The single nucleotide polymorphism rs700518 is an independent risk factor for metabolic syndrome and benign prostatic hyperplasia (MetS‐BPH)

Abstract

Studies have shown that 48.59% of benign prostate hyperplasia (BPH) is combined with metabolic syndrome (MetS). The mainstream view supports the correlation between MetS and BPH, but the pathogenesis of MetS-BPH is not fully understood. Four hundred and seventy-four men, aged 47 years or older, were recruited into this study by consecutive routine physical examination programs, and several parameters were obtained from each participant. Based on the diagnosis of BPH, MetS, and MetS-BPH, the participants were divided into BPH and Non-BPH groups, MetS and Non-MetS groups, as well as MetS-BPH and Non-MetS-BPH groups. The values of the obtained parameters were evaluated using Student's t-test, chi-square test, and logistic regression analysis. The value of estradiol (E2) was higher in the diseased groups (BPH, MetS, and MetS-BPH groups) compared with the corresponding control groups (Non-BPH, Non-MetS, and Non-MetS-BPH groups), and the differences were statistically significant. Also, E2 had an independent association with BPH (OR = 2.286, 95% CI: 1.723-3.593, p < 0.001), MetS (OR = 1.406, 95% CI: 0.585-2.315, p < 0.001), and MetS-BPH (OR = 1.249, 95% CI: 0.795-1.962, p < 0.001). Regarding SNPs of CYP19A1 gene, both the rs4646 genotypes (CC, CA, and AA) and the rs700518 genotypes (CC, CT, and TT) were present in every group, and all genotypes had statistically significant differences between the diseased and corresponding control groups. However, only the TT genotype of rs700518 was independently associated with BPH, MetS, and MetS-BPH after adjusting for age. The TT genotype of rs700518 is an independent risk factor for the MetS-BPH populations, and the CYP19A1 gene regulation of estrogen leads to MetS-BPH.

The association between metabolic syndrome and benign prostatic hyperplasia: a systematic review and meta-analysis

“…Moreover, epidemiological evidence suggested that patients with MetS had a greater risk of developing T2DM [57]. The correlation between MetS and BPH has been widely discussed, but the controversy still exists [26,31,33,36]. Thus, a meta-analysis is needed to clarify the correlation between the two diseases, and provide the latest medical evidence for clinical work.…”

“…In the final statistical analysis, there were 18 studies reported the PSA level [16,17,19,20,[22][23][24][25][26][27][28][30][31][32][33][34][35][36]. There was no statistical difference in PSA level between the presence of MetS and the absence of MetS (WMD ¼ 0.04; 95% Cl: À0.06 to 0.13; p ¼ .43; Figure 3).…”

“…The data of Qmax was gained in 8 studies [23,27,28,[30][31][32]35,36]. The Qmax of the MetS group was lower than the non-MetS group (WMD ¼ À0.48; 95% Cl: À0.77 to À0.19; p ¼ .001; Figure 4(a)).…”

Polygenic risk score predicting susceptibility and outcome of benign prostatic hyperplasia in the Han Chinese

“…The exact cause of BPH is not fully understood, but it is believed to be a complex interplay between genetic and environmental factors [3][4][5]. Genetic factors play a crucial role in the development of BPH, with several genes and single nucleotide polymorphisms (SNPs) identified to be associated with an increased risk of BPH [6][7][8]. These genetic variations may influence the growth of prostate glandular cells, androgen and androgen receptors expression, epithelial-stromal interactions, inflammation, and other biological processes involved in the pathogenesis of BPH [9].…”

Polygenic risk score predicting susceptibility and outcome of benign prostatic hyperplasia in the Han Chinese

“…The exact cause of BPH is not fully understood, but it is believed to be a complex interplay between genetic and environmental factors [3][4][5] . Genetic factors play a crucial role in the development of BPH, with several genes and single nucleotide polymorphisms (SNPs) identi ed to be associated with an increased risk of BPH [6][7][8] . These genetic variations may in uence the growth of prostate glandular cells, androgen and androgen receptors expression, epithelial-stromal interactions, in ammation, and other biological processes involved in the pathogenesis of BPH 9 .…”