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PubMedDate not supplied

Estrogen: physiology, pharmacology, and formulations for replacement therapy.

Estrogen is the central component in 6 of the 100 most widely prescribed medications in the United States today. This steroid has several therapeutic uses including contraceptive applications, treatment of menopausal symptoms, and the prevention of osteoporosis. A wide variety of estrogen replacement therapy (ERT) and estrogen plus progestational hormonal replacement therapy (HRT) preparations are available. In addition, there are an increasing number of products with estrogenic properties that are being promoted as alternatives to drugs containing estrogen, such as phytoestrogens and selective estrogen receptor modifiers (SERMs). This article reviews the physiology of estrogenic effects, estrogen metabolism, and the pharmacokinetics of marketed preparations.

Adult↗
PubMed2004

A mouse model of cardiac rhabdomyoma generated by loss of Tsc1 in ventricular myocytes.

Tuberous sclerosis is a hamartoma syndrome due to mutations in TSC1 or TSC2 in which cardiac rhabdomyomas are seen in approximately 60% of patients. These lesions have an unusual natural history as they are usually most prominent immediately after birth and spontaneously resolve in most cases. To develop a mouse model of this lesion, we used a conditional, floxed allele of Tsc1 and a modified myosin light chain 2v allele in which cre recombinase expression occurs in ventricular myocytes. Mice with ventricular loss of Tsc1 had a median survival of 6 months and developed a dilated cardiomyopathy with the occurrence of scattered foci of enlarged ventricular myocytes. The enlarged cells were periodic acid-Schiff positive indicating the presence of excess glycogen and expressed elevated levels of phospho-S6, similar to findings in patient rhabdomyoma cells. The observations confirm that rhabdomyomas occur through a two hit mechanism of pathogenesis. However, the mice showed no evidence of fetal/neonatal demise, and there was no evidence of proliferation in the lesions. We propose that these differences are due to the timing of loss of Tsc1 in the ventricular myocytes and/or the truncated gestational period in the mouse compared with humans, during which progestational hormones may accentuate the growth of patient rhabdomyomas.

Alleles↗
PubMed1994

Hypothalamo-pituitary effects of RU486: inhibition of progesterone-induced hyperprolactinaemia.

Monkeys given oestrogen priming at physiological levels for at least 1 week become hyperprolactinaemic upon the addition of physiological progesterone administration. Here, using RU486, we test whether that this oestrogen/progestin-induced hyperprolactinaemia results from classical progesterone actions at the hypothalamo-pituitary level. Blood samples were collected daily from study day 1-67. Each monkey (n = 2) received daily injections of 25 micrograms/kg oestradiol benzoate, i.m., on study days 5-60. Progesterone-filled silastic capsules (3 cm) were inserted on study day 14 and removed on day 53. On study days 39-45, each monkey received RU486 (25 mg/day, p.o.). Serum samples were stored at -20 degrees C until assayed for prolactin, oestradiol, progesterone and RU486 by radioimmunoassay. Hyperprolactinaemia was induced in all three monkeys upon insertion of progesterone capsules. Prolactin concentrations fell sharply during RU486 treatment to nadirs some 10-fold less than prior to RU486 treatment. The time series was modelled by the Box-Jenkins autoregressive-integrated moving average (ARIMA) method with progesterone producing a gradual increase in prolactin concentrations and RU486 producing a sudden decrease. Statistically significant effects of progesterone and RU486 were found. Thus, the addition of progesterone to an oestrogenized milieu significantly increased prolactin concentrations, and RU486 fully reversed this effect. This evidence indicates that the progesterone-induced hyperprolactinemia in an oestrogenized milieu results from classical progesterone effects.

Animals↗
PubMed1976

Hormone-dependent mammary tumors in strain GR/A mice. II. Preneoplastic and neoplastic properties.

In a series of transplant experiments, we investigated interactions between normal, ductal phase, and tumorous phase mammary tissues in GR/A mice, with particular respect to growth regulation. Transplants from hormone-dependent mammary tumors (HDT) transplanted into mammary fat pads already containing normal mammary ducts usually could not be located subsequently or, at best, displayed minimal growth. Growth regulation was also normal when two HDT transplants, placed in a single gland-free fat pad in nonpregnant hosts, produced ductal outgrowths displaying mutual avoidance behavior in which ducts did not touch and were normally spaced. A normal and HDT transplant in a single gland-free fat pad also showed identical, normal regulatory behavior. In contrast, HDT transplants in pregnant hosts or in hosts receiving exogenous hormone therapy displayed altered growth patterns in which neighboring tumors touched and eventually fused. When surrounded by normal tissues, the HDT continued to proliferate and often appeared to overgrow and engulf normal elements. We concluded that HDT tissues grown in nonpregnant hosts fully responded to those short-range regulatory influences characteristic of normal morphogenesis. When exposed to hormones of pregnancy, however, these interactions changed, and HDT tissues exhibited many characteristics of ductal carcinomas.

Animals↗
PubMed1977

Potent inhibitory effect of a new antiestrogen (RU 16117) on the growth of 7,12-dimethylbenz[a]anthracene-induced rat mammary tumors.

At the daily dose of 24 mug for a period of 4 weeks, RU 16117 (11alpha-methoxyethinyl estradiol), a new antiestrogen, led to 65% reduction of the number of already established dimethylbenz[a]anthracene (DMBA)-induced mammary tumors in female Sprague-Dawley rats. Not only the tumor number but also the tumor size was reduced by RU 16117 in a manner similar to that seen after ovariectomy. The absence of an inhibitory effect of doses of 0.1 to 12.5 mug 17beta-estradiol (E2) per day, a dose-range which covers the low estrogenic activity of the RU 16117 doses used, suggested that the inhibitory effect of RU 16117 was not due to its estrogenic activity. Decreased levels of receptors for E2, progesterone, and prolactin were found in the tumors remaining after ovariectomy; treatment with the dose of RU 16117 sufficient to inhibit tumor growth (24 mug) had a similar inhibitory effect on the levels of E2 and prolactin receptors. These data suggested that a reduction of hormone receptor levels in the tumor tissue could be a mechanism by which RU 16117 acts as a potent inhibitor of the growth of DMBA-induced mammary carcinoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Inhibition of ovulation: comparison between the mechanism of action of steroids and GnRH analogues.

The pulsatile secretion of GnRH is achieved by the fine regulation of oestrogens and progesterone. Progesterone is mainly responsible for a negative feedback effect at the hypothalamic level which decreases GnRH pulse frequency. Oestradiol exerts both a positive and a negative feedback effect, mostly at the pituitary level, and the use of steroids to prevent ovulation combines both effects. Recent developments in steroid research suggest a potential interest in the use of non-androgenic progestins which reproduce the negative feedback effect of progesterone with fewer metabolic side effects. GnRH agonists, although responsible for low plasma levels of oestradiol, may be useful in women at risk for steroid contraception. GnRH antagonists suppress transient gonadotrophin-dependent events in the menstrual cycle. Studies with the second generation GnRH antagonist, Nal--Glu, suggest a potential use of these compounds in suppressing ovulation.

Contraceptive Agents, Female↗
PubMed1990

The effects of the antiprogestin mifepristone, in vivo, and progesterone in vitro on prolactin production by the human decidua in early pregnancy.

This study investigated the regulatory effect of progesterone on decidual prolactin (dPRL) production during early human pregnancy (6-7 weeks). Patients (n = 7) were treated with the antiprogestin-mifepristone (RU 486; 600 mg single oral dose) for 24-36 h before termination of pregnancy by curettage. Tissue was also obtained from patients without pretreatment in vivo (n = 8) and acted as controls. Decidual tissue was incubated in vitro with and without progesterone and mifepristone for 5 days and the medium changed daily. Prolactin production by decidua parietalis decreased over the period of incubation and was unaffected by addition of progesterone or mifepristone. However, in the group pretreated in vivo with mifepristone, the production of dPRL was markedly lower than in the control group. In contrast, the production of dPRL by decidua capsularis to which trophoblast was attached, was maintained at a constant level over 5 days of culture and was unaffected by pretreatment with mifepristone in vivo or its addition in vitro, or by progesterone. Prolactin was immunolocalized using avidin-biotin immunoperoxidase staining to decidualized cells within the decidua and the intensity of staining was reduced or absent in the decidua parietalis from the mifepristone group compared to controls, but was similar in decidua capsularis in both control and mifepristone groups, in good agreement with the in-vitro production of dPRL. Our findings suggest that the effect of progesterone may be only facilitative, maintaining decidual differentiation, and dPRL production might only be associated with the presence of progesterone-dependent differentiated decidual cells. Apart from progesterone, factors from trophoblast cells can maintain dPRL production during pregnancy.

Abortion, Induced↗
PubMed1985

Comparative study of nursing mothers in Africa (Zaire) and in Europe (Sweden): breastfeeding behaviour, nutritional status, lactational hyperprolactinaemia and status of the menstrual cycle.

A total of 1036 nursing mothers were investigated for their nursing behaviour, status of nutrition and menstrual cycle, serum prolactin and progesterone; 61 in Sweden, 457 in an urban area of Zaïre (Bukavu, Kivu) and 518 in a rural area of the same region (Kabare, Kivu). Lactational hyperprolactinaemia is influenced by the frequency but not by the duration of suckling. The return of luteinization of follicles, but not that of menstrual bleeding, was inversely related to the degree of lactational hyperprolactinaemia. Significant luteinization took place in only some 10% of the mothers during the first three months of lactation in Sweden and within the first year in Zaïre. In these mothers with luteinized follicles the average progesterone was only slightly above 1.0 ng/ml indicating poor luteinization. Lactational hyperprolactinaemia, the return of menstruation and luteinization during lactation were not related to the nutritional status as evaluated by the body weight indices and serum albumin. However, suckling and hyperprolactinaemia do not appear to be the only factors involved in the control of fertility during lactation. When serum prolactin levels were equally low, i.e. below 500 microU/ml, twice the number of lactating mothers with signs of luteinization were found in the urban than in the rural population of Zaïre.

Body Weight↗
PubMed1976

The influence of pharmaceutical compounds on male fertility.

1. Steroid hormones can affect spermatogenesis and thereby fertility directly and/or indirectly. All antigonadotropically active steroids inhibit spermatogenesis via inhibition of gonadotropin secretion, mainly that of H. Androgens and steroids occurring in the biosynthetic chain of testosterone synthesis have a direct promoting effect on spermatogenesis if applied in high doses. It has not been possible as yet to make clinical use of this positive effect since it is obviously not possible to achieve the necessary intratesticular androgen concentrations. 2. As concerns the different androgens and the steroids in the androgen biosynthetic chain, and also all synthetic anabolics, there is no parallelism between the direct spermatogenic activity, the androgenic activity and the antigonadotropic activity. 3. Estrogens and synthetic gestagens do not inhibit spermatogenesis directly at the testicular level. All effects of estrogens can be abolished experimentally by adequate substitution with gonadotropins or androgens, or a combination of androgens and gonadotropins. 4. Only those antiandrogens inhibit spermatogenesis with additional antigonadotropic properties (e.g. cyproterone acetate). Pure antiandrogens, like flutamide or cyproterone, have a slight and transient influence on spermatogenesis at the most. If at all, they merely cause transient subfertility. 5. Beside steroids and several centrally active pharmaceutics (e.g. psychotropic drugs and several antihypertensive compounds), only siloxanes and methallibur seem to affect spermatogenesis via inhibition of gonadotropin secretion. Other antispermatogenic agents act by inhibition of mitosis (Colchicine, alkylating agents) or presumably via damage of the Sertoli cells. 6. Based on present knowledge, contraception in men could be principally managed by administration of a) androgens alone, b) gestagen/androgen combinations, c) estrogen/androgen combinations, d) certain antiandrogens. 7. The difficulties of contraception in men by steroid hormones or steroid hormone combinations have been pointed out. As regards the usefulness of antiandrogens for contraception, no definite conclusions can be drawn at the moment. All non-steroidal inhibitors of spermatogenesis which have been found up to the present are not suitable because of toxic effects.

Androgen Antagonists↗
PubMed1979

The relation between plasma oestrogen, progesterone and prolactin concentrations and the efficacy of vaginal prostaglandin E2 gel in initiating labour.

In an attempt to relate the efficacy of treatment to endogenous hormone levels, plasma oestrogen, progesterone and prolactin levels were analysed in women at term following the vaginal administration of prostaglandin E2 gel to induce labour. Patients who went into labour after treatment had significantly higher oestradiol-17 beta levels before treatment compared with those requiring formal surgical induction the following day. No difference could be demonstrated in levels of progesterone or prolactin in the two groups of patients. The significance of these results is discussed.

Estradiol↗
PubMed1979

Hormonal profiles in lactating and non-lactating women immediately after delivery and their relationship to breast engorgement.

Prolactin, human placental lactogen (HPL), oestrone, oestradiol and progesterone levels in plasma were measured before and during the first seven days after delivery in women who did not breast feed. The results confirmed the rapid clearance of placental steroids from the circulation after delivery. Plasma prolactin levels remained elevated during the early puerperium and the range of values were the same in non breast-feeding women and a group of breast feeding women. Of the 25 women studied, six developed breast engorgement. No difference in hormonal profiles were found leading to the conclusion that there is no endocrine basis for breast engorgement in non-breast feeding women.

Adult↗
PubMed1984

Rat pregnancy induces two suppressor cell activities.

Pregnancy in rat is able to stimulate two suppressor cell activities. One is specific to the paternal histocompatibility antigens and it resides in the T-lymphocyte population. The second is nonspecific and is of non-T nature. The use of various methods for pseudopregnancy and deciduoma installation has allowed the demonstration of two inducing circuits: (a) the presence of fertilized ova in the female genital tract and (b) the progestation hormonal status.

Animals↗
PubMed1979

Hormone serum levels and hormone receptor contents of endometria in women with normal menstrual cycles and patients bearing endometrial carcinoma.

Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (HPRL), 17 beta-estradiol (E2) and progesterone (P) were estimated in 46 subjects with normal menstrual cycles in whom hysterectomies were performed. Estrogen (ER) and progesterone receptor (PgR) levels in endometrial samples of these patients were estimated, and histological dating of the cycle day was carried out. Similarly, hormone serum levels and ER as well as PgR were estimated in 17 patients with endometrial carcinoma. No correlation between LH, FSH, HPRL and ER as well as PgR was noted in the normal subjects. Correlation between P and ER was observed in this group. Parallel variations between E2 and PgR were recorded in the normal females. In the carcinoma group no correlations between hormone serum levels and receptor contents were found, but ER and PgR correlated with each other. Receptor levels was highest in the well-differentiated group of endometrial carcinoma. The present experiments provide a rationale for progestagen therapy of carcinoma of the endometrium.

Endometrium↗