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11 beta-hydroxylase deficiency in hyperandrogenism.
Fertil Steril. 1991 Apr; 55(4):733-41.FS

Abstract

OBJECTIVE

to determine the 11-deoxycortisol (S) response and incidence of 11 beta-hydroxylase deficiency in hyperandrogenism.

DESIGN

Hyperandrogenic women prospectively and consecutively underwent acute adrenal stimulation studies.

SETTING

Tertiary institution.

PATIENTS

Two hundred sixty women complaining of hirsutism and/or hyperandrogenic oligomenorrhea were studied, excluding five unrelated families (1.9% of total) suffering from 21-hydroxylase deficient late-onset adrenal hyperplasia. Forty-one healthy premenopausal eumenorrheic women served as controls.

MAIN OUTCOME MEASURES

Only two unrelated women (0.8%) had a poststimulation or net increment S level value greater than or equal to threefold the upper 95th percentile of controls and were presumed to suffer from 11 beta-hydroxylase deficient late-onset adrenal hyperplasia. One hundred nine (42%) of hyperandrogenic women had at least one S value above the 95th percentile of controls. These women also demonstrated higher basal (F0) and stimulated cortisol levels, but a similar increment compared with controls.

RESULTS

Patients with high S measures had higher testosterone, dehydroepiandrosterone sulfate, and androstenedione levels, but similar luteinizing hormone/follicle-stimulating hormone ratios, than hyperandrogenic cohorts with no abnormal S measures. Basal values of S (S0), F0, or S0/F0 were not useful to predict an abnormal S response to stimulation.

CONCLUSIONS

Although adrenocortical hyperactivity was present in 42% of our hyperandrogenic patients, only 0.8% were presumed to suffer from 11 beta-hydroxylase deficient late-onset adrenal hyperplasia. A systemic search for this deficiency in hyperandrogenism is probably unwarranted.

Authors+Show Affiliations

Department of Obstetrics and Gynecology, University of Alabama, Birmingham 35294.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

2009997

Citation

Azziz, R, et al. "11 Beta-hydroxylase Deficiency in Hyperandrogenism." Fertility and Sterility, vol. 55, no. 4, 1991, pp. 733-41.
Azziz R, Boots LR, Parker CR, et al. 11 beta-hydroxylase deficiency in hyperandrogenism. Fertil Steril. 1991;55(4):733-41.
Azziz, R., Boots, L. R., Parker, C. R., Bradley, E., & Zacur, H. A. (1991). 11 beta-hydroxylase deficiency in hyperandrogenism. Fertility and Sterility, 55(4), 733-41.
Azziz R, et al. 11 Beta-hydroxylase Deficiency in Hyperandrogenism. Fertil Steril. 1991;55(4):733-41. PubMed PMID: 2009997.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 11 beta-hydroxylase deficiency in hyperandrogenism. AU - Azziz,R, AU - Boots,L R, AU - Parker,C R,Jr AU - Bradley,E,Jr AU - Zacur,H A, PY - 1991/4/1/pubmed PY - 2001/3/28/medline PY - 1991/4/1/entrez SP - 733 EP - 41 JF - Fertility and sterility JO - Fertil Steril VL - 55 IS - 4 N2 - OBJECTIVE: to determine the 11-deoxycortisol (S) response and incidence of 11 beta-hydroxylase deficiency in hyperandrogenism. DESIGN: Hyperandrogenic women prospectively and consecutively underwent acute adrenal stimulation studies. SETTING: Tertiary institution. PATIENTS: Two hundred sixty women complaining of hirsutism and/or hyperandrogenic oligomenorrhea were studied, excluding five unrelated families (1.9% of total) suffering from 21-hydroxylase deficient late-onset adrenal hyperplasia. Forty-one healthy premenopausal eumenorrheic women served as controls. MAIN OUTCOME MEASURES: Only two unrelated women (0.8%) had a poststimulation or net increment S level value greater than or equal to threefold the upper 95th percentile of controls and were presumed to suffer from 11 beta-hydroxylase deficient late-onset adrenal hyperplasia. One hundred nine (42%) of hyperandrogenic women had at least one S value above the 95th percentile of controls. These women also demonstrated higher basal (F0) and stimulated cortisol levels, but a similar increment compared with controls. RESULTS: Patients with high S measures had higher testosterone, dehydroepiandrosterone sulfate, and androstenedione levels, but similar luteinizing hormone/follicle-stimulating hormone ratios, than hyperandrogenic cohorts with no abnormal S measures. Basal values of S (S0), F0, or S0/F0 were not useful to predict an abnormal S response to stimulation. CONCLUSIONS: Although adrenocortical hyperactivity was present in 42% of our hyperandrogenic patients, only 0.8% were presumed to suffer from 11 beta-hydroxylase deficient late-onset adrenal hyperplasia. A systemic search for this deficiency in hyperandrogenism is probably unwarranted. SN - 0015-0282 UR - https://www.unboundmedicine.com/medline/citation/2009997/11_beta_hydroxylase_deficiency_in_hyperandrogenism_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0015-0282(16)54239-3 DB - PRIME DP - Unbound Medicine ER -