Adrenal Involvement in Polycystic Ovary Syndrome

Abstract

The etiology of hyperandrogenic chronic anovulation is heterogeneous and relatively unknown in the majority of cases. Affected individuals in this latter segment are considered to have polycystic ovary syndrome (PCOS) of which 50 to 60% exhibit androgen excess of adrenal origin. An understanding of normal adrenal function provides insight into the factors that contribute to adrenal androgen excess in PCOS. Since pituitary ACTH secretion promotes developmental growth and overall steroidogenic efficiency within the adrenal cortex, it is probable that these actions of ACTH along with the adrenal's unique centripetal circulation play a major role in the induction of adrenarche. This latter phenomenon is characterized by alterations in adrenocortical morphology and steroidogenic enzyme activities culminating in increases in adrenal androgens to normal circulating adult levels. Thus, it is not surprising that adrenal dynamic testing has revealed increased 17,20 lyase activity or adrenal androgen hyper-responsiveness to ACTH as the two abnormalities leading to adrenal androgen excess in PCOS. Whereas 17,20 lyase hyperactivity diagnosed by defined criteria in response to pharmacological ACTH may be an intrinsic genetic defect, increases in 17,20 lyase activity and adrenal androgen hyper-responsiveness to ACTH in response to physiological ACTH may be promoted by the functional elevation of estrogen of ovarian origin in PCOS. The latest in vitro data suggest the estrogen may elicit its effect on the adrenal cortex through a receptor mediated mechanism. Therefore, the currently available data indicate that adrenal androgen excess in PCOS is also heterogeneous in etiology.

Effect of pioglitazone treatment on the adrenal androgen response to corticotrophin in obese patients with polycystic ovary syndrome

“…Similarly, a continuation of exaggerated adrenarche suggests a chronic adrenal hyperfunction in these women (Lucky et al, 1986). Furthermore, most authors agree on the presence of an adrenal androgen hyper-responsiveness to ACTH in at least a proportion of the PCOS population (Lanzone et al, 1992;Gonzalez, 1997;Azziz et al, 1998).…”

Hyperandrogenism and Its Possible Effects on Endometrial Receptivity: A Review

“…About 50% of women with PCOS have elevated circulating levels of dehydroepiandrosterone sulphate (DHEAS) and 11β-hydroxyandrostenedione, two androgens secreted almost exclusively by the zona reticularis of the adrenal glands [28,29]. The ele-vated DHEAS levels in women with PCOS are likely due to the cumulative effect of several factors, including increased circulating unbound oestradiol levels and altered cortisol metabolism [30,31]. Indeed, decreased peripheral cortisol has been observed in PCOS, due to increased inactivation of this steroid by 5-alpha-reductase or impaired reactivation of cortisol from cortisone by 11beta-hydroxysteroid dehydrogenase type 1 [32,33].…”

A review of the hormones involved in the endocrine dysfunctions of polycystic ovary syndrome and their interactions

“…Since DHEA-S is almost solely produced by the adrenal cortices, increased DHEA-S is often used as an indicator for overactive adrenal cortex production of androgens. Approximately 50-60% of women with PCOS exhibit adrenal originating androgen excess by increased DHEA-S ( 88 ). Currently, it is thought the ovary has a limited to negligible effect on the adrenocortical function ( 89 ).…”