup analysis based on ethnicities, comprising Asian, European, American, and African, showed that only in African population, Fokl polymorphism was associated with reduced odds of EH under additive (OR=0.36; 0.17–0.74), p=0.005 and recessive model (OR=0.31; 0.14–0.7), p=0.005. Conclusions VDR gene polymorphism of Fokl was significantly associated with EH in a particular genetic model and could be affected by ethnicity. However, further studies are needed to make the robust evidence. Funding Acknowledgement Type of funding sources: None.