b.不妊治療と黄体機能不全(2.生殖)

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This review discussed recent findings of scientific basis and treatment for defect. The primary function of the corpus luteum is secretion of progesterone, which is required for maintenance of normal pregnancy. Luteinizing hormone (LH) from the anterior pitiutary is important for normal development and function of the corpus luteum. The mature corpus luteum is composed of two steroidogenic cell types ; luteinized granulosa cell and luteinized theca cell. Angiogenesis mediated by vascular endothelial growth factor (VEGF) is an important feature of the luteinization process. Phosphorylation of steroidogenic acute regulatory protein (StAR) resulting in enhancement of cholesterol transport from the outer to the inner mitochondrial membrane appears to be a key step in LH action of progresterone synthesis. If pregnancy does not occur, the corpus luteum regresses (luteolysis). Although the role of PGF_<2α> in human remains controversial, local PGF_<2α> and endothelin-1 may be mediators of luteolysis. Down-regulation of StAR appears to be a primary site of negative regulation of progesterone synthesis by PGF_<2α>. Loss of luteal cells follows an influx of calcium, activation of endonucleases, and an apoptotic form of cell death. If pregnancy is established, continual secrtion of progesterone from the corpus luteum is required to provide an appropriate uterine environment for the maintenance of pregnancy. In the uterus, progesterone facilitates implantation and maintains pregnancy, by promoting uterine growth and suppression of myometrial contraction. In early pregnancy, human chorionic gonadotrophin (HCG) directly stimulates the corpus luteum to secrete progesterone until placental steroid production is well established. Normal luteal function requires optimal preovulatory follicular development (especially adequate FSH stimulation) and continued tonic LH support. In cases in which luteal defect is presumed to be a cause of infertility, inadequate progesterone secretion is believed to lead to poor secretory endometrial development manifest by a delay in endometrial maturation. The underlying causes of luteal defect may include inadequate follicular development, inadequate FSH secretion, abnormal LH secretion, or an abnormal effect of progesterone on the endometrium. Controversies regarding the concept of luteal defect have revolved around issues of diagnosis, endometrial biopsy versus progesterone levels, and treatment, progesterone versus clomiphene citrate. Based on findings that low FSH values prior to ovulation can be associated with luteal defect, it would seem reasonable to use clomiphene citrate. Clomiphene citrate is the first choice of many clinicians for the treatment of luteal defect. Because there is a suspected deficiency of progesterone in luteal defect, exogenous progesterone has been utilized. Vaginal administration of progesterone accomplishes targeted delivery to the uterus without producing high circulating levels. The micronized progesterone could a potential drug for the treatment of luteal defect. Luteal support is thought to be more imporatnt in IVF cycles in which GnRH agonist is used because of the poor development of the corpus luteum. HCG improved pregnancy rates in IVF when GnRH agonist was used. Progresterone was also beneficial for luteal support in IVF. However we prefer the routine use of HCG in IVF cycles, but recommend progesterone for high responder patients at risk for ovarian hyperstimulation syndrome.
社団法人日本産科婦人科学会の論文
2000-08-01

b.不妊治療と黄体機能不全(2.生殖)

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