Sezer Aksel

Vasomotor symptoms, serum estrogens, and gonadotropin levels in surgical menopause

Hormonal parameters of young women who developed vasomotor symptoms in the immediate postoperative period following castration are compared to those who remained asymptomatic. Only 37.5 per cent of 16 premenopausal women developed hot flushes after operation. Perimenopausal women with vasomotor symptoms and elevated follicle-stimulating hormone levels demonstrated normal luteinizing hormone and estrogen values preoperatively. There were no statistically significant differences in total serum estrogen, follicle-stimulating hormone, or luteinizing hormone concentrations between the group of patients with symptoms and the group withoyt symptoms. The results of the study indicate that rising gonadotropin or declining estrogen values appear to have no direct correlation to the onset of vasomotor symptoms in the immediate postoperative period. Thus, the precise etiology of the hot flush remains to be elucidated.

The Diagnosis and Therapy of Luteal Phase Deficiency

Between 1973 and 1975, 16 patients evaluated for infertility at Duke University Medical Center were diagnosed as having luteal phase deficiency. A majority had had prior infertility surveys, and the average duration of their infertility exceeded 2 years. The diagnosis was suspected after study of basal body temperature charts and menstrual patterns in more than 80% of the patients. This diagnosis was established by timed endometrial biopsy. The primary method of therapy was supplementation of the luteal phase with progesterone vaginal suppositories. The pregnancy rate after therapy was 50% and pregnancy occurred after a mean of five treatment cycles. The minimal follow-up of patients who failed to conceive was 8 months. To date, the majority of these pregnancies have been completed without complication and the remainder are progressing satisfactorily. Two additional patients developed luteal phase deficiency while taking clomiphene citrate and became pregnant with progesterone supplementation.

Luteinizing Hormone-Releasing Hormone in the Human Fetal Brain*†

Hypothalamic and other brain tissues were obtained after death from human fetuses aborted by hysterectomy at various conceptional ages. Immunoreactive luteinizing hormone-releasing hormone (LHRH) activity in tissue extracts was determined by a double-antibody radioimmunoassay method. Fetal hypothalamic and cortical tissue at 5 weeks after conception showed no assayable LHRH activity. At 6 weeks, immunoreactive LHRH was detectable in extracts of both the hypothalamus and the cortex, and levels appeared to fluctuate with a trend to increase until the 20th week. Two of four fetuses at 13 and 14 weeks conceptional age had significantly higher LHRH activity in the thalamus than in the rest of the central nervous system. After 16 weeks, LHRH activity was detected in the hypothalamus, thalamus, cerebrum, and cerebellum in decreasing concentrations, respectively. As the age of the fetus progressed from 16 to 20 weeks, the LHRH concentration in the hypothalamus increased significantly, from 1.2 pg/mg to 29.3 pg/mg of wet tissue. LHRH concentrations in specimens of comparable conceptional age that could not be promptly dissected were lower than in those dissected within 30 minutes after the ligation of uterine arteries.

Effect of progesterone and 17-hydroxyprogesterone caproate on normal corpus luteum function

A group of infertility patients were evaluated by an endometrial biopsy, timed with a basal body temperature chart, serum luteinizing hormone radioimmunassay to pinpoint ovulation, and daily serum progesterone values during a control and a treatment cycle. Progesterone in the suppository or intramuscular form and 17-hydroxyprogesterone caproate* were administered during the luteal phase to a group of volunteer patients with normal corpus luteum function to determine if these compounds would depress serum progesterone levels as do certain progestational agents. There was no apparent inhibition of corpus luteum function as no decrease in progesterone production occurred. Despite the additive effect of progesterone administration demonstrated by elevated serum levels, endometrial biopsies remained in phase when dated from the estimated day of ovulation.

