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PubMed1990

The physiological and clinical effects of progesterone inhibition with mifepristone (RU 486) in the second trimester.

A double-blind placebo-controlled trial was performed in 20 primigravidae to assess the physiological and clinical effects of oral mifepristone on myometrial contractility and sensitivity in the second trimester. Ten women received 600 mg of oral mifepristone and 10 women a placebo 24 h before abortion was induced in both groups, with extra-amniotic PGE2 instillation. Intrauterine pressure recordings demonstrated increased spontaneous uterine activity and increased sensitivity to PGE2 and ergometrine, but no change in oxytocin sensitivity after mifepristone treatment. There were no significant differences in PGE or PGF metabolite concentrations in peripheral maternal plasma over the 24-h study period after treatment between the mifepristone and placebo groups. The mean induction abortion interval in the mifepristone group was 512 (SD 321) min compared with 1128 (SD 606) min in the placebo group (P less than or equal to 0.02). The mechanism whereby mifepristone provokes enhanced uterine contractility and sensitivity to prostaglandins, with a reduction in abortion times, does not appear to be through endogenous production of PGE or PGF.

Abortion, Induced↗
PubMed1994

Prostaglandins and progesterone receptor antagonists in human fertility regulation.

Anti-progesterone medicines have now been extensively studied for human fertility regulation. The combination of the anti-progesterone Mifepristone with prostaglandin analogues such as Gemeprost and Misoprostol have been used in several European centres for medical abortion. Used before nine weeks gestation, these medicines have similar efficacy to surgical abortion. In addition, administration of progesterone antagonists within five days of unprotected intercourse appear effective in pregnancy prevention. Anti-progesterone medicines are not currently available in Australia. The introduction of progesterone receptor antagonists and modern prostaglandins would save approximately $10,000,000 per year to the Australian Health Budget. Furthermore, the introduction of progesterone receptor antagonists for emergency contraception would have even greater financial and emotional savings for Australian women. In Australia, when known carcinogens can be purchased over the counter, it is surely time for Australians to consider effective emergency contraception bought over the counter.

Abortion, Induced↗
PubMed1976

A synergistic effect of oestradiol and prolactin influencing the incidence of 3-methylcholanthrene induced cerivical carcinomas in mice.

Castrated NMRI mice were laparotomized and a thread impregnated with beeswax-methylcholanthrene was inserted into the uterine cervix. Beginning on the day of operation and for a further 5 days the animals were injected with oestradiol, prolactin, oestradiol-prolactin, oestradiol-prolactin-progesterone, or the solvents for the hormones only. One group of animals were injected with oestradiol-prolactin for 6 days and later with progesterone every third day until death. The animals were killed one or 4 weeks after the operation. Among the one-week animals the number of cervices presenting epithelial downgrowths ("buds") into the stroma was higher after treatment with a combination of oestradiol and prolactin than after treatment with each hormone separately or among the controls. Four weeks after operation, the incidence of squamous cervical carcinomas was seen to be significantly higher among animals injected with both oestradiol and prolactin than in controls or in those injected with oestradiol or prolactin alone. Progesterone had no definite effect on the oestradiol-prolactin induced incidence. The mechanism behind the synergistic effect of prolactin and oestradiol is discussed.

Animals↗
PubMed1978

The relationship of changes in serum estradiol and progesterone during the menstrual cycle to the thyrotropin and prolactin responses to thyrotropin-releasing hormone.

The responses of serum TSH and PRL to TRH (500 microgram) were studied in normal young women in the early follicular, periovulatory, and midluteal phases of the menstrual cycle in order to examine the relationship of these responses to the levels of estradiol relationship of these responses to the levels of estradiol (E2) and progesterone. Each woman was studied twice in each phase in order to assess intraindividual variability. There was no significant difference in either the TSH or PRL responses among the phases of the menstrual cycle nor was either response affected by the periovulatory rise in E2 or by the luteal rise in both E2 and progesterone. Thus, the interpretation of the TSH and PRL responses to TRH in normal women is not affected by the menstrual cycle although both responses are greater in women that in men. Both the peak TSH and peak PRL after TRH were highly correlated with the basal levels of TSH (r = 0.85; P less than 0.01) and PRL (r = 0.67; P less than 0.01), respectively, indicating that the TSH and PRL responses to TRH in women are directly proportionate to the basal levels of the respective hormones, as previously shown for the TSH response in men. The mean intraindividual variability (coefficient of variation) of the TSH response to TRH was 18%, but ranged as high as 56%, while that of the PRL response was 16% and ranged up to 31%; variability was not affected by the phase of the menstrual cycle. The normal range of the peak TSH after TRH in women is 7-33 microU/ml (mean +/- 2 SD); however, because of the variability, a normal woman may sometimes have a peak TSH after TRH as low as 4 microU/ml. Repeating the test will result in a normal value if the woman is truly normal. Similarly, the normal peak PRL after TRH in women is 22-111 ng/ml (mean +/- 2 SD); usually, however, the lower limit is 30 ng/ml with lower values due to intraindividual variation. The data suggest that the higher average level of E2 in women compared to women, but that the cyclic changes in serum E2 or progesterone in women have little or no additional effect.

