Background: The prevalence of adrenal hyperandrogenism (AH), as defined by
increased circulating dehydroepiandrosterone-sulfate (DHEAS) levels, ranges from 15 to
45% in women with polycystic ovary syndrome (PCOS).
Methods: The aim of this review is to update the pathogenesis and consequences of AH in
PCOS, from molecular genetics to the clinical setting.
Results: Mounting evidence derived from animal models suggests that genetically or enviromentally
determined prenatal androgen excess, by influencing the hormonal and metabolic
phenotype of susceptible female fetuses later in life, may be the capital event for the development
of AH in PCOS. Because human placental aromatase activity is likely to prevent any
deleterious effect of maternal hyperandrogenemia on the fetus, inheritance of the maternal
steroidogenic defect is the more likely culprit, even though other factors such as changes in
placental steroidogenesis itself or its nutritional efflux may also be involved in the building a
deregulated enzymatic pathway from utero to adult life. Anyhow, the most important issue is whether or not AH
influences the cardiometabolic risk of women with PCOS. On the one hand, AH has shown a controversial relationship
with carbohydrate metabolism and adiposity, and is also associated with abnormalities in blood pressure
regulation in these patients. On the other hand, DHEAS may exert a beneficial effect on the lipid profile of both
lean and obese patients. Lastly, available studies in women with PCOS cast doubt upon a protective role of
DHEAS levels on subclinical atherosclerosis, despite opposite data from the general population.
Conclusion: AH is frequent in patients with PCOS yet unraveling its consequences for the management of this
disorder requires future longitudinal studies.