The purpose of this study was to re‐evaluate the quantitative and qualitative responses of LH to exogenous and endogenous GnRH stimulation in normally cycling women and in polycystic ovarian disease (PCOD). Responses of serum LH to GnRH (100g i.v.) and the opioid antagonist naloxone (10 mg i.v.) were determined in healthy women in the early ( n = 5) and late ( n = 4) follicular phase, and in patients with PCOD ( n = 20). Serum bioactive (B) LH was determined by a mouse interstitial cell in vitro bioassay, and immunoreactive LH by a conventional RIA (I‐LH) and a novel sensitive (0.05 IU/I) and specific immunofluorimetric assay (F‐LH). The B/I (2.4 ± 0.1) and B/F (2.7 ± 0.6) ratios in basal serum samples of the PCOD patients were significantly higher ( p < 0.05) than the corresponding ratios (1.6‐1.8 and 1.8‐2.0) of the control women. GnRH stimulated the secretion of I‐LH (2‐4‐fold), F‐LH and B‐LH (3‐5‐fold each) in all groups studied. There were no apparent changes of the BII and BIF ratios in normal women during early follicular phase or in patients with PCOD. However, the normal women during late follicular phase displayed a significant (pCO.05) increase in the BII ratio, albeit no change was found in the BIF ratio. During naloxone‐induced endogenous GnRH responses, the control women during late follicular phase showed a %‐fold increase in B‐LH, I‐LH and F‐LH, with unchanged B/I and B/F ratios. No LH responses to naloxone were found in normal women during early follicular phase or in patients with PCOD. We conclude that, hy utilizing an immunofluorimetric assay, the basally elevated biohmmuno ratio of LH could be confirmed in PCOD patients. However, there were no qualitative changes in LH during the response to GnRH stimulation in normal women or in PCOD.
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Ding et al. (1991) studied this question.
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