title: Polymorphisms in the vitamin D receptor gene and the androgen receptor gene and the risk of benign prostatic hyperplasia.
abstract: OBJECTIVE
  Little is known about risk factors for the development of benign prostatic hyperplasia (BPH). Recently, associations were observed between prostate cancer (CaP) risk and polymorphisms in the vitamin D receptor (VDR) gene and the androgen receptor (AR) gene. Since both receptors are relevant for prostate growth, the VDR and AR are also expected to be involved in the development of BPH. The objective of this study is to establish the relationship between the risk of BPH and a polymorphism in the number of CAG repeats in the AR gene and a TaqI restriction enzyme polymorphism in the VDR gene.
  
  
  METHODS
  For this study, 98 patients who had been treated for BPH-related complaints and 61 convenience controls (predominantly bladder cancer patients) were recruited from the outpatient clinic. DNA was isolated from peripheral blood, and genotyping was performed with PCR-based methods. Means as well as odds ratios (ORs) with 95% confidence intervals (CI) were calculated using SPSS software.
  
  
  RESULTS
  The mean number of CAG repeats in the AR gene in patients and controls was found to be similar: 21.8 (SD = 2.8) and 21.9 (SD = 2.9), respectively. In the subgroup of patients with a prostate volume of at least 50 cm(3), the mean number of repeats was 21.5 (SD = 2.6). The OR for BPH for individuals with homozygous presence of the VDR TaqI restriction fragment length polymorphism (RFLP) (tt) versus individuals with homozygous absence (TT) or heterozygotes (Tt) was found to be 1.0 (95% CI 0.4-2.4). For individuals with a prostate volume of at least 50 cm(3), the OR was 1.2 (95% CI 0.5-3. 2).
  
  
  CONCLUSIONS
  Unlike earlier observations in prostate cancer, we did not find an association between the CAG repeat polymorphism in the AR gene and the TaqI RFLP polymorphism in the VDR gene and the risk of BPH.
authors.affiliation: Urology, University of Nijmegen, The Netherlands.
authors.forename: J T
authors.initials: JT
authors.lastname: Bousema
authors.forename: M J
authors.initials: MJ
authors.lastname: Bussemakers
authors.forename: K P
authors.initials: KP
authors.lastname: van Houwelingen
authors.forename: F M
authors.initials: FM
authors.lastname: Debruyne
authors.forename: A L
authors.initials: AL
authors.lastname: Verbeek
authors.forename: J J
authors.initials: JJ
authors.lastname: de La Rosette
authors.forename: L A
authors.initials: LA
authors.lastname: Kiemeney
mesh_terms: D000368:Aged; D006801:Humans; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics*; D011470:Prostatic Hyperplasia / Q000235:genetics*; D011944:Receptors, Androgen / Q000235:genetics*; D018167:Receptors, Calcitriol / Q000235:genetics*; D012307:Risk Factors
chemical_list: D011944:Receptors, Androgen; D018167:Receptors, Calcitriol