title: Genetic susceptibility to urinary incontinence: implication of polymorphisms of androgen and oestrogen pathways.
abstract: OBJECTIVE
  Although existence of genetic factors predisposing to urinary incontinence in women is widely admitted, precise molecular and genetic variations implicated are still unknown. Given the established influence of steroids metabolism in incontinence, we studied the correlation between polymorphisms of genes of oestrogen/androgen pathways and urinary incontinence in women, in order to raise evidence of genetic susceptibility.
  
  
  METHODS
  A case-control study included 121 cases and 66 controls. Age, familial history of incontinence, gynaecologic history and age of menopause were collected. Patients were classified into three groups: control, urge urinary incontinence (UUI), stress urinary incontinence (SUI). Genetic polymorphisms were determined after amplification by PCR for the following genes: CYP-19, CYP17, androgen receptor (AR) and oestrogen receptor (ESR-1). Statistical analysis was performed to study correlation between genotype and presence of a subtype of incontinence.
  
  
  RESULTS
  A total of 187 patients were analysed: 66 were controls, 30 presented UUI and 107 presented SUI. Patients presenting incontinence had significantly more often familial history of incontinence than controls. AR polymorphism (combination of 2 alleles containing more than 21 CAG repeats) is significantly associated with UUI (P = 0.02). Polymorphisms of ESR-1, CYP17 and CYP19 were not associated with any subtype of urinary incontinence.
  
  
  CONCLUSIONS
  This study shows that AR polymorphism is linked to genetic susceptibility to urinary incontinence. This result suggests that this disease is partly gene-related and encourages larger studies to explore the genetics factors of urinary incontinence.
authors.affiliation: Department of Urology, Tenon Hospital, Groupe Hospitalo-Universitaire EST, Assistance Publique-Hôpitaux de Paris (AP-HP), University Paris VI, 4 rue de la Chine, 75970, Paris Cedex 20, France. jncornu@hotmail.fr
authors.forename: J N
authors.initials: JN
authors.lastname: Cornu
authors.forename: B
authors.initials: B
authors.lastname: Merlet
authors.forename: O
authors.initials: O
authors.lastname: Cussenot
authors.forename: G
authors.initials: G
authors.lastname: Cancel-Tassin
authors.forename: C
authors.initials: C
authors.lastname: Ciofu
authors.forename: G
authors.initials: G
authors.lastname: Amarenco
authors.forename: F
authors.initials: F
authors.lastname: Haab
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001141:Aromatase / Q000235:genetics; D016022:Case-Control Studies; D047628:Estrogen Receptor alpha / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006801:Humans; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D011944:Receptors, Androgen / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics*; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics; D014550:Urinary Incontinence, Stress / Q000235:genetics*; D053202:Urinary Incontinence, Urge / Q000235:genetics*
chemical_list: C506487:ESR1 protein, human; D047628:Estrogen Receptor alpha; D011944:Receptors, Androgen; D001141:Aromatase; D013254:Steroid 17-alpha-Hydroxylase