Plasma Prostaglandin F2α Levels in Dysmenorrheic Women

Plasma prostaglandin F 2 α (PGF 2 α ) concentrations were compared in nine ovulatory dysmenorrheic women, one dysmenorrheic oral contraceptive user, and two nondysmenorrheic control subjects, in an effort to demonstrate a relationship between plasma PGF 2 α levels and dysmenorrhea. In addition, the effects of aspirin, a known inhibitor of prostaglandin synthesis, on dysmenorrhea and on PGF 2 α levels were investigated. No statistical difference was demonstrated between the plasma PGF 2 α levels of dysmenorrheic and nondysmenorrheic subjects throughout the menstrual cycle. Attainment of an adequate salicylate level was accompanied by a significant decrease in PGF 2 α levels. All dysmenorrheic subjects reported improvement in symptoms while taking aspirin. The greatest subjective relief was reported by women who began taking aspirin (10 grains every 4 hours) 3 or more days prior to the onset of bleeding.

Prostaglandin F2α Levels in Human Ovarian Plasma in Pregnancy and in a Case of Halban's Disease

It has been demonstrated that the ovary bearing the corpus luteum in the human is responsible for the major portion of prostaglandin F2α(PGF2α), total estrogen, and progestin production during the luteal phase of a normal menstrual cycle.1 This study was performed with the intent to gain more information about the secretion of PGF2α in conditions that prolong the life span of the corpus luteum, such as pregnancy and Halbans disease. Utilizing a specific radioimmunoassay for PGF2α, ovarian venous plasma levels were measured in 7 pregnant women and in a patient with Halbans disease. During the first and second trimester of pregnancy, PGF2α values in plasma from the active and inactive ovary were comparable and were significantly lower than concentrations in plasma from the active ovary during the luteal phase of the normal cycle. In a patient with persistent corpus luteum or Halbans disease, PGF2α concentrations of venous plasma from the ovary bearing the corpus luteum were significantly lower than those obtained from the contralateral ovary. These observations indirectly support the hypothesis that prostaglandins produced within the ovary may have a role in luteal regression.

Prostaglandin F2α Levels in Human Ovarian Plasma in Pregnancy and in a Case of Halbanʼs Disease

It has been demonstrated that the ovary bearing the corpus luteum in the human is responsible for the major portion of prostaglandin F2alpha (PGF2alpha), total estrogen, and progestin production during the luteal phase of a normal menstrual cycle. This study was performed with the intent to gain more information about the secretion of PGF2alpha in conditions that prolong the life span of the corpus luteum, such as pregnancy and Halbans disease. Utilizing a specific radioimmunoassay for PGF2alpha, ovarian venous plasma levels were measured in 7 pregnant women and in a patient with Halbans disease. During the first and second trimester of pregnancy, PGF2alpha values in plasma from the active and inactive ovary were comparable and were significantly lower than concentrations in plasma from the active ovary during the luteal phase of the normal cycle. In a patient with persistent corpus luteum or Halbans disease, PGF2alpha concentrations of venous plasma from the ovary bearing the corpus luteum were significantly lower than those obtained from the contralateral ovary. These observations indirectly support the hypothesis that prostaglandins produced within the ovary may have a role in luteal regression.

Luteinizing Hormone-Releasing Hormone and the Human Menstrual Cycle

Plasma concentrations of LHRH were measured by radioimmunoassay in daily samples obtained from 10 normally ovulating women. The normalcy of each menstrual cycle was determined by measuring luteinizing hormone (LH), follicle-stimulating hormone (FSH), total estrogen, and progesterone concentrations. Six women had consistently measurable immunoreactive LH-releasing hormone (LHRH) in every blood sample. In four, LHRH could not be detected in some of the samples, more frequently during the follicular phase. LHRH levels varied between 10 and 35 pg/ml during the menstrual cycle. At midcycle, coincident with the LH surge, the mean LHRH level (17.6 +/- 4.4 pg/ml) was not significantly different from the mean follicular or luteal phase values. The lowest LHRH level, 11.4 +/- 4.6 pg/ml, was observed on the day of the estrogen surge. A detailed evaluation was made of the specific days of the cycle. Blood samples obtained from an indwelling venous catheter every 20 minutes over a 3 or a 5 hour period during the days of the estrogen surge and the LH surge and on the following day showed no correlation between OHRH, LH, and FSH values.