This study aims to explore the effect of gene polymorphisms of 5a-reduction enzyme (), steroidogenic cytochrome P-450 17alpha-hydroxylase (), aromatase cytochrome P450 family 19 () and vita-min D receptor () on benign prostatic hyperplasia (BPH) susceptibility and clinical progress. A total of 452 BHP patients and 501 healthy individuals were selected in Harbin Medical University Daqing School from October 2014 and December 2015 as the case and control groups. All BPH patients received drug treatment and were subsequently divided into the progression and non-progression groups based on their therapeutic efficacy. PCR-RFLP was applied to detect the genotype distributions of , which were further tested with Hardy-Weinberg (H-W) equilibrium. Logistic regression analysis was applied to determine the risk factors for BPH progression. Compared with subjects carrying VV genotype and V allele at V89L, those with LL genotype and L allele at V89L may have reduced risk of BPH susceptibility or progression (all < 0.05). Compared with subjects carrying TT genotype and T allele at -34T>C, those with CC genotype and C allele at -34T>C may have increased risk of BPH susceptibility or progression (all < 0.05). Compared with individuals carrying FF genotype and F allele at Fok I, those with ff genotype and f allele at Fok I may have increased susceptibility to BPH (all < 0.05). Logistic regression analysis showed that V89L and polymorphisms and -34T>C (TC + CC)/ V89L (VV) combined genotypes were significantly related with the clinical progression of BHP. These results revealed that V89L and -34T>C polymorphisms were associated with the risk of BPH and its clinical progression.
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