R.L. Vande Wiele

Ovarian hyperstimulation syndrome: Report of a case with notes on pathogenesis and treatment☆

Abstract A case of ovarian hyperstimulation is described. This syndrome infrequently appears as a complication of induction of ovulation with human menopausal and chorionic gonadotropins. The clinical manifestations are weight gain, extreme ovarian enlargement, ascites with pleural effusion, oliguria, and hypotension. Severe cases may become life-threatening due to marked fluid shifts, electrolyte imbalance, intravascular hypovolemia, and hypercoagulability. The pathogenesis of this syndrome is discussed, and suggestions are made about management. Therapy is symptomatic, expectant, and conservative unless surgical intervention becomes necessary in cases of intraperitoneal bleeding due to ovarian rupture. Physicians using gonadotropins for the treatment of infertility should be thoroughly familiar with the physiopathology of this complication.

Pulsatile administration of gonadotropin-releasing hormone for induction of ovulation

Chronic pulsatile administration of gonadotropin-releasing hormone (GnRH) was used to induce ovulation in 12 women with various ovulatory disorders. In the first group of eight patients with normal to low baseline levels of gonadotropin, seven responded favorably to the treatment. Follicular maturation was observed in 57% of the treated cycles, and normal ovulatory cycles were induced in 24% of the patients. Two patients became pregnant. The intravenous route of administration was more effective than the subcutaneous one, possibly in response to the GnRH profile after each pulse. (The amplitude of GnRH peaks after an intravenous pulse was four times that seen after a subcutaneous one.) In contrast, follicular maturation and ovulation could not be induced in four women of a second group of patients with normal baseline levels of follicle-stimulating hormone but with high and frequent pulses of luteinizing hormone. The conclusion reached was that pulsatile administration of GnRH can be a new therapeutic tool in the treatment of ovulatory disorders in women who have an insufficient endogenous release of GnRH.

Intravenous infusion of prostaglandin F2α in the mid-luteal phase of the normal human menstrual cycle

The luteolytic effect of PGF2alpha was studied in 3 normal women. Plasma levels of estrogens progesterone and gonadotropins were measured daily. Following a control cycle an infusion of 100 mcg/minute of PGF2alpha over an 8 hour period was given. 2 subjects received the PGF2alpha on the 9th and one on the 5th postovulatory day. The steroid patterns during the control and treatment cycles were not significantly different and the length of the luteal phases was identical. To accentuate luteal activity 2 subjects received in subsequent cycles 10000 i.u. HCG 48 hours prior to the PGF2alpha infusion. In these cycles despite the PGF2alpha the steroids continued to rise and then gradually declined in a normal fashion. The luteal phase was not curtailed. All subjects experienced nausea vomiting painful uterine contractions staining and temperature elevations above 100 degrees Fahrenheit during infusion. It is concluded that in the human PGF2alpha at the given dose was not luteolytic. (authors)

A COMPARISON OF THE EFFECTS OF ACTIVE IMMUNIZATION OF FEMALE RHESUS MONKEYS TO ESTRADIOL-17 OR PROGESTERONE-20-PROTEIN CONJUGATES

Abstract Eleven out of 14 female monkeys were successfully immunized against estradiol-17 hemisuccinyl-BSA. The elicited antibodies were highly specific for phenolsteroids. Intervals between uterine bleedings were lengthened and anovulation occurred consistently in animals with titers above 25% binding. Circulatory estrogens were extremely elevated throughout immunization, reaching levels of 10 ng/ml or more. The disappearance rate of injected 3 H-estradiol was significantly prolonged in comparison to non-immunized controls. Four out of 5 monkeys developed high titers after immunization against progesterone-20-O-carboxymethyl-oxime-BSA. These antibodies cross-reacted significantly with a number of 4-ene-3 keto steroids, e.g. 20-dihydroprogesterone, testosterone and 4-androstene dione. The length of the menstrual cycle remained unchanged in 3 out of 4 animals. More than half of the cycles remained ovulatory, as evidenced by the presence of fresh corpora lutea and increases in plasma progestins during the luteal phase. These results indicate that estrogens are causatively related to the midcycle LH ovulatory surge, while progesterone appears not to be essential in this event. The occurrence of anovulatory cycles in monkeys immunized to progesterone-20-BSA may be explained by the lack of specificity of the antiserum.