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Adrenocortical hyperresponsiveness to corticotropin in polycystic ovary syndrome patients with adrenal androgen excess.
Fertil Steril. 2004 Jan; 81(1):126-31.FS

Abstract

OBJECTIVE

To test the hypothesis that adrenal androgen (AA) excess in the polycystic ovary syndrome (PCOS) is due to a generalized exaggeration in AA output in response to adrenocorticotropic hormone (ACTH), and that this abnormality is due to an identifiable alteration in the biosynthesis of AAs.

DESIGN

Cross-sectional prospective controlled study.

SETTING

Academic tertiary care medical center.

PATIENT(S)

Patients with PCOS (n = 9) and without (n = 9) AA excess and controls (n = 12) without hyperandrogenism, matched for age and body mass.

INTERVENTION(S)

Acute 60-minute ACTH test was performed on patients.

MAIN OUTCOME MEASURE(S)

Basal levels of dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), free T, and basal (Steroid(0)) and the 60-minute ACTH-stimulated levels (Steroid(60)) of pregnenolone (PREG), progesterone (P4), 17-hydroxypregnenolone (17-HPREG), 17-hydroxyprogesterone (17-HP), dehydroepiandrosterone (DHEA), and androstenedione (A4) were measured. Adrenocortical activities of 17-hydroxylase (17-OH), 17,20-lyase, and 3beta-hydroxysteroid dehydrogenase were estimated from product to precursor ratio, using Steroid(60) values.

RESULT(S)

Compared with PCOS patients without AA excess, PCOS patients with AA excess demonstrated significantly greater levels of DHEA(0) and A4(60). PCOS patients with AA excess had significantly higher activity of delta(5)17-OH, compared with PCOS patients without AA excess.

CONCLUSION(S)

Adrenal androgen excess in PCOS is associated with a greater delta(5)17-OH activity in response to ACTH.

Authors+Show Affiliations

Moran C
Department of Obstetrics and Gynecology, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
Reyna R
No affiliation info available
Boots LS
No affiliation info available
Azziz R
No affiliation info available

MeSH

17-alpha-Hydroxyprogesterone3-Hydroxysteroid DehydrogenasesAdrenal CortexAdrenocorticotropic HormoneAdultAndrostenedioneCase-Control StudiesCross-Sectional StudiesDehydroepiandrosteroneDehydroepiandrosterone SulfateFemaleHumansHyperandrogenismPolycystic Ovary SyndromePregnenoloneProgesteroneProspective StudiesSteroid 17-alpha-HydroxylaseTestosterone

Pub Type(s)

Clinical Trial
Comparative Study
Controlled Clinical Trial
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

14711555

Citation

Moran, Carlos, et al. "Adrenocortical Hyperresponsiveness to Corticotropin in Polycystic Ovary Syndrome Patients With Adrenal Androgen Excess." Fertility and Sterility, vol. 81, no. 1, 2004, pp. 126-31.
Moran C, Reyna R, Boots LS, et al. Adrenocortical hyperresponsiveness to corticotropin in polycystic ovary syndrome patients with adrenal androgen excess. Fertil Steril. 2004;81(1):126-31.
Moran, C., Reyna, R., Boots, L. S., & Azziz, R. (2004). Adrenocortical hyperresponsiveness to corticotropin in polycystic ovary syndrome patients with adrenal androgen excess. Fertility and Sterility, 81(1), 126-31.
Moran C, et al. Adrenocortical Hyperresponsiveness to Corticotropin in Polycystic Ovary Syndrome Patients With Adrenal Androgen Excess. Fertil Steril. 2004;81(1):126-31. PubMed PMID: 14711555.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Adrenocortical hyperresponsiveness to corticotropin in polycystic ovary syndrome patients with adrenal androgen excess. AU - Moran,Carlos, AU - Reyna,Rosario, AU - Boots,Larry S, AU - Azziz,Ricardo, PY - 2004/1/9/pubmed PY - 2004/4/2/medline PY - 2004/1/9/entrez SP - 126 EP - 31 JF - Fertility and sterility JO - Fertil Steril VL - 81 IS - 1 N2 - OBJECTIVE: To test the hypothesis that adrenal androgen (AA) excess in the polycystic ovary syndrome (PCOS) is due to a generalized exaggeration in AA output in response to adrenocorticotropic hormone (ACTH), and that this abnormality is due to an identifiable alteration in the biosynthesis of AAs. DESIGN: Cross-sectional prospective controlled study. SETTING: Academic tertiary care medical center. PATIENT(S): Patients with PCOS (n = 9) and without (n = 9) AA excess and controls (n = 12) without hyperandrogenism, matched for age and body mass. INTERVENTION(S): Acute 60-minute ACTH test was performed on patients. MAIN OUTCOME MEASURE(S): Basal levels of dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), free T, and basal (Steroid(0)) and the 60-minute ACTH-stimulated levels (Steroid(60)) of pregnenolone (PREG), progesterone (P4), 17-hydroxypregnenolone (17-HPREG), 17-hydroxyprogesterone (17-HP), dehydroepiandrosterone (DHEA), and androstenedione (A4) were measured. Adrenocortical activities of 17-hydroxylase (17-OH), 17,20-lyase, and 3beta-hydroxysteroid dehydrogenase were estimated from product to precursor ratio, using Steroid(60) values. RESULT(S): Compared with PCOS patients without AA excess, PCOS patients with AA excess demonstrated significantly greater levels of DHEA(0) and A4(60). PCOS patients with AA excess had significantly higher activity of delta(5)17-OH, compared with PCOS patients without AA excess. CONCLUSION(S): Adrenal androgen excess in PCOS is associated with a greater delta(5)17-OH activity in response to ACTH. SN - 0015-0282 UR - https://www.unboundmedicine.com/medline/citation/14711555/Adrenocortical_hyperresponsiveness_to_corticotropin_in_polycystic_ovary_syndrome_patients_with_adrenal_androgen_excess_ DB - PRIME DP - Unbound Medicine ER -