Association between allergic rhinitis and hypertension risk: A bidirectional 2-sample mendelian randomization study

Abstract

Previous studies have suggested a potential association between allergic rhinitis (AR) and hypertension, but the genetic basis remains unclear. In this study, we aimed to explore the genetic correlation and potential causal association between AR and hypertension. Using a large-scale genome-wide association study (GWAS) public database, we conducted meticulous screening to acquire the most up-to-date GWAS data on single nucleotide polymorphisms (SNPs) relevant to AR and hypertension, with a significance threshold of P < 5 × 10-8. Then, we investigated the causal association between AR and hypertension through mendelian randomization (MR) analysis. We also performed reverse MR analysis to assess the possibility of reverse causality. Sensitivity analyses encompassed various factors, including horizontal pleiotropy, heterogeneity testing, and stepwise exclusion sensitivity checks. To investigate the causal relationship between AR and hypertension, we utilize the odds ratio (OR) and 95% confidence interval (CI) as our evaluative metric. This study leveraged a database comprising 112583 samples for AR and 461880 samples for hypertension. After meticulous screening, we identified 32 SNPs as instrumental variables. By employing the aforementioned 2-sample Mendelian randomization approaches, the estimated causal effects showed striking concordance. A discernible causal association between AR and hypertension was found using the IVW method (OR = 0.91, 95% CI: 0.86–0.98, P = .008), with horizontal pleiotropy and heterogeneity tests supporting the validity of our MR study. MR-Egger regression findings provided reassurance against bias stemming from genetic pleiotropy (intercept = -0.0006802, P = .6947). Interestingly, “leave-one-out” analysis yielded no evidence of nonspecific SNP influences, further consolidating our findings. Moreover, our reverse MR analysis yielded no indication of reverse causality from hypertension to AR, effectively discounting any influence from the latter on the former. Our study found evidence of a causal association between AR and hypertension in individuals of European ancestry. It demonstrated that AR reduced the risk of hypertension, suggesting a protective effect on hypertension due to the negative correlation with AR.