Comparison of luteinizing hormone pulsatility in the serum of women suffering from polycystic ovarian disease using a bioassay and five different immunoassays.
Bioassays and immunoassays of protein hormones often read different parts of the molecule and give conflicting results. Therefore, we studied the LH bioactivity (bLH; mouse Leydig cell testosterone production assay) and immunoreactive LH (irLH) using five immunoassays [one conventional polyclonal RIA and four immunometric sandwich assays using monoclonal antibodies (mAB)] in five women suffering from polycystic ovarian disease (PCOD). Blood samples were taken from these patients at 10-min intervals for 24 h. Data were analyzed by the PC Pulsar pulse detection program. As described by others, bLH is increased in PCOD patients, and LH pulse frequency is largely accelerated (18-28 pulses/24 h). Almost every LH pulse was detected by the polyclonal RIA, whereas all mAB immunoassays detected significantly fewer pulses than the bioassay or the RIA. Occasionally, irLH pulses were detected by some assay systems when bLH activity did not increase, and there was a great difference in the temporal occurrence of bLH and irLH pulses. It is concluded that the type of immunoassay used for the detection of LH levels is also of importance for the number of detected LH pulses. Furthermore, each mAB immunoassay appears to detect different epitopes on the LH molecule, such that different conformational and/or glycosilated states are identified. Often, irLH pulses occur with no concurrent bLH pulses, which may indicate that the pituitary in PCOD patients releases pulses of biologically inactive LH in response to hypothalamic GnRH release. Hence, the pituitary gonadotrophs must be in some degree of synchrony in producing such biologically inactive material.[1]References
- Comparison of luteinizing hormone pulsatility in the serum of women suffering from polycystic ovarian disease using a bioassay and five different immunoassays. Imse, V., Holzapfel, G., Hinney, B., Kuhn, W., Wuttke, W. J. Clin. Endocrinol. Metab. (1992) [Pubmed]
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