The induction of premature luteolysis in normal women—follicular phase luteinizing hormone secretion and corpus luteum function in the subsequent cycle***

Women with luteal phase deficiency have been shown to have an increased frequency of luteinizing hormone pulses in the early follicular phase of the menstrual cycle. Because progesterone is known to modulate luteinizing hormone secretion, it has been hypothesized that the decreased progesterone secretion in a previous luteal phase deficiency cycle could lead to the abnormal luteinizing hormone secretory pattern in the ensuing early follicular phase. With the possibility that the higher luteinizing hormone pulse frequency might lead to another deficient luteal phase, it becomes conceivable that luteal phase deficiency could be self-perpetuating. To test this hypothesis, luteal phase deficiency was induced in six normal women by decreasing luteinizing hormone support of the corpus luteum with a gonadotropin-releasing hormone antagonist Nal-Glu, administered twice daily beginning in the midluteal phase after a control cycle. During the antagonist-treated luteal phase, each subject met the predetermined criteria for induced luteal phase deficiency: a 33% or greater decrease in integrated progesterone from the control cycle and an integrated progesterone level p = 0.5; (2) luteinizing hormone pulse amplitude was 11.0 ± 1.3 vs 12.0 ± 2.2 ng/ml, p = 0.6; and (3) luteinizing hormone mean level was 19.4 ± 2.3 vs 22.2 ± 3.3 ng/ml, p = 0.1. Corpus luteum function was also compared between the control and posttreatment cycles. Luteal phase length was 13.7 ± 0.6 vs 12.7 ± 0.6 days, p = 0.08. Integrated progesterone values were 136.9 ± 12.9 vs 130.5 ± 11.3 ng/ml per day, p = 0.5. Therefore no discernible abnormalities in early follicular luteinizing hormone secretions or corpus luteum secretion of progesterone occurred after an induced luteal phase deficiency cycle. We conclude that luteal phase deficiency is not self-perpetuating and that the rapid luteinizing hormone secretion pattern found in the early follicular phase in women with luteal phase deficiency is not a result of decreased progesterone levels in the preceding luteal phase, but rather appears to be a result of dysfunctional suprahypothalamic neuroendocrine modulation of the gonadotropin-releasing hormone pulse generator.