Hayashi M, Suginami H, Taii S, Mori T
Department of Obstetrics and Gynecology, Tenri Hospital, Japan.
Endocr J. 1993 Jun;40(3):297-309. doi: 10.1507/endocrj.40.297.
To investigate endocrine pathophysiology of luteal phase deficiency (LPD), GnRH/TRH stimulation tests were performed in the early follicular (EFP) and midluteal phases (MLP) of the menstrual cycle in 52 infertile women with a history of short luteal phase, in whom pituitary responsiveness to GnRH/TRH and steroidogenic competency of the corpus luteum were analyzed. Twelve women with either elevated basal-LH or exaggerated PRL response to GnRH/TRH in EFP were eliminated, and the remaining 40 women were studied. Basal-FSH in EFP inversely correlated with steroidogenic parameters in MLP, indicating that compromised folliculogenesis causes LPD. In a fraction of LPD women, decreased basal-LH in MLP was associated with decreased basal-progesterone (p), in spite of normal steroidogenic potential of the corpus luteum, suggesting that aberrant LH secretion is another progenitor of LPD. The other group of LPD women showed shortening of high phase period and/or extravagant discrepancy in endometrial dating without apparent abnormal endocrine parameters, suggesting that unknown factors are involved in establishment of LPD. From the diagnostic point of view, they were discriminated into three groups, normal, incomplete LPD and complete LPD groups, with a modified classification of LPD; 1) shortening of high phase period < 11 days, 2) delay in histological to chronological dating of the endometrium > 2 days, and 3) decreased max-P in MLP < 10 ng/ml. Normal (n = 14) and complete LPD (n = 7) groups consisted of women having all the criteria of classification within and out of the cut-off values, respectively. The remainders were enrolled into incomplete LPD group (n = 19). Complete LPD group mainly consisted of women having compromised folliculogenesis as a cause of LPD. In contrast, incomplete LPD group appeared a mixture of heterogeneous populations as to the genesis of LPD. GnRH/TSH stimulation test, especially when performed in MLP, would unveil endocrine pathophysiology of LPD and provide an accurate standard for diagnosis of LPD.
为研究黄体期缺陷(LPD)的内分泌病理生理学,对52例有黄体期短病史的不孕妇女在月经周期的卵泡早期(EFP)和黄体中期(MLP)进行了GnRH/TRH刺激试验,分析了垂体对GnRH/TRH的反应性和黄体的类固醇生成能力。12例在EFP时基础LH升高或对GnRH/TRH的PRL反应过度的妇女被排除,对其余40例妇女进行了研究。EFP时的基础FSH与MLP时的类固醇生成参数呈负相关,表明卵泡生成受损导致LPD。在一部分LPD妇女中,尽管黄体的类固醇生成潜力正常,但MLP时基础LH降低与基础孕酮(p)降低有关,提示LH分泌异常是LPD的另一个起因。另一组LPD妇女表现为高相期缩短和/或子宫内膜日期测定的过度差异,而无明显的内分泌参数异常,提示未知因素参与了LPD的发生。从诊断角度来看,根据改良的LPD分类,她们被分为三组,即正常组、不完全LPD组和完全LPD组;1)高相期缩短<11天,2)子宫内膜组织学与时间测定延迟>2天,3)MLP时最大p降低<10 ng/ml。正常组(n = 14)和完全LPD组(n = 7)分别由符合分类标准全部在临界值内和外的妇女组成。其余的归入不完全LPD组(n = 19)。完全LPD组主要由卵泡生成受损导致LPD的妇女组成。相比之下,不完全LPD组在LPD的发生原因方面似乎是异质性人群的混合。GnRH/TSH刺激试验,尤其是在MLP时进行,将揭示LPD的内分泌病理生理学,并为LPD的诊断提供准确标准。