4.7 Article

Clinical and endocrine characteristics of the main polycystic ovary syndrome phenotypes

Journal

FERTILITY AND STERILITY
Volume 94, Issue 6, Pages 2197-2201

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.fertnstert.2010.02.014

Keywords

PCOS; hyperandrogenism; anovulation

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Objective: To evaluate the clinical and endocrine differences between main polycystic ovary syndrome (PCOS) phenotypes. Design: To evaluate clinical and hormone parameters in a large group of consecutive women with PCOS diagnosed according Rotterdam criteria and divided according their phenotype. Setting: University department of medicine. Patient(s): Three hundred eighty-two consecutive women with PCOS and 85 ovulatory controls. Intervention(s): Evaluation of clinical and hormone parameters. Main Outcome Measure(s): Blood levels of gonadotropins, testosterone, sex-hormone-binding globulin, dehydroepiandrosterone sulfate, 17 alpha-hydroxyprogesterone, progesterone, glucose, and insulin, and calculation of the free androgen index and insulin sensitivity. Result(s): The severe PCOS phenotype (hyperandrogenism, chronic anovulation, and polycystic ovaries: type I classic PCOS) was the most common phenotype in 53.9% of the patients. The phenotype of 8.9% of patients was characterized by hyperandrogenism and chronic anovulation but normal ovaries (type II classic PCOS). The two phenotypes of classic PCOS had similar clinical and endocrine characteristics, but the patients with polycystic ovaries had a higher luteinizing hormone/follicle-stimulating hormone (LH/FSH) ratio. Ovulatory PCOS was relatively common (28.8% of PCOS patients) and presented milder clinical and endocrine alterations than the classic PCOS phenotypes. The normoandrogenic phenotype was relatively uncommon. These patients had a normal body mass index, insulin sensitivity, and free androgen index but showed increased levels of LH and LH/FSH ratio. Conclusion(s): Ovulatory PCOS represents the mild form of classic PCOS, but the normoandrogenic phenotype, although part of the spectrum, may represent a different disorder or have a different pathogenetic pathway. (Fertil Steril (R) 2010; 94: 2197-201. (C) 2010 by American Society for Reproductive Medicine.)

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