Adult↗
PubMed1986

Fourteen-day versus twenty-one-day regimens of intermittent intranasal luteinizing hormone-releasing hormone agonist combined with an oral progestogen as antiovulatory contraceptive approach.

This study was designed to determine the effect of discontinuous administration of a LHRH agonist on pituitary-ovarian function in normal women. The LHRH agonist buserelin (200 micrograms/12 h or 400 micrograms/24 h) was given intranasally for four consecutive cycles for 14 or 21 days in 26 normally cycling women. Five milligrams of medroxyprogesterone acetate were given orally twice daily from days 15-21. There was a 7-day pause between each medication cycle. Blood samples were drawn every other day for RIA of LH, FSH, estradiol (E2), and progesterone (P). Serum FSH increased for only a few days at the beginning of each cycle, whereas sustained elevation of serum LH occurred during LHRH agonist administration. Serum E2 increased rapidly and remained elevated during the administration of buserelin. Serum P remained in the follicular phase range or increased briefly after the initiation of buserelin occasionally in the 14-day regimens. After discontinuation of buserelin, E2 fell rapidly, and uterine withdrawal bleeding occurred. During the pause, FSH increased progressively. The patterns of gonadotropin response to buserelin were similar in the four cycles. Based on measurement of the areas of the response curves, serum LH and E2 levels were higher during the administration of 200 micrograms/12 h compared to 400 micrograms/24 h buserelin. However, down-regulation of the pituitary-ovarian axis, as evaluated by the acute gonadotropin response to buserelin on day 14, was more pronounced with 200 micrograms/12 h than with 400 micrograms/24 h. Breakthrough bleeding occurred in the 14-day schedules, whereas withdrawal bleeding occurred during the pause in the 21-day schedules. The immediate cycles following buserelin administration were normal ovulatory cycles. Intermittent LHRH agonist administration for 21 days avoided constant down-regulation of the pituitary-ovarian axis and allowed regular uterine bleeding. Combined with an appropriate P complement, it could be a useful contraceptive approach.

Administration, Intranasal↗
PubMed1977

Pituitary gonadotrophin secretion during the first weeks of pregnancy.

A longitudinal study of basal plasma LH and FSH and their responses to 25 microng LRH iv as well as basal levels of oestradiol, progesterone, prolatin and HCG was performed every week in 3 women, pregnant after heterologous insemination, from conception until the 6th week of gestation. A comparative study was carried out in 7 women in cycles in which no conception occurred after insemination. All hormones were assayed with radioimmunoassay. LH was measured with a specific assay for native HL, which did not cross-react with HCG. A decrease in basal levels of LH and FSH as well as decreasing responses to LRH was found during the first 2 weeks of gestation. These changes did not differ from what was observed during the luteal phase in the non-conception cycles. One week later the basal FSH levels and the FSH response in the pregnant women showed a further decrease, while in the non-pregnant women, now reaching the early follicular phase, a rise in FSH basal levels occurred. The basal levels of LH and the LH response, however, did not differ from that found in the non-pregnant woment at this time. FSH basal levels remained below the lower normal limit in eumenorrhoic women from the 3rd week of gestation. By this time the FSH response was almost completely inhibited. The LH basal levels, however, remained above the lower normal limit in eumenorrhoic women, but the LH response to LRH progressively decrease and was completely inhibited by the 5th week of gestation. In the non-conception cycles the LH response varied with the levels of oestradiol in plasma. This was not found in the pregnant women as the decrease in gonadotrophin response occurred while oestradiol remained at mid-cycle levels during the first 4 weeks of gestation. Rather it seems that the increasing and continuously elevated level of progesterone, in the presence of appropriate levels of oestradiol, might be the main go nadal steroid responsible for the diminishing pituitary secretion. The contribution of HCG to the further decrease in gonadotrophin secretion after the 2nd week of pregnancy cannot be answered by the present studies. Prolactin remained at non-pregnant levels until the 6th week of gestation, and appeared to have no influence on the secretion of gonadotrophins during early pregnancy.

Adult↗
PubMed1982

Danazol has progestin-like actions on the human endometrium.

The administration of danazol, 200 mg three times daily, from the 3rd to the 23rd day of the cycle to normally menstruating women exhibited the following actions on the human endometrium: significantly reduced cytosol oestrogen and progestin receptor concentrations, and declined 17 beta-hydroxysteroid dehydrogenase activity. Very similar results were obtained during medroxyprogesterone acetate (100 mg daily) treatment for the same period of time. Danazol administration did not decrease circulating gonadotrophin levels but clearly suppressed luteal serum oestradiol and progesterone concentrations. Danazol was found to bind in vitro to endometrial progestin receptor with an affinity approximately 3% of that of progesterone. These findings are compatible with the notion that a local progestin-like rather than a systemic action of danazol is the way by which its therapeutic effect is exerted. This may be potentiated by the suppression of circulating oestradiol levels.

