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This work was supported by Grants PI1501686, PIE1600050, and PI1801122 from Instituto de Salud Carlos III, Spanish Ministry of Economy and Competitiveness, and co-financed by the European Development Regional Fund “A way to achieve Europe” (EDRF). CIBERDEM and IRYCIS are also initiatives of from Instituto de Salud Carlos III.
The author declares no competing interests.
Polycystic ovary syndrome (PCOS) is nothing more, but also nothing less, than a very common female phenotype consisting of a combination of signs and symptoms of androgen excess (hirsutism and/or hyperandrogenemia) and ovarian dysfunction [oligo-ovulation and/or polycystic ovarian morphology (PCOM)], provided that other specific diagnoses such as hyperprolactinemia and nonclassic congenital adrenal hyperplasia have been excluded . The prevalence of PCOS in premenopausal women ranges from ~ 6% (using the older more restrictive criteria) to ~ 20% (when applying current more inclusive definitions) , possibly making this syndrome the most common endocrine and metabolic disorder in women of reproductive age .
Even though PCOS is quite homogeneous in a few characteristics such as its peripubertal onset and similar worldwide prevalence , the PCOS phenotype may result from different combinations of pathophysiological mechanisms making heterogeneity intrinsic to the syndrome . I will here provide hypotheses to explain how the pathophysiological heterogeneity of PCOS is translated into most aspects of the disorder, from clinical presentation to management, but very particularly to its definition.
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