The adrenal and polycystic ovary syndrome

Yildiz B. O., Azziz R.

REVIEWS IN ENDOCRINE & METABOLIC DISORDERS, cilt.8, sa.4, ss.331-342, 2007 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 8 Sayı: 4
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1007/s11154-007-9054-0
  • Dergi Adı: REVIEWS IN ENDOCRINE & METABOLIC DISORDERS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.331-342
  • Anahtar Kelimeler: PCOS, DHEA, adrenal, hyperandrogenism, cortisol, heritability, DEHYDROEPIANDROSTERONE-SULFATE LEVELS, EXAGGERATED 17-HYDROXYPROGESTERONE RESPONSE, CORTICOSTEROID-BINDING GLOBULIN, CORTICOTROPIN-RELEASING FACTOR, IMPAIRED GLUCOSE-TOLERANCE, ANDROGEN EXCESS, INSULIN-RESISTANCE, ADRENOCORTICAL STEROIDOGENESIS, HYPERANDROGENIC WOMEN, 21-HYDROXYLASE GENE
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30% of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.