17-Hydroxysteroid Dehydrogenases↗
PubMed1975

Plasma hormones and pituitary luteinizing hormone in the rat during the early stages of pregnancy and after post-coital treatment with tamoxifen (ICI 46,474).

Plasma levels of oestradiol-17beta, progesterone and luteinizing hormone (LH) and pituitary levels of LH have been measured during the first 6 days of pregnancy, in normal rats and in rats receiving two doses of Tamoxifen (trans-1-(rho-beta dimethylamino-ethoxyphenyl)-1-2-diphenylbut-1-ene) on day 2 of pregnancy. In normal rats oestradiol rose strongly from early on day 3 to reach a peak concentration between 22.00 h on day 3 and 08.00 h on day 4. Progesterone concentrations rose from day 2 to reach peak values on day 3-4. In animals in which implantation was delayed 20-24 h by administration of Tamoxifen (0.1 mg/kg) orally on day 2 the increased level of plasma oestrogen was also delayed by 20 h. A higher dose of Tamoxifen (0.2 mg/kg) on day 2, which prevented implantation, completely eliminated the increase in plasma oestradiol. Neither dose of Tamoxifen affected the levels of progesterone. In both normal rats and rats treated with 0.1 mg Tamoxifen/kg, plasma LH levels declined by day 3 while pituitary levels rose steadily. There was no detectable change in either plasma or pituitary LH levels, accompanying the increase in plasma oestradiol in the normal rats. In animals receiving Tamoxifen (0.2 mg/kg), plasma LH increased to a maximum by day 4 while levels of pituitary LH decreased. The results show that the oestrogen "surge" of early pregnancy, occurs normally about midnight on day 3 and not late on day 4 as previously thought. It is considered that the plasma oestradiol peak in early pregnancy results from an increased release of FSH rather than an increased release of LH. Tamoxifen may owe part of its antifertility action to a capacity to inhibit the synthesis of oestradiol from progesterone.

Adrenalectomy↗
PubMed1975

Serotonin, 5-hiaa, total estrogen and pregnanediol excretion in urine during therapeutic saline abortion.

In 24 patients, who underwent therapeutic abortion for various reasons between the 17th and 26th week of pregnancy, urinary excretion of serotonin, 5-HIAA, total estrogens, and pregnanediol were measured before, during and after the intra-amniotic injection of hypertonic saline. 20% hypertonic saline solution (160-500 ml) was given by transabdominal injection over a period of 5 min. The four hormones or metabolites were measured during six periods: I; 12-24 hrs, and II: 0-12 hrs before saline administration, III: 0-12 hrs after saline administration, IV: 0-12 hrs during aborion, V: 0-12 hrs and VI: 12-24 hrs after abortion. The results point to the active participation of serotonin in the process of fetal expulsion, as serotonin was increased by over 100% (from 20-22 to 43-47 mu-g/12 hrs) during periods III-IV, and its metabolite 5-HIAA, too, increased by nearly 60% (from 2.4-2.5 to 3.3-3.9 mg/12 hrs). They decreased during the post-abortive periods V-VI. On the other hand, total estrogens decreased only slowly, but continuously, during all 6 periods (4.9, 4.3, 3.4, 3.1, 1.8 and 1.4 mg/12 hrs). Pregnanediol, beginning with 12 mg/12 hrs showed a slight increase during periods III-IV (14.5 and 15.6 mg/12 hrs) and a decrease during periods V-VI (8.0 and 5.8 mg/12 hrs). These findings are interpreted as indicating the disruption of feto-placental function affecting estrogens during periods III-VI. They might demonstrate an accelerated hydrogenation of progesterone into pregnanediol during periods III-IV, followed by a sharp decreased in progesterone/pregnanediol production during periods V-VI.

Abortion, Therapeutic↗
PubMed1989

Termination of early pregnancy with RU 486 (mifepristone) in combination with a prostaglandin analogue (sulprostone).

The antiprogestin RU 486 (mifepristone) has been shown to induce abortion when administered in early pregnancy, but the rate of incomplete abortion is high, around 40%. As blockage of the progesterone receptor increases the myometrial sensitivity to prostaglandins, a combination of RU 486 and a prostaglandin E2-analogue was tested for termination of pregnancy. One hundred and sixteen women, with a gestational length of less than 49 days from the first day of the last menstrual period, were treated with a daily dose of 50 or 100 mg RU 486 for 3 to 6 days, complemented with an intramuscular dose of 0.25 mg sulprostone (16-phenoxy-PGE2-sulfonylamide) on the last day of RU 486 treatment. The results confirmed that a reduction of treatment duration to 3 days is just as effective for inducing abortion (91% complete abortion) as a 4-6-day treatment regimen (95% complete abortion). Six patients had an incomplete abortion and in one the pregnancy continued unaffected. Side effects included intense uterine pain after the prostaglandin administration (16%), vomiting associated with the antiprogestin intake (9%) and after the prostaglandin administration (9%). One woman needed emergency curettage due to heavy bleeding. Six percent of the treated patients had a decrease in hemoglobin exceeding 20 g/l during the first week but no patient needed blood transfusion. No serious side effects were recorded.

Abortifacient Agents↗