Circulating Levels of Plasma Adrenocorticotropin in Polycystic Ovary Disease

In polycystic ovarian disease (PCO), excessive andro-gen production arises from both the adrenal glands and the ovaries. The mechanism responsible for increased adrenal androgen production is not clear. Several lines of evidence indicate that ACTH is a major, though not necessarily exclusive, modulator of such production. The purpose of this study was to determine the concentration of plasma ACTH in PCO patients and to correlate its level with that of circulating adrenal androgens.Twenty-nine patients with the clinical diagnosis of PCO based on the presence of hirsutism and oligomenorrhea were studied. Twenty-four normal cycling women without evidence of endocrine disease, and not receiving any medication, served as controls.In PCO patients, the serum LH concentration (1 5.0 + 1.5 mlU/ml) was significantly greater, and the FSH level (8.8 ± 0.4 mlU/ml) was slightly less than those found in normal subjects studied throughout the menstrual cycle (9.9 ± 1.3 and 9.8 ± 0.7 mlU/ml, respectively). Significant increases in testosterone (407 ± 27 pg/ml), androstenedione (2083 ± 119 pg/ml), and dehydroepiandrosterone sulfate (2.9 ± 0.3 μg/ml) were observed in PCO patients, as compared to normal values (268 ± 21 pg/ml, 1189 ± 93 pg/ml, and 2.0 ± 0.2 μg/ ml, respectively). Basal circulating concentrations of dehydroepiandrosterone did not differ statistically between groups. Measurements of 17-hydroxyprogesterone and 1 7-hydroxypregnenolone were less than 1.0 and 2.5 ng/ ml, respectively, in PCO patients and not different from those in normal control subjects during the early follicular phase of the menstrual cycle.In the measurement of individual and mean (± SE) plasma ACTH and serum cortisol levels in PCO patients and normal subjects, the minimal detectable concentration of ACTH was 10 pg/ml. The results in the controls were consistent with previous values established for normal women. In PCO patients, the distribution of ACTH levels was similar to that observed in the normal group. Accordingly, the mean basal ACTH concentration in PCO patients (22 ± 2 pg/ml) was not different from that in normal controls (20 ± 2 pg/ml). Mean serum cortisol levels also were not different between groups. Individual ACTH concentrations did not correlate with respective cortisol or androgen levels. The mean ratio of circulating dehydroepiandrosterone sulfate to ACTH in individual PCO patients (0.17 ± 0.01) was significantly greater than that observed in normal subjects (0.13 ± 0.02). By