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Departments of Obstetrics and Gynecology (R.A., L.A.S., E.S.K., C.M., J.L., K.C.S., K.T., L.R.B.) and Medicine (R.A.), University of Alabama at Birmingham, Birmingham, Alabama 35233; Caracas Fertility Center (L.A.S.), Caracas, Federal District, Venezuela 1050; and the Health Research Council (C.M.), Mexican Institute of Social Security, Federal District, Mexico City, Mexico
Address all correspondence and requests for reprints to: Ricardo Azziz, M.D., M.P.H., M.B.A., Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, 8635 West Third Street, Suite 160 W, Los Angeles, California 90048. E-mail: azzizr{at}cshs.org.
The objective of the present study was to estimate the prevalence of the different pathological conditions causing clinically evident androgen excess and to document the degree of long-term success of suppressive and/or antiandrogen hormonal therapy in a large consecutive population of patients.
All patients presenting for evaluation of symptoms potentially related to androgen excess between October 1987 and June 2002 were evaluated, and the data were maintained prospectively in a computerized database. For the assessment of therapeutic response, a retrospective review of the medical chart was performed, after the exclusion of those patients seeking fertility therapy only, or with inadequate follow-up or poor compliance.
A total of 1281 consecutive patients were seen during the study period. Excluded from analysis were 408 patients in whom we were unable to evaluate hormonal status, determine ovulatory status, or find any evidence of androgen excess. In the remaining population of 873 patients, the unbiased prevalence of androgen-secreting neoplasms was 0.2%, 21-hydroxylase-deficient classic adrenal hyperplasia (CAH) was 0.6%, 21-hydroxylase-deficient nonclassic adrenal hyperplasia (NCAH) was 1.6%, hyperandrogenic insulin-resistant acanthosis nigricans (HAIRAN) syndrome was 3.1%, idiopathic hirsutism was 4.7%, and polycystic ovary syndrome (PCOS) was 82.0%. Fifty-nine (6.75%) patients had elevated androgen levels and hirsutism but normal ovulation. A total of 257 patients were included in the assessment of the response to hormonal therapy. The mean duration of follow-up was 33.5 months (range, 6155). Hirsutism improved in 86%, menstrual dysfunction in 80%, acne in 81%, and hair loss in 33% of patients. The major side effects noted were irregular vaginal bleeding (16.1%), nausea (13.0%), and headaches (12.6%); only 36.6% of patients never complained of side effects.
In this large study of consecutive patients presenting with clinically evident androgen excess, specific identifiable disorders (NCAH, CAH, HAIRAN syndrome, and androgen-secreting neoplasms) were observed in approximately 7% of subjects, whereas functional androgen excess, principally PCOS, was observed in the remainder. Hirsutism, menstrual dysfunction, or acne, but not alopecia, improved in the majority of patients treated with a combination suppressive therapy; although more than 60% experienced side effects.
This work was supported in part by National Institutes of Health Grants RO1-HD29364 and K24-D01346 (to R.A.).
Abbreviations: ASN, Androgen-secreting neoplasm; BMI, body mass index; BTB, breakthrough bleeding; CAH, classic adrenal hyperplasia; DHEAS, dehydroepiandrosterone sulfate; FAE, functional androgen excess; GLU, glucose; HA, hyperandrogenemia; HAIRAN, hyperandrogenic insulin-resistant acanthosis nigricans; HOMA, homeostatic model assessment method; HOMA-%ß-cell, percentage of ß-cell function calculated by HOMA; HOMA-IR, insulin resistance calculated by HOMA; 17-HP, 17-hydroxyprogesterone; IH, idiopathic hirsutism; INS, insulin; mF-G, modified Ferriman-Gallwey; NCAH, non-classic adrenal hyperplasia; OC, oral contraceptive; 21-OH, 21-hydroxylase; PCOS, polycystic ovary syndrome; P4, progesterone; SPA, spironolactone; T, testosterone; WHR, waist to hip ratio.
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