Ovarian Hyperstimulation Syndrome: A Current Survey

Publisher Summary This chapter discusses the mechanisms regulating the menstrual cycle in women. It discusses the events in the early and late proliferative period of the menstrual cycle, the main emphasis being on the relationship between FSH and estrogens. The chapter presents evidence indicating that the rising titer of estrogens is the trigger of the preovulatory LH release. It also discusses studies that relate to the control of the secretion of progesterone by the corpus luteum and of the duration of the postovulatory period. The chapter describes the manner in which the available physiological information may be incorporated into a model of the menstrual cycle. It presents some results of computer simulation studies based on this model. In a study described in the chapter, FSH and LH were measured by radioimmunoassay and progesterone by the radioligand method. To measure plasma estradiol and estrone, a radioimmunoassay was used employing antibodies that were made by the application of the hapten principle.

Mechanisms regulating the menstrual cycle in women.

Ovarian stimulation by a combination of a gonadotropin-releasing hormone agonist and gonadotropins for in vitro fertilization.

According to the 2-cell theory, ovarian steroidogenesis requires the coordinate action of both FSH and LH. To evaluate the relative importance of these hormones in follicular maturation, a randomized cross-over study was performed in 10 women with complete gonadotropin deficiency (absence of pulsatile LH secretion and no LH response to LHRH). Five women were treated with highly purified FSH (LH bioactivity, 0.09%) and 3 months later with human menopausal gonadotropin (hMG; LH bioactivity, 65%), each given for 10 days at a daily dose of 225 IU FSH, im. The sequence was reversed in the other 5 women. hCG (5000 IU) was administered im 24 h after the last injection of FSH or hMG. Plasma estradiol (E2), estrone (E1), androstenedione (A), testosterone, LH, and FSH concentrations and urinary LH and FSH were measured daily by RIA. Ultrasonography was performed during each treatment and 2 days after each hCG injection. After FSH treatment, mean plasma and urinary FSH levels increased, mean plasma LH did not change, and urinary LH increased slightly but not significantly from 91 +/- 32 (SE) to 164 +/- 55 mIU/24 h (10(-3) IU/24 h). After hMG treatment, mean plasma and urinary LH and FSH levels increased accordingly. The mean basal plasma E2 [11 +/- 1 pg/mL (40 +/- 4 pmol/L)] and E1 [14 +/- 4 pg/mL (52 +/- 15 pmol/L)] levels increased after FSH treatment to 207 +/- 69 pg/mL (760 +/- 253 pmol/L) and 82 +/- 21 pg/mL (303 +/- 78 pmol/L), respectively (P less than 0.01), but plasma A did not change. In response to hMG, the mean plasma E2, E1, A, and testosterone levels increased more than during FSH treatment. Ultrasonography revealed multiple preovulatory follicles (greater than or equal to 16 mm) in 2 women after hMG and 1 woman after FSH treatment; therefore, hCG was not administered. In 3 women given FSH, hCG did not induce ovulation. hCG induced ovulation in 8 women given hMG and in 6 women given FSH, based on ultrasonography and plasma progesterone levels. Thus, in the presence of profound gonadotropin deficiency pharmacological doses of FSH, with minute LH contamination, are capable of stimulating ovarian follicular maturation, underlining the key role of FSH in folliculogenesis.

John R. Marshall

Papers

Ovulatory Response Rate with Human Menopausal Gonadotropins of Varying FSH/LH Ratios