Relationship of GnRH‐stimulated LH release to episodic LH secretion and baseline endocrine‐metabolic measures in women with polycystic ovary syndrome

Summary background and objective  In polycystic ovary syndrome (PCOS) inappropriate gonadotrophin secretion is characterized by increased pulse frequency and amplitude, elevated 24-h mean serum concentrations, and greater responses to GnRH. While the mechanism(s) responsible for this increased release of LH are not well understood, enhanced LH secretion has been attributed to increased pituitary sensitivity to GnRH and feedback influences from circulating steroid hormones. To address these considerations, we conducted a study to examine the relationships between GnRH-stimulated LH responses, episodic gonadotrophin secretion, and baseline measurements of endocrine-metabolic function in PCOS. patients  Serum LH responses to sequential multidose GnRH administration and pulsatile gonadotrophin secretion were examined in 13 PCOS and 13 normal women. measurements  Serum LH, steroid hormone, insulin and glucose levels were determined in blood samples obtained during assessment of episodic gonadotrophin secretion and LH responses to GnRH stimulation. design  Each subject was studied on two consecutive days. On study day 1 each subject underwent frequent blood sampling every 10 min for 12 h. On study day 2 each received sequential doses of GnRH, 2 µg, 10 µg and 20 µg, administered intravenously at 4-h intervals over a continuous 12-h period. results  Serum LH responses following GnRH were markedly greater in PCOS compared to normal women, as expected. In individual PCOS, peak LH responses to GnRH were significantly correlated with corresponding basal LH and LH pulse amplitude, but not LH pulse frequency. In the PCOS group, LH responses were positively correlated with serum oestradiol (E2) and inversely related to body mass index (BMI). Between-group differences in LH responsiveness disappeared when controlling for serum testosterone (T) levels. conclusions  These results indicate that the absolute LH increment following GnRH is largely dependent on baseline LH levels and may account for the well-documented difference in LH responsiveness between PCOS and normal women. That neither LH responses to GnRH nor LH pulse amplitude were correlated to LH pulse frequency suggests involvement of other factors along with GnRH to account for increased LH secretion in PCOS. In addition to E2 and BMI, serum testosterone appears to be, at least in part, responsible for differences in LH secretion and release between PCOS and normal women.