THE CORPUS-LUTEUM INSUFFICIENCY - A MULTIFACTORIAL DISEASE

The pulsatile release pattern of LH during the entire menstrual cycle is well defined; however, the response of corpora lutea to these LH pu lses in patients suffering from corpus luteum insufficiencies (GLI) is largely unknown. Patients suffering from CLI were selected from infer tile patients on the basis of low progesterone (P < 25 nmol/L) in a bl ood sample withdrawn during a monitoring cycle. During the next cycle, nine blood samples were collected during the follicular and luteal ph ase and follicular development was assessed by vaginal sonography. Of 109 patients who had a CLI in the monitoring cycle, 55 had a CLI again , and 38 women agreed to undergo assessment of pulsatile hormone secre tion. These women again had P < 25 nmol/L at days 6 and 7 of the lutea l phase and blood samples were withdrawn through antecubital vein cath eters from 0900-1700 h at 10-min intervals on days 7, 8, or 9 followin g ovulation. From 38 patients with such defined CLI, 16 (42%) had no L H episode and significantly lower basal LH levels in comparison with 1 4 control subjects. Thirteen (34%) of the patients had normal appearin g LH episodes despite too low P and E(2) concentrations, but their CL did not react to the LH episodes. The remaining 9 patients (24%) had n ormal LH episodes; their CL reacted to these episodes, but their basal P levels were too low. In all blood samples LH was not only determine d using an immunoassay but also by the mouse Leydig cell testosterone production bioassay. It could be established that no CLI exists, which is due to the release of bioinactive LH. It is anticipated that the d ifferentiation of three different types of CLI, one of hypothalamic an d two of ovarian origin, may allow the development of differential dia gnostic and therapeutic tools in the future.