Corpus luteum defects

During the review period a number of experimental works dealing with structure and function of different cell populations constituting the corpus luteum have been published. The function of luteinizing hormone receptors and their response to luteinizing hormone stimulation at different phases of the luteal phase have been studied. The synthesis, localization, and levels within the endometrium of a series of proteins such as insulin-like growth factor I, its binding protein, placental protein 14, and CA 125 have been examined. The possible implications of these studies on normal and disturbed corpus luteum functions are briefly discussed. The clinical assessment of corpus luteum function is still neither simple nor accurate. Histologic dating of endometrial biopsy has been reexamined, showing that readings of the same slide by the same evaluator were in exact agreement only in 43.1% of instances, and the dating differences among five various evaluators were even larger. An examination of 28 young, healthy volunteers participating in a 2-month strenuous exercise program indicated that in normal women, exercise, change of living conditions, stress, or other extraneous impacts may result in menstrual disturbances affecting either the entire cycle course or the luteal phase only. However, in the majority of cases, these effects are transient. Another study established that the prolactin secretion characteristics in women with luteal phase deficiency did not differ from those observed in 36 normal, apparently ovulating women. Another clinical study showed that deficient plasma lipoprotein levels are not connected with luteal phase deficiency. In another study, injection of anti-follicle-stimulating hormone serum to fertile bonnet monkeys on day 7 of the menstrual cycle resulted in a significant shortening of the luteal phase. In a study of 175 women with unexplained infertility, 29% had elevated follicle-stimulating hormone levels combined with reduced concentrations of estradiol and follicular growth pattern within the low normal range during the follicular phase and reduced progesterone levels during early- and midluteal phase. Endometrial defect coexistent with luteal phase deficiency can be corrected by treatment with follicle-stimulating hormone. Another study showed that clomiphene treatment during follicular phase increased the number of corpora lutea and the concentration of their luteinizing hormone receptors. The questions of whether stimulated (or overstimulated) cycles are frequently connected with luteal phase deficiency and whether all stimulated cycles require luteal support, and what type of support is preferable, are still open.