Soules M R, Bremner W J, Dahl K D, Rivier J E, Vale W W, Clifton D K
Department of Obstetrics and Gynecology, University of Washington, Seattle 98195.
Am J Obstet Gynecol. 1991 Apr;164(4):989-94; discussion 994-6. doi: 10.1016/0002-9378(91)90571-8.
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 less than 100 ng/ml per day. Luteinizing hormone secretion patterns were determined by frequent blood sampling performed every 10 minutes for 12 hours in the early follicular phase of the control cycle and the cycle after antagonist administration. Daily luteal progesterone levels were measured in the control, treatment, and posttreatment cycles. Each volunteer served as her own control. Standard parameters were compared between the control and posttreatment pulse studies in the early follicular phase: (1) luteinizing hormone pulse frequency was 9.5 +/- 1.0 vs 10.0 +/- 0.9 pulses/12 hours, control vs posttreatment, respectively, 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.(ABSTRACT TRUNCATED AT 400 WORDS)
黄体期缺陷的女性在月经周期的卵泡早期促黄体生成素脉冲频率增加。由于已知孕酮可调节促黄体生成素的分泌,因此有人推测,在前一个黄体期缺陷周期中孕酮分泌减少可能导致随后卵泡早期促黄体生成素分泌模式异常。鉴于较高的促黄体生成素脉冲频率可能导致另一个黄体期缺陷,黄体期缺陷可能会自我延续。为了验证这一假设,在六个正常女性中诱导黄体期缺陷,方法是从对照周期后的黄体中期开始,每天两次给予促性腺激素释放激素拮抗剂Nal-Glu,以减少黄体对促黄体生成素的支持。在拮抗剂治疗的黄体期,每个受试者都符合诱导黄体期缺陷的预定标准:与对照周期相比,孕酮积分下降33%或更多,且孕酮积分水平低于每天100 ng/ml。在对照周期和拮抗剂给药后的周期的卵泡早期,通过每10分钟频繁采血12小时来测定促黄体生成素的分泌模式。在对照、治疗和治疗后周期中测量每日黄体孕酮水平。每个志愿者都作为自己的对照。比较对照周期和治疗后卵泡早期脉冲研究的标准参数:(1)促黄体生成素脉冲频率分别为9.5±1.0次/12小时和10.0±0.9次/12小时,对照与治疗后相比,p = 0.5;(2)促黄体生成素脉冲幅度为11.0±1.3 ng/ml和12.0±2.2 ng/ml,p = 0.6;(3)促黄体生成素平均水平为19.4±2.3 ng/ml和22.2±3.3 ng/ml,p = 0.1。还比较了对照周期和治疗后周期的黄体功能。黄体期长度分别为13.7±0.6天和12.7±0.6天,p = 0.08。孕酮积分值分别为每天136.9±12.9 ng/ml和130.5±11.3 ng/ml,p = 0.5。因此,在诱导黄体期缺陷周期后,卵泡早期促黄体生成素分泌或黄体孕酮分泌没有明显异常。(摘要截断于400字)