Plasma beta-endorphin and the menstrual cycle.

beta-Endorphin (beta-E) takes part in the regulation of luteinizing hormone (LH) and prolactin secretion, but little is known about its role in the menstrual cycle. Using a specific assay, plasma concentration of beta-E was followed in healthy women in the periovulatory period and before and during menstruation. The mean concentration of beta-E in the eight women studied showed an increase at the midcycle, being 3.2 +/- 0.5 (standard error) pmol/l on day LH -1 and rising to 4.6 +/- 0.7 pmol/l on day LH 0 and further to 7.5 +/- 1.2 pmol/l on day LH +1. Thereafter, the mean beta-E level remained at 5.3 +/- 0.8 pmol/l and 5.2 +/- 0.4 pmol/l on days LH +2 and LH +3, respectively. Ten additional women were studied before and during menstruation. The highest mean plasma concentration of beta-E, 5.1 +/- 0.9 pmol/l, was found at the onset of menstruation, declining to 3.3 +/- 0.6 pmol/l and 2.9 +/- 0.6 pmol/l on the second and fifth days of menstruation, respectively. These findings suggest that beta-E secretion increases at the time of ovulation. At the onset of menstruation, pain may increase endorphin secretion.

Obesity, serum steroid levels, and pulsatile gonadotropin secretion in polycystic ovarian disease.

Serum binding capacity of sex-hormone binding globulin (SHBG-BC), steroid concentrations, and secretion patterns of LH and FSH were compared between groups of seven nonobese and seven obese patients with polycystic ovarian disease (PCOD). Obese patients with PCOD differed from those with normal weight in having very low SHBG-BC and elevated serum levels of free and albumin bound testosterone. Compared to healthy women in the follicular phase, both nonobese and obese patients with PCOD showed equally elevated serum levels of androstenedione, estrone, and albumin-bound and free estradiol. Pattern of gonadotropin secretion was studied from blood samples taken at 15 min intervals for 6 h. In 6 patients of both groups low pulses of FSH were found coincidently with pulses of LH. Serum level of LH showed a clear pulsatile pattern in all patients with PCOD, varying from 4.5 to 7.5 pulses per 6 h. The mean pulse rate in the groups of nonobese and obese patients with PCOD was similar, 5.9 pulses per 6 h. In the obese patients the mean LH levels were, however, less elevated and the pulse amplitudes were smaller than those in the nonobese patients. We suggest that this difference is due to high levels of biologically active testosterone in obese patients with PCOD.

Maternal serum bile acid levels and fetal distress in cholestasis of pregnancy.

Cardiotocography (CTG) and serum total bile acid level were used in the perinatal surveillance of 117 pregnancies with intrahepatic cholestasis. Signs of fetal distress occurred more commonly in cholestasis pregnancies with high maternal bile acid levels. Despite careful monitoring one intrauterine fetal loss occurred without any warning signs in CTG. In this case the serum bile acid level was only moderately elevated. CTG seems to be suitable for detection of fetal distress in cholestasis pregnancies. Those with high maternal bile acid level should be subjected to a more intensive follow-up. Some fetal risk, however, seems to remain despite of the use of these methods.

Prolactin pulsatility in polycystic ovarian disease.

Secretion patterns of LH and prolactin were studied in 5 nonobese (group A) and 7 obese (group B) women with polycystic ovaries (PCO) by taking blood samples at 15-min intervals for 6 h. Serum LH level showed a distinct pulsatility in all patients. There was no significant difference in the mean pulse rate of LH between group A (6.2 +/- 0.45, mean +/- SE) and group B (5.8 +/- 0.24). A pulsatile secretion pattern in prolactin was also found in 11 of the 12 PCO patients studied, the pulse rate being 3.2 +/- 1.0 in group A and 3.9 +/- 0.45 in group B. 79% of prolactin pulses coincided with those of LH but their amplitude was significantly lower than that of LH. In the total group of PCO patients a positive correlation was found between the serum concentrations of prolactin and free estradiol (r = 0.85), and prolactin and estrone (r = 0.78) indicating that estrogens participate in the regulation of prolactin secretion in polycystic ovarian disease. Four patients showed a steep decrease in the plasma prolactin level at the beginning of the study period suggesting a sensitive stress response.

Plasma beta-endorphin immunoreactivity in premenstrual tension.

Plasma samples were collected twice during the follicular phase and three times during the luteal phase of the menstrual cycle in 12 women with premenstrual tension (PMT) and in 14 control subjects without symptoms. Concentrations of beta-endorphin (beta-E) immunoreactivity, cortisol, oestradiol, progesterone and LH were determined. Comparison of the mean concentrations of LH, cortisol, oestradiol and progesterone did not reveal any statistically significant differences between the PMT and the control groups. In the early luteal phase, the mean plasma beta-E immunoreactivity was lower in the PMT group (10.7, SE 0.7 pg/ml) than in the control group (14.6, SE 1.6 pg/ml, P less than 0.05), suggesting that endorphin secretion is decreased in PMT. No significant change in the plasma beta-E level was found in the PMT patients between the follicular and luteal phase when symptoms appeared. This does not exclude the possibility that in the central nervous system abnormal changes occur in the activity of endogenous opioids in PMT.