title: Steroid hormone metabolism in women with pelvic organ prolapse.
abstract: OBJECTIVE
  To identify whether endogenous steroid hormone metabolism in women with pelvic organ prolapse (POP) is different from that in normal women and the relationship between endogenous steroid hormone metabolites and POP stage.
  
  
  METHODS
  Twenty postmenopausal women who were clinically diagnosed as having POP and 20 volunteer postmenopausal women without prolapse were included in the study. We compared the urinary profiles of endogenous steroids between the two groups and investigated the relationship between urinary profiles of endogenous steroids and degree of prolapse. Urinary profiles of endogenous steroids were assayed by gas chromatography/mass spectrometry.
  
  
  RESULTS
  The ages of the patients and control group were 64.6 +/- 6.5 and 63.5 +/- 3.9 years, and the body mass index was 23.96 +/- 3.14 and 24.11 +/- 2.73 kg/m2 in patients and normal subjects, respectively. The number of patients were 4 at stage I, 4 at stage II, 6 at stage III and 6 at stage IV. 5-Androstene-3 beta,16 beta,17 beta-triol (5-AT), 11 beta-hydroxy an and 17 beta-estradiol were significantly increased in the POP group as compared with the control group (0.76 +/- 0.67 vs. 0.06 +/- 0.03 mumol/g creatinine, P = .002, 1.16 +/- 0.83 vs. 0.65 +/- 0.23 mumol/g creatinine, P = .04; and 15.08 +/- 9.81 vs. 8.53 +/- 6.19 mumol/g creatinine, P = .04). However, tetrahydrocortisone (THE) was significantly increased in the control group as compared with the patient group (9.80 +/- 6.21 vs. 5.22 +/- 4.89 mumol/g creatinine, P = .04). Androgen metabolites 5-AT and THE significantly correlated with the pelvic organ prolapse quantitation (POP-Q) stage (R = .418; P = .027; R = .46, P = .016). Among the estrogen metabolites, 17 beta-estradiol correlated with POP-Q stage, but not significantly so (R = .38, P = .05), and the 17 beta-estradiol/estrone ratio weakly correlated with stage (R = .14, P = .49).
  
  
  CONCLUSIONS
  The metabolites of endogenous steroid hormones could be contributing factors in the pathogenesis of POP.
authors.affiliation: Departments of Obstetrics and Gynecology and of Urology, College of Medicine, Yonsei University, Seoul, Korea 120-752. swbai@yumc.yonsei.ac.kr
authors.forename: Sang Wook
authors.initials: SW
authors.lastname: Bai
authors.forename: Byung Hwa
authors.initials: BH
authors.lastname: Jung
authors.forename: Bong Chul
authors.initials: BC
authors.lastname: Chung
authors.forename: Sang Un
authors.initials: SU
authors.lastname: Kim
authors.forename: Jeong Yeon
authors.initials: JY
authors.lastname: Kim
authors.forename: Koon Ho
authors.initials: KH
authors.lastname: Rha
authors.forename: Sei Kwang
authors.initials: SK
authors.lastname: Kim
authors.forename: Ki Hyun
authors.initials: KH
authors.lastname: Park
mesh_terms: D000368:Aged; D015992:Body Mass Index; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D012739:Gonadal Steroid Hormones / Q000378:metabolism* / Q000652:urine; D006801:Humans; D008875:Middle Aged; D012307:Risk Factors; D012720:Severity of Illness Index; D013256:Steroids / Q000378:metabolism* / Q000652:urine; D014596:Uterine Prolapse / Q000209:etiology / Q000378:metabolism* / Q000652:urine
chemical_list: D012739:Gonadal Steroid Hormones; D013256:Steroids