The control of bioactive luteinizing hormone secretion in women with polycystic ovary syndrome.

Serum bioactive luteinizing hormone (LH) is elevated in virtually all patients with polycystic ovary syndrome, whereas serum immunoreactive LH may not be increased. The resultant increase in the bioactive: immunoreactive LH ratio in polycystic ovary syndrome leads to the suggestion that a more biologically active form of LH may be secreted in patients with polycystic ovary syndrome. This study was designed to investigate the control of bioactive LH in polycystic ovary syndrome. Compared to matched control subjects, seven patients with polycystic ovary syndrome had higher levels of serum immunoreactive LH (24 +/- 3 mlU/ml), immunoreactive LH: follicle-stimulating hormone (FSH) ratios (4.6 +/- 0.6), bioactive LH (98 +/- 27 mlU/ml), and bioactive: immunoreactive LH ratios (4.6 +/- 0.5). Serum testosterone (64 +/- 10 ng/ml), unbound testosterone (16 +/- 3 mg/dl), and unbound estradiol (49 +/- 5 pg/ml) were also higher. In response to 150 micrograms of intravenous gonadotropin-releasing hormone, increments of both bioactive LH and immunoreactive LH were higher than those in control subjects, but the bioactive: immunoreactive LH ratio was unaltered. Although urinary homovanillic acid was lower in polycystic ovary syndrome, it did not correlate with the bioactive: immunoreactive LH ratio. Similarly, the bioactive: immunoreactive LH ratio was not altered by 1 week of L-dopa (500 mg) or after another week of L-dopa (400 mg) with carbidopa (100 mg) 1 month later. Although baseline unbound estradiol correlated with the delta maximum response of bioactive LH after gonadotropin-releasing hormone (r = 0.65, p less than 0.05), unbound estradiol did not correlate with the bioactive: immunoreactive LH ratio. However, there was a significant positive correlation between the baseline bioactive: immunoreactive LH and the increased delta maximum responses of both immunoreactive LH (r = 0.55) and bioactive LH (r = 0.58), p less than 0.05. These data suggest that, although gonadotropin-releasing hormone stimulation, dopamine, and estrogen may not selectively increase the pituitary secretion of bioactive LH, the sensitivity of the pituitary gland itself and the hyperdynamic state of gonadotropin secretion in polycystic ovary syndrome may result in the increased secretion of bioactive LH.