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Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups.
Fertil Steril. 2005 Jun; 83(6):1717-23.FS

Abstract

OBJECTIVE

We tested the hypothesis that the three clinical phenotypes of polycystic ovary syndrome (PCOS) represent forms of the same metabolic disorder.

DESIGN

Prospective cohort analysis.

SETTING

University-based tertiary care.

PATIENT(S)

Three-hundred sixteen untreated consecutive women diagnosed as having PCOS.

INTERVENTION(S)

None.

MAIN OUTCOME MEASURE(S)

Each subject underwent an evaluation of ovulatory function, body habitus, acne, and hirsutism; serum free and total testosterone (T), 17-hydroxyprogesterone (17-HP), and DHEAS; and fasting plasma glucose and insulin levels. Insulin resistance and beta-cell function were assessed using the homeostatic assessment model equation (HOMA-IR and HOMA-beta-cell, respectively).

RESULT(S)

The Oligo+HA+Hirsutism phenotype was present in 48% of subjects, Oligo+HA in 29%, and Oligo+Hirsutism in 23%. The three phenotypes did not differ in mean body mass index, waist-to-hip ratio, racial composition, degree of oligo-ovulation, prevalence of acne, or family history of hyperandrogenic symptomatology. However, subjects demonstrating the Oligo+HA+Hirsutism phenotype were the youngest and had the greatest degrees of hyperandrogenemia, hyperinsulinemia, and beta-cell function; patients with the Oligo+Hirsutism phenotype where the oldest and had the mildest degrees of hyperandrogenemia, hyperinsulinemia, and beta-cell function. Subjects with the Oligo+HA phenotype demonstrated intermediate degrees of hyperandrogenemia and metabolic dysfunction.

CONCLUSION(S)

We conclude that the three clinical phenotypes of PCOS do not represent forms of the same metabolic disorder and may be the result of varying degrees of metabolic dysfunction; greater degrees of beta-cell function and circulating insulin levels favored the development of hirsutism and frank hyperandrogenemia.

Links

Publisher Full Text

Authors+Show Affiliations

Chang WY
Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles, California, USA.
Knochenhauer ES
No affiliation info available
Bartolucci AA
No affiliation info available
Azziz R
No affiliation info available

MeSH

AdultAnalysis of VarianceBody Mass IndexChi-Square DistributionFemaleHirsutismHumansPhenotypePolycystic Ovary SyndromeProspective Studies

Pub Type(s)

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

Language

eng

PubMed ID

15950641

Clinical Trial Links

Study of Testosterone and Athlete Response

Citation

Chang, Wendy Y., et al. "Phenotypic Spectrum of Polycystic Ovary Syndrome: Clinical and Biochemical Characterization of the Three Major Clinical Subgroups." Fertility and Sterility, vol. 83, no. 6, 2005, pp. 1717-23.
Chang WY, Knochenhauer ES, Bartolucci AA, et al. Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups. Fertil Steril. 2005;83(6):1717-23.
Chang, W. Y., Knochenhauer, E. S., Bartolucci, A. A., & Azziz, R. (2005). Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups. Fertility and Sterility, 83(6), 1717-23.
Chang WY, et al. Phenotypic Spectrum of Polycystic Ovary Syndrome: Clinical and Biochemical Characterization of the Three Major Clinical Subgroups. Fertil Steril. 2005;83(6):1717-23. PubMed PMID: 15950641.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups. AU - Chang,Wendy Y, AU - Knochenhauer,Eric S, AU - Bartolucci,Alfred A, AU - Azziz,Ricardo, PY - 2004/05/19/received PY - 2005/01/28/revised PY - 2005/01/28/accepted PY - 2005/6/14/pubmed PY - 2006/1/4/medline PY - 2005/6/14/entrez SP - 1717 EP - 23 JF - Fertility and sterility JO - Fertil Steril VL - 83 IS - 6 N2 - OBJECTIVE: We tested the hypothesis that the three clinical phenotypes of polycystic ovary syndrome (PCOS) represent forms of the same metabolic disorder. DESIGN: Prospective cohort analysis. SETTING: University-based tertiary care. PATIENT(S): Three-hundred sixteen untreated consecutive women diagnosed as having PCOS. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Each subject underwent an evaluation of ovulatory function, body habitus, acne, and hirsutism; serum free and total testosterone (T), 17-hydroxyprogesterone (17-HP), and DHEAS; and fasting plasma glucose and insulin levels. Insulin resistance and beta-cell function were assessed using the homeostatic assessment model equation (HOMA-IR and HOMA-beta-cell, respectively). RESULT(S): The Oligo+HA+Hirsutism phenotype was present in 48% of subjects, Oligo+HA in 29%, and Oligo+Hirsutism in 23%. The three phenotypes did not differ in mean body mass index, waist-to-hip ratio, racial composition, degree of oligo-ovulation, prevalence of acne, or family history of hyperandrogenic symptomatology. However, subjects demonstrating the Oligo+HA+Hirsutism phenotype were the youngest and had the greatest degrees of hyperandrogenemia, hyperinsulinemia, and beta-cell function; patients with the Oligo+Hirsutism phenotype where the oldest and had the mildest degrees of hyperandrogenemia, hyperinsulinemia, and beta-cell function. Subjects with the Oligo+HA phenotype demonstrated intermediate degrees of hyperandrogenemia and metabolic dysfunction. CONCLUSION(S): We conclude that the three clinical phenotypes of PCOS do not represent forms of the same metabolic disorder and may be the result of varying degrees of metabolic dysfunction; greater degrees of beta-cell function and circulating insulin levels favored the development of hirsutism and frank hyperandrogenemia. SN - 1556-5653 UR - https://www.unboundmedicine.com/medline/citation/15950641/Phenotypic_spectrum_of_polycystic_ovary_syndrome:_clinical_and_biochemical_characterization_of_the_three_major_clinical_subgroups_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0015-0282(05)00405-X DB - PRIME DP - Unbound Medicine ER -