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KMID : 0377619920570040281
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Korean Jungang Medical Journal
1992 Volume.57 No. 4 p.281 ~ p.281
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PATHOPHYSIOLOGY OF LUTEAL PHASE INADEQUACY
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Wentz, Anne Colston
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Abstract
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Luteal phase inadequency (I:PI) clearly exists and can be identified. However, most studies are unable to prove that diagnosis of LPI change focundity. Many mechanisms for the development of LPI can be postulated, and a defect in any could result in deficient progesterone production during the luteal phase.. An adequate pool of primordial follicles is essential to follicular development. Hormonal inadequacy, including gonadotropin and steroid defects, and insufficient receptor synthesis may result in abnormal corpus luteum function. An inadequate FSH output, a defective granulosa cell response, a poor quantitative LH surge, or in adequate pulsatile LH stimulation can all result in poor formation of the corpus luteum. LPI occurs in association with well-described clinical entitles. A higher incidence of LPI is found hi association with: 1) recurrent early fetal wastage, 2) ovulation induction regimens, 3) hyperprolactinemia, 4) the extremes of reproductive life post menarche, premenopausal, 5) scranuous athletic conditioning (running, baller, gymnastics), 6) low body weight, 7) unexplained infertility, 8) long follicular phase, 9) hyperandrogenism, 10) follicular aspiration (oocyte retrieval), 11) the first 1 -2 cycles after an abortion, delivery of stopping oral contraceptives, and 12) endometriosis(?). LPI should be diagnosed using the late luteal phase endometrial biopsy as a biopsy; the histologic pattern of the endometrium should reflect an adequate output of progesterone, and an appropriate ratio of progesterone to estradiol. When endometrial inadequacy is associated with normal progesterone output, the endometrial biopsy represents the only way to diagnose an inappropriately developed implantation site. Once a properly timed biopsy has been diagnosed to be out-of-phase, several required tests must be accomplished. To make the diagnosis, a second biopsy is needed. In addition, a hysterosalpingogram (HS(,) and serum prolactin level must be obtained. Approaches to therapy are straight-forward, involving either stimulation of luteal function or substitution for the deficiency. Agents which stimulate luteal activity include hCG, pure Li-i and indirectly, bromocriptine (Parlodel). Substitution therapy is accomplished using vaginal, rectal or intramuscular progesterone, but never a progestational agent. The choice of progesterone supplementation is best reserved for those patients; 1) with normal follicular phase length. 2) who are 35 years of age or less, 3) who have normal prolactin levels, 4) who have a normal HSO, and 5) who have no other clearly diagnosable cause of LPI. LPI is an unusual cause of infertility but has a higher incidence in pa-tie. is preseting early recurrent abortion, probably because of endometrial derangement.
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KEYWORD
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