Functional hyperandrogenism detected by corticotropin and GnRH-analogue stimulation tests in women affected by apparently idiopathic hirsutism

Abstract

The etiologic diagnosis of hirsutism is often difficult. Previous studies have reported normal basal androgen and SHBG concentrations in 33-50% of hirsute women, suggesting the presence of an "idiopathic" form of hirsutism as the most frequent cause of this problem. The recent use of GnRH-analogues together with the corticotropin stimulation test allows better understanding of whether the cause of hirsutism is androgen excess and, if so, whether the origin of the latter is ovarian, adrenal or both. The present study evaluated adrenal and ovarian function in 48 young hirsute women as well as in 78 normal women matched for body mass index and age, who acted as control group. To determine ovarian function, a single 100-microg dose of GnRH analogue triptorelin was injected s.c.; thereafter, gonadotropins, 17-hydroxyprogesterone (17-OHP), delta4-androstenedione (delta4), total testosterone (T) and estradiol were determined. To better understand the adrenal function, 250 microg of 1,24 ACTH were administrated as i.v. infusion for 5 h, and plasma cortisol (F), 17-OHP, A4, DHEAS, T, 11-desossicortisol were measured. The combined use of these two stimulation tests was able to detect mild to moderate abnormalities in the steroidogenesis of ovaries alone (23%), adrenals alone (16.6%), or both (35.4%) in most hirsute women (75%) with otherwise normal baseline androgen concentrations. In particular, patients showed significantly increased responses of 17-OHP, delta4, total T, 11-desossicortisol, and F to 1,24-ACTH administration. Moreover, they also had significantly higher 17-OHP and T responses to triptorelin. In conclusion, milder forms of functional ovarian and/or adrenal hyperandrogenism, similar to those found in clearly hyperandrogenic women, were observed and could be an underlying mechanism of idiopathic hirsutism.

Insulin resistance in women with hirsutism

“…The pathophysiology of IH is presumed to involve a primary increase in skin 5α-reductase activity and possibly an alteration in androgen receptor function [2]. In these patients there may be present mild forms of ovarian and adrenal functional hyperandrogenism [3]. In the light of this information, we investigated whether this peripheral increased androgen activity is associated with insulin metabolism.…”

“…Idiopathic hirsutism is defined as hirsutism associated with normal ovulatory function and normal circulating serum androgen concentrations [2]. In these patients mild forms of ovarian and adrenal functional hyperandrogenism may be present [3]. Polycystic ovary syndrome (PCOS) is characterized by chronic anovulation, obesity and hyperandrogenism.…”

The Investigation of Insulin Resistance in Patients with Idiopathic Hirsutism

“…This deficiency is due to the fact that most previous studies have included patients in whom the diagnosis of IH was not strictly established. Although IH is thought to be caused by the increased sensitivity of the pilosebaceous unit to the circulating androgens, recently Rossi et al (18) evaluated the adrenal and ovarian function in 48 young hirsute women by using GnRH analog and the ACTH stimulation test. The authors demonstrated that milder forms of functional ovarian and/or adrenal hyperandrogenism, similar to those found in hyperandrogenic women, were observed and could be an underlying mechanism of IH.…”

The lack ofassociationbetween idiopathic hirsutism and metabolic disturbances: Iranian PCOS Prevalence Study

“…Increase in skin 5a-reductase activity [8], hyper-response of pilosebaceous unit to normal levels of circulating androgen [9], or genetic alteration in androgen receptor [10,11] has been postulated as the possible pathogenesis of IH; mild forms of ovarian and adrenal functional hyperandrogenism have been reported in some patients with IH [12][13][14][15].…”