Endocrine Abstracts

PCOS is the most common hyperandrogenic disorder, with a high prevalence of metabolic comorbidities, including obesity and central fat distribution, insulin resistance and the metabolic syndrome. With this background, it should be accepted that androgen excess must be present in all women with PCOS. Thanks to the advance in measuring blood androgen levels by LC-MS/MS, it has become clear that almost all typical cases of PCOS have a variable pattern of androgen excess. An androgen profile including all major androgens should therefore be used for research purposes and clinical practice. The phenotype characterized by menses abnormalities and polycystic ovarian morphology but without androgen excess should be regarded as a separate entity. The presence of a dysmetabolic profile should also be used in the characterization of PCOS, specifically insulin resistance, which is commonly present in obese PCOS women but can also be detected in their normal-weight counterpart. In fact, there is evidence that androgen excess may play a crucial role in disrupting the metabolic pathway, in favouring aberrant visceral fat morphology and function, in favouring the development of insulin resistance and in increasing the susceptibility to develop glucose intolerance states and type 2 diabetes. Hirsutism is common in PCOS, however its correlation with blood androgen levels is weak or absent. Apart from the opportunity to use more objective methodologies to define it, much more research is needed on the potential role of cutaneous androgens. Finally, due to the relevant impact of obesity on PCOS and the fact that in many developed countries most PCOS women are obese, it can be suggested that a secondary form of PCOS related to obesity may exist. The concept of secondary PCOS can be extended to other pathological entities, particularly to the severe insulin resistant states, but also to other endocrinopathies and, finally, to specific drugs (particularly antiepileptics). As with other endocrine syndromes, we should therefore consider that PCOS, precisely because it is a ‘syndrome’, may include many different phenotypes, ranging from the classic to milder forms, and that a secondary PCOS may occur. Additional mild phenotypes without well defined androgen excess may have different pathophysiological mechanisms.