title: Sex steroids, adiposity and smoking in the pathogenesis of idiopathic hirsutism and polycystic ovary syndrome.
abstract: Hyperestronemia may be central to the development of polycystic ovary syndrome. The present study was designed to examine whether increased availability of androstenedione or increased aromatase closely associated with adiposity, plays the dominant role in the development of hyperestronemia. We measured plasma androstenedione, estrone and the estrone/androstenedione ratio (an indirect index of peripheral aromatase activity), in 141 patients with idiopathic hirsutism and in 88 patients with polycystic ovary syndrome. Estrone levels were higher in polycystic ovary syndrome, 250.4 +/- 129 (mean +/- standard deviation) than in idiopathic hirsutism, 210.6 +/- 119 pmol/l, p less than 0.05. Plasma androstenedione levels were higher in polycystic ovary syndrome, 8.24 +/- 3.5, than in idiopathic hirsutism, 7.1 +/- 1.7 nmol/l, p less than 0.0025. However, the estrone/androstenedione ratio was similar in the two groups. In all patients who smoked, androstenedione was higher, 8.14 +/- 3.22 than in nonsmokers, 6.99 +/- 2.96 nmol/l, p less than 0.005. Smokers had a lower body mass index, 23.9 +/- 2.3, than non-smokers 25.6 +/- 4.8 kg/m2, p less than 0.025. However, estrone levels were similar in smokers and in non-smokers. These data indicate that elevated estrone is more closely related to increased availability of androstenedione than to increased aromatase activity. While cigarette smoking appears to increase androstenedione levels, it may inhibit aromatase activity either directly or indirectly because of an associated reduction in adiposity. However, since the relative frequency of polycystic ovary syndrome and idiopathic hirsutism was similar in smokers and non-smokers, smoking did not appear to reduce estrone bioactivity as had been claimed.
authors.affiliation: Department of Endocrinology and Diabetes Mellitus, St. Vincent's Hospital, Dublin, Eire.
authors.forename: B
authors.initials: B
authors.lastname: Byrne
authors.forename: S
authors.initials: S
authors.lastname: Cunningham
authors.forename: D
authors.initials: D
authors.lastname: Igoe
authors.forename: R
authors.initials: R
authors.lastname: Conroy
authors.forename: T J
authors.initials: TJ
authors.lastname: McKenna
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism; D000328:Adult; D000728:Androgens / Q000097:blood; D000735:Androstenedione / Q000097:blood; D015992:Body Mass Index; D001835:Body Weight / Q000502:physiology; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D004967:Estrogens / Q000097:blood; D004970:Estrone / Q000097:blood; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood*; D006628:Hirsutism / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D009765:Obesity / Q000453:epidemiology / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D012189:Retrospective Studies; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D012907:Smoking / Q000453:epidemiology / Q000503:physiopathology*; D013739:Testosterone / Q000097:blood
chemical_list: D000728:Androgens; D004967:Estrogens; D012739:Gonadal Steroid Hormones; D012738:Sex Hormone-Binding Globulin; D004970:Estrone; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate