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PubMed1990

[Female sex hormones and thrombocytopoiesis].

The influence of estradiol, estriol and progesterone was studied on basic parameters of thrombocytopoiesis and thrombocytopoietic activity of plasmas of female rats. It was established that the investigated hormones increased highly the number of thrombocytes, the percentage of 75-selenomethionine incorporated in newly formed thrombocytes and the total number of megakaryocytes. Thrombocytopoietic activity of the plasma was raised considerably only in rats, injected with estradiol, but the remaining hormones did not induce significant changes in this activity. It is accepted that estradiol, estriol and progesterone stimulate thrombocytopoiesis of female rats by various mechanisms. Estradiol increases highly the formation of specific humoral regulator of thrombocytopoiesis--throbocytopoietin. The stimulating effect of estriol and progesterone is most probably nonspecific (thrombocytopoietin-independent), as the first hormone activates proliferation of megakaryocytes greatly, but the second hormone-the differentiation of these cells.

Animals↗
PubMed1986

[Study on the clinical evaluation of DHAS loading as a fetoplacental function test--effect of DHAS on estrogen metabolism at a fetoplacental unit].

To evaluate estrogen metabolism in the fetoplacental unit after dehydroepiandrosterone-sulfate (DHAS) injection to the mother, unconjugated estrone, estradiol, estriol and estetrol in maternal vein (MV), umbilical vein (UV), umbilical artery (UA) and amniotic fluid (AF) were measured after DHAS injection. Eighteen normal obstetric patients (37-39W) on whom was performed elective repeat cesarean section were injected with 100 mg of DHAS 30-60 minutes (7 cases), 120 minutes (6 cases), 180-240 minutes (5 cases) before delivery. The injection of DHAS to the mother resulted in a rapid marked rise in estradiol levels in MV (400% of control) and estrone levels in UV (1480% of control). The rise in estrone levels in MV was slower than that of estradiol. The increase in estradiol in UV and UA was significant, but the values were lower than that in MV. No significant changes in estriol levels in each compartment were demonstrated. However, a significant increase in estetrol was observed in each compartment by 4 hours. A significant correlation was found between individual MV and UV plasma estetrol concentrations. These results indicate that placenta secretes estrone and estradiol asymmetrically to maternal and fetal circulation after DHAS injection. Determination of the maternal estradiol and estetrol rise after DHAS injection may reflect placental and fetoplacental function, but estriol may not.

Dehydroepiandrosterone↗
PubMed1987

[Studies on the interrelation of fetal heart rate change, placental findings and fetal outcome].

The relation between antepartum fetal heart rate (FHR) non stress test (NST), maternal serum estriol, intrapartum FHR change, birth weight, placental findings and Apgar score were studied in 168 normal gestations and 36 high-risk pregnancies including 25 EPH-gestosis cases. The frequency of placental infarcts was higher in severe gestosis than in other high-risk pregnancies and normal gestation. Abnormal NST was more frequent in high-risk pregnancy than normal. Light for date (LFD) infants were more numerous in high-risk pregnancy than normal, and also frequent in the cases of placental infarcts. Particularly in high-risk pregnancy patients with abnormal NST and placental infarcts, 3 out of 5 showed LFD infants. Intrapartum fetal distress was more common in the cases of abnormal NST than normal. The five minute Apgar score was lower in the patients with abnormal NST and in the cases of placental infarcts than normal. The placental infarct ratio was higher in high-risk pregnancies with abnormal NST than normal. The maternal serum estriol level was not changed in cases of high-risk pregnancy, abnormal NST or placental infarcts when compared to normal gestation. The cases of succeeding fetal death, however, showed a low serum estriol level. In conclusion, antepartum abnormal NST suggests severe placental dysfunction caused by its infarcts and the prognosis is poor in patients with high-risk pregnancies, particularly EPH-gestosis. Coping with abnormal antepartum NST is regarded as important in fetal management.

Apgar Score↗
PubMed1981

[Endocrino-pharmacological study of reproduction: Role and biosynthesis of steroid hormones in the feto-placental unit].

Although considerable information is available concerning steroidogenesis in the human fetus, the function of the different steroids formed during pregnancy and the factors regulating this delicate hormones balance are poorly understood. During human pregnancy, the placenta synthesizes large quantities of progesterone, estradiol, estrone and estriol and secretes these hormones into both the maternal and fetal circulations; progesterone from maternal lipoprotein-cholesterol, estradiol and estrone from maternal and fetal dehydroepiandrosterone sulfate (DHAS), and estriol largely from fetal 16 alpha-OH-DHAS. It has been demonstrated that preimplantation blastocysts of several animal species have the capacity to accumulate steroids to pregnenolone to progesterone, and to interconvert estrone and estradiol. Estetrol (E4), 15 alpha-hydroxy derivative of estriol is an interesting compound, since its formation is relatively unique to fetal liver function. Of special interest is that placental sulfatase deficiencies result in an extension of the gestation, and Cesarean section has to be done. This raises the question of the role of estrogens in determining the onset of labor, much as in the case of anencephaly. In general, progesterone may decline prior to an abortion, but there has not been a direct application to clinical practice. Estrogen levels during pregnancy are influenced by factors other than fetal well-being and include fetal weight, placental enzyme function, fetal adrenal function, maternal intestinal flora, maternal renal excretion and maternal liver function. Although not yet extensively utilized, such a dynamic test as the infusion of DHAS may yield useful information within a short period in otherwise complicated cases related to fetal and placental function.

Androgens↗
PubMed1983

Abnormal estrogen conjugation in women at risk for familial breast cancer at the periovulatory stage of the menstrual cycle.

The present study was designed to establish whether women with a family history of breast cancer exhibit endocrine abnormalities which could be responsible for their increased risk for the disease. Plasma hormone levels were measured every second day throughout the menstrual cycle in 30 women at risk for familial breast cancer and in an equal number of matched controls. Thirteen of the 14 substances measured exhibited no differences between the two populations, but plasma androsterone sulfate was significantly lower in the high-risk subjects. Thirteen urinary hormones were measured every day throughout the cycle with only the mean estrone and estradiol glucuronide but not estriol glucuronide content being significantly lower in the high-risk subjects. A compensatory increase in the urinary estrogen sulfates was observed. Daily analysis of these differences showed that they were most pronounced in thry day throughout the cycle with only the mean estrone and estradiol glucuronide but not estriol glucuronide content being significantly lower in the high-risk subjects. A compensatory increase in the urinary estrogen sulfates was observed. Daily analysis of these differences showed that they were most pronounced in thry day throughout the cycle with only the mean estrone and estradiol glucuronide but not estriol glucuronide content being significantly lower in the high-risk subjects. A compensatory increase in the urinary estrogen sulfates was observed. Daily analysis of these differences showed that they were most pronounced in the periovulatory period of the cycle. These results suggest that the genetic risk for breast cancer is associated with an abnormality in estrogen conjugation at a specific time of the ovulatory cycle.

Androgens↗
PubMed1981

Betamethasone administration to the mother and problems in foeto-placental monitoring.

The administration of betamethasone to the mother in order to accelerate maturation of foetal lungs induces significant modifications in the foeto-placental hormonal secretion. Both the total estriol and unconjugated estriol present a sharp fall in the days immediately following the administration and a rise 10-12 days later, depending on a rebound effect. The HPL levels do not variate except for a progressive and constant rising due probably to better cardiocirculatory maternal condition with, consequently, a higher utero-placental blood-flow. All these phenomena increase when the administration of betamethasone to the mother is repeated more then once. The AA. believe that the sharp fall of the estriol doesn't represent a danger for the foetus being only an effect of maternal and fetal adrenal depression. Consequently the AA. suggest to drive the management during and after the administration of betamethasone to the mother on the basis of other foeto-placental functional tests, as cardiotocography. The results were analysed.

Betamethasone↗
PubMed2000

Hormonal placental function tests for fetal assessment in high risk pregnancies.

BACKGROUND: Biochemical tests of fetal well-being such as placental hormone levels have not always shown direct benefits for mothers and babies. OBJECTIVES: The objective of this review was to assess the effects of measuring placental hormone levels during high risk pregnancies. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group trials register and MEDLINE. We also contacted study authors. SELECTION CRITERIA: Adequately controlled trials comparing availability with no availability of hormone placental tests in high risk pregnancy. DATA COLLECTION AND ANALYSIS: Trial quality was assessed and data were extracted by two reviewers and this was checked by a colleague. Study authors were contacted for additional information. MAIN RESULTS: Two trials involving 3355 women were included. Methodological quality of the trials was acceptable, but results for only 230 out of 2733 women (abnormal hormone levels) were available from one trial. One trial compared oestriol levels reported promptly with levels measured but not reported. The overall perinatal mortality rate was 30.5 per 1000 live births weighing 500 grams or more. No beneficial effects of oestriol measurement on fetal outcome could be identified (odds ratio of perinatal death 0.87, 95% confidence interval 0.35 to 2.18). For abnormal test results only, the reported oestriol group showed a statistically non-significant trend to less perinatal mortality (odds ratio 0.48, 95% confidence interval 0.15 to 1.60). The other trial compared human placental lactogen measurements reported promptly with measurements not reported until after pregnancy. For abnormal test results, the reported group showed significantly less perinatal mortality with four (3.4%) deaths compared to 17 (15%) in the control group (odds ratio 0.25, 95% confidence interval 0.10 to 0.61). Data from normal test results was not available for this trial. REVIEWER'S CONCLUSIONS: The measurement of human placental lactogen levels may be of some value in high risk pregnancies, but there is not enough evidence to evaluate the use of hormone placental tests generally.

Female↗
PubMed1988

Effect of various steroids on the biosynthesis of arachidonic acid in isolated hepatocytes and HTC cells.

The effect of various steroids on the incorporation and desaturation of eicosa-8,11,14-trienoic acid in normal hepatocytes and HTC cells was investigated. After 3 hr incubation with 11-deoxycorticosterone, both kinds of cells showed an increase in the incorporation of eicosatrienoic acid. In contrast, progesterone, cortexolone, 17-beta-estradiol, testosterone, estriol, aldosterone, corticosterone, dexamethasone, dehydroepiandrosterone, 11-beta-hydroxyandrosterone, 11-ketoaetiocholanolone, epiaetiocholanolone and 5-beta-pregnane-3 alpha,20 alpha-diol, provoked no significant changes in the uptake of the exogenous acid. Of all the steroids tested, only 11-deoxycorticosterone, dexamethasone and 17-beta-estradiol evoked a significant inhibition on the arachidonate biosynthesis in both kinds of cells. Testosterone, estriol, aldosterone and corticosterone provoked a significant inhibition of delta 5-desaturase in HTC cells. In dexamethasone, this effect was dose-dependent (0 to 10(-4) M). Simultaneous incubation with 17-beta-estradiol or 11-deoxycorticosterone with dexamethasone led to an extent of inhibition on arachidonate biosynthesis that did not surpass the effect of each drug. Pretreatment of isolated hepatocytes with the antiglucocorticoid, cortexolone, prevented the dexamethasone-induced inhibition of arachidonate biosynthesis. Normal rat liver microsomes preincubated in vitro with dexamethasone, 11-deoxycorticosterone, 17-beta-estradiol, corticosterone or estriol (10(-6) or 10(-4) M concentration), showed no significant changes in the delta 5-desaturase activity. The results obtained suggest that the effect of the steroids on arachidonic acid biosynthesis in normal hepatocytes and HTC cells requires receptor occupancy and probably is mediated through a common biochemical mechanism.

8,11,14-Eicosatrienoic Acid↗
PubMed1998

Long-term effects of continuous combined HRT on bone turnover and lipid metabolism in postmenopausal women.

This study was undertaken to investigate the effect of 10 years of hormone replacement therapy (HRT) on bone turnover and lipid metabolism in postmenopausal women. The single-centre trial was initiated as a 1-year, double-masked, randomized, parallel-group study of continuous combined HRT with 2 mg 17 beta-estradiol and 1 mg norethisterone acetate administered once daily with or without 1 mg estriol. Following preliminary results which showed no difference between the addition and omission of estriol, patients continued on an open-label extension phase of continuous combined HRT without estriol for a further 9 years. Of the 52 women who entered the original double-masked study, 32 entered the open-label extension phase. The 10-year analysis was based on 27 patients. Major increases in bone mineral density (BMD) of the lumbar spine were seen during the first 3 years of treatment, remaining statistically significant compared with baseline at all visits throughout the 10-year follow-up (p < or = 0.025). Statistical modelling confirmed that there were no decreases in BMD after these initial increases. BMD remained 5.5% higher than baseline values after 10 years of continuous combined HRT. Mean total cholesterol levels were significantly reduced after 10 years of therapy (p = 0.012), with no significant changes in serum triglyceride and low-density lipoprotein (LDL)-cholesterol levels from baseline values at this time. High-density lipoprotein (HDL)-cholesterol levels, however, were reduced by 15.4% (p < 0.001). In conclusion, 10 years of continuous combined HRT resulted in a significant and sustained increase in BMD. This treatment regimen therefore appears to be well suited for the long-term prevention of osteoporosis in postmenopausal women.

Adult↗
PubMed1975

On the regulation of fetal and maternal 16 alpha- hydroxydehydroepiandrosterone and its sulfate by cortisol and ACTH in human pregnancy at term.

In studying the mechanisms which govern estriol production in human pregnancy at term, 16 alpha OH-DHEA, 16alpha-OH-DHEA sulfate, and unbound unconjugated cortisol were measured in peripheral venous plasma of 28 healthy women and in cord venous and arterial plasms of their newborn infants at the time of elective cesarean section prior to the onset of labor. In eight cases treated with 150 mg. of cortisol, maternal and cord plasma 16alpha-OH-DHEA and its sulfate were considerably lower than in 10 control cases. Approximately 4 to 8 1/2 hours after injection of 40 I.U. of Depot-ACTH, both of these estriol precursors were also significantly decreased. It is concluded from these experiments that cortisol causes a decrease of estriol mainly by suppressing fetal 16alpha-OH-DS.

Adrenocorticotropic Hormone↗
PubMed1977

Effect of pregnancy hormones on herpesvirus and other deoxyribonucleic acid viruses.

Clinical impressions and observations of genital herpesvirus infections indicate that lesions are more persistent and more severe during pregnancy. Several explanations are possible: an altered immune state, increased vascularity and blood flow, and/or increased viral infectivity due to increase in one or more hormones during pregnancy. Studies presented here were directed toward investigating the latter possibility. Herpesvirus, type 2, isolated from a genital lesion was titrated in WI-38 cells in the absence and presence of estriol, progesterone, human chorionic gonadotropin (hCG) and human placental lactogen. Two other deoxyribonucleic acid (DNA) viruses, adenovirus type 7 and vaccinia virus, were included for control purposes. Although estriol significantly inhibited and hCG significantly enhanced the single-cycle production of herpesvirus, there was little or no effect on these hormones on adenovirus. Progesterone, after 48 hours but not after two hours of preincubation, inhibited production of herpesvirus and vaccinia virus but had no effect on aderiovirus. When end-point titers were measured after multiple cycles of viral growth, there were no differences in viral titers with any of the hormones, except for a slight reduction with estriol. Except for the uniform effect of progesterone on DNA viruses, hormonal effects on viral production cannot be generalized from experiments with one virus.

Adenoviruses, Human↗
PubMed1987

Pharmacology and pharmacokinetics of estrogens.

The primary source of estrogen, ovarian 17 beta-estradiol, is normally converted to estrone and estriol, both of which are metabolized to their sulfate and glucuronide forms, as well as oxidated to nonestrogens. In postmenopausal women, the primary sources of estrogen are nonovarian, including the production of androstenedione from the adrenal cortex and its metabolism to estrone by the liver, adipose tissue, skeletal muscle, kidney, brain, and hair follicles. Estrogen circulates bound to sex hormone-binding globulin and albumin. The sulfate form may be a storage form of this hormone and is freely converted back to estrone and estriol. The glucuronide and sulfate forms have limited cell penetration; they are excreted mainly in the kidney, with little tubular reabsorption. Several theories have been advanced to explain the effects of estrogens on the basis of their receptors. A consideration of pharmacologic and pharmacokinetic characteristics reveals specific advantages and disadvantages of the preparations currently available for estrogen replacement therapy. Oral agents have the disadvantage of being subject to a considerable first-pass hepatic effect, resulting in their conversion to estriol, oxidation to nonestrogens, and conjugation to sulfate and glucuronide salts. These preparations can also be associated with poor patient compliance, as can injectable, topical, or suppository preparations. On the other hand, transdermal patches are not subject to a first-pass hepatic effect, provide relatively uniform serum levels, and may help alleviate the problem of noncompliance.

Estradiol↗
PubMed1990

Characterization of [3H]estradiol-17 beta-(beta-D-glucuronide) binding sites in basolateral and canalicular liver plasma membranes.

The specific binding of [3H]estradiol-17 beta-(beta-D-glucuronide) ([3H]E217G) was examined in isolated basolateral (bLPM) and canalicular (cLPM) liver plasma membranes. Two distinct binding sites were identified in each membrane fraction by competition and saturation experiments. Binding parameters obtained from competition studies were: Kd1 = 26 nM, Bmax1 = 0.26 pmol/mg protein; Kd2 = 2.6 microM, Bmax2 = 27 pmol/mg protein for bLPM; and Kd1 = 81 nM, Bmax1 = 0.61 pmol/mg protein; Kd2 = 6.7 microM, Bmax2 = 79 pmol/mg protein for cLPM. Binding parameters obtained from saturation experiments were not significantly different. There was no Na+ requirement for binding. Kinetic dissociation experiments showed that binding was reversible and revealed two components. The dissociation rate constants did not vary with the method of dilution of radioligand, i.e. by "infinite" volume, or excess unlabeled ligand, thus ruling out the possibility of cooperativity. The ability of a series of compounds to inhibit the binding of [3H]E217G was also examined. In bLPM, taurocholate (TC), estrone sulfate (E1SO4) and bromosulfophthalein (BSP) were able to compete with both binding sites, whereas estriol-17 beta-(beta-D-glucuronide) (E317G), estriol-16 alpha-(beta-D-glucuronide) (E316G), testosterone glucuronide (TG), estradiol-3-(beta-D-glucuronide) (E23G), estriol-3-(beta-D-glucuronide) (E(3)3G), cholate and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) were able to inhibit binding to only the low-affinity site. In cLPM, only the cholestatic steroid D-ring glucuronides (E(3)17G, E(3)16G and TG) and TC were able to compete with both sites, whereas the non-cholestatic steroid A-ring glucuronides (E(2)3G and E(3)3G), BSP and DIDS competed for only the low-affinity site. Based on the observed substrate specificities, the low-affinity sites in bLPM and cLPM are postulated to represent multispecific organic anion carriers. The high-affinity site in cLPM may play a role in mediating steroid D-ring glucuronide-induced cholestasis.

Animals↗
PubMed1981

Effect of ACTH infusion on induction of uterine contraction in prolonged human pregnancy in association with endocrine function.

The role of hormonal interactions in the mechanism initiating labor in women was studied. The serum levels in women was studied. The serum levels of cortisol, progesterone, estradiol estriol, human chorionic somatomammotropin, and prolactin were measured simultaneously before, during and after infusion of ACTH at a rate of 50 microgram/h in 100 ml of physiological saline or infusion of physiological saline without ACTH (as control) at a rate of 100 ml/h into 14 pregnant women of 10 days or more beyond term. In five (group A) of the 10 women infused with ACTH. uterine contractions were induced within 5-15 min after beginning of ACTH infusion. Although the serum progesterone levels in group A were slightly, but not significantly, lower than those in the other five women (group B) in whom uterine contractions were not induced, the ratio of progesterone to estriol was 13/1 in group A and 18/1 in group B, respectively (P less than 0.05). The endocrine levels in group A may be favorable for the initiation of uterine contraction. The serum cortisol levels in group A were higher, but not significantly higher, than those in group B after ACTH infusion. And the serum estriol levels 6 h after ACTH infusion were significantly lower than control levels before ACTH infusion (P less than 0.01 in group A, P less than 0.05 in group B). To the contrast, in all the four control women infused with physiological saline only (group C), neither uterine contractions nor changes in the serum levels of ACTH and cortisol were found. This work may show that ACTH infusion induced uterine contractions by increased corticosteroids via placenta in lower ratio of progesterone to estrogen but it does not provide any precise information on the mechanism of initiation of human labor.

Adrenocorticotropic Hormone↗
PubMed1986

The molecular structure of 16 alpha-iodo-17 beta-estradiol, a high affinity ligand for the estrogen receptor.

16 alpha-Iodoestradiol is an estrogenic steroid with high affinity for the estrogen receptor. When labelled with a gamma emitting isotope, such as 125I, the resulting radioactive steroid is an excellent ligand for the sensitive analysis of the estrogen receptor. The X-ray study of the crystal structure of 16 alpha-iodoestradiol reveals that the bond distances and angles of the iodinated estrogen are similar to those of estradiol and estriol. The substitution of iodine for the 16 alpha-hydroxyl group has little effect on geometric and electronic properties of the molecule and does not interfere with the hydrogen bonding ability of the 17 beta-hydroxyl group. The difference in receptor binding affinity between 16 alpha-estradiol and estriol may be due to competition for intermolecular hydrogen bond formation between the hydroxyls at C(16) and C(17) on estriol. X-Ray data indicate that the 16-hydroxyl can form significantly shorter and presumably stronger hydrogen bonds.

Chemical Phenomena↗
PubMed1978

Separation of estrogen conjugates by high pressure liquid chromatography.

High pressure liquid chromatography using a prepacked commercial strong anion exchanger column (mu Partisil 10 SAX, 25 cm x 4.6 mm) was used to separate a mixture of eight estrogen conjugates. Chromatographic conditions using a 0.01 M potassium phosphate or 0.1 M NaCl as solvent in the isocratic mode are described for the separation of estrone glucosiduronate, 17beta-estradiol-3-glucosiduronate, 17beta-estradiol-17-glucosiduronate, estriol-3-glucosiduronate, estriol-16alpha-glucosiduronate, estriol-17-glucosiduronate, estrone sulfate and 17beta-estradiol-3-sulfate. This system gives high resolution of the estrogen conjugates in small eluent volumes in less than 30 min. The advantages of this high pressure liquid chromatographic system over other methods of separation are discussed.

Chromatography, High Pressure Liquid↗
PubMed1992

Progesterone and estradiol suppress human mononuclear cell cytotoxicity.

Fetal trophoblast is generally resistant to lysis by cytotoxic cells. We hypothesized that progesterone and estrogens secreted by the trophoblast act at the choriodecidual interface where they are present in high concentrations to provide a local, paracrine immunosuppressive effect on cellular cytotoxicity. Using peripheral blood mononuclear cells as effector cells in a cytotoxicity assay, we evaluated the effects of progesterone, estrone, estradiol and estriol, either alone or in combination, on cellular cytotoxicity. Both progesterone and estradiol suppressed cytotoxicity in a dose-dependent manner. Estrone, estriol, pregnenolone and cholesterol had no effect. A synergistic suppression of cytotoxicity was observed when estrone, estradiol, estriol and progesterone were combined. We speculate that trophoblast production of progesterone and estradiol may be an important local immunosuppressive mechanism contributing to fetal survival.

Cells, Cultured↗