Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome
| Autor: | Theresa Horab, Rogerio A. Lobo, Frank González, Lilly Chang |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Adult
endocrine system medicine.medical_specialty 3-Hydroxysteroid Dehydrogenases Adrenocortical Hyperfunction endocrine system diseases Adrenal disorder medicine.drug_class Biology 17-alpha-Hydroxypregnenolone Dexamethasone Basal (phylogenetics) Adrenocorticotropic Hormone Cytochrome P-450 Enzyme System Internal medicine Adrenal Glands Hydroxyprogesterones medicine Humans Testosterone Prospective Studies Prospective cohort study 17-alpha-Hydroxyprogesterone Obstetrics and Gynecology Estrogens Luteinizing Hormone Androgen Polycystic ovary Endocrinology Reproductive Medicine Androgens Hydroxyprogesterone Female hormones hormone substitutes and hormone antagonists Polycystic Ovary Syndrome Blood sampling Endocrine gland |
| Zdroj: | Fertility and Sterility. 66:354-361 |
| ISSN: | 0015-0282 |
| Popis: | Objective To examine the hypothesis that, in polycystic ovary syndrome (PCOS), ovarian steroids induce adrenal enzyme dysfunction or adrenal androgen hyperresponsiveness to ACTH. Design Prospective controlled clinical study. Setting Reproductive endocrinology unit of an academic medical center. Patients Twelve women with PCOS who had adrenal androgen excess were compared with five weight-matched ovulatory women. In half of the women with PCOS, prestudy screening was suggestive of mild 3 β -hydroxysteroid dehydrogenase (HSD) deficiency. Interventions Basal and adrenal dynamic blood sampling before and after GnRH agonist (GnRH-a) administration for 6months. Main Outcome Measures Basal E 2 and androgen levels as well as dexamethasone-suppressed, ACTH-stimulated 17 α -hydroxyprogesterone, 17 α -hydroxypregnenolone, and androgen levels before and after ovarian suppression. Results Although none of the subjects with PCOS proved to have mild 3 β -HSD deficiency, the majority of them (58%) met the criteria for 17,20 lyase hyperactivity before and after GnRH-a therapy. As a group, the remaining subjects with PCOS exhibited an elevated DHEAS response to ACTH before GnRH-a treatment, which may have normalized after GnRH-a treatment. Conclusion Adrenal androgen excess in PCOS may be heterogeneous in etiology, whereas 17,20 lyase hyperactivity appears to be an intrinsic adrenal disorder, adrenal androgen hyper-responsiveness to ACTH may be ovarian induced. Reliance on historical controls may lead to overdiagnosis of mild 3 β -HSD deficiency. |
| Databáze: | OpenAIRE |
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