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PubMed1995

Salivary estriol as risk assessment for preterm labor: a prospective trial.

OBJECTIVE: Increased understanding of human parturition allows for novel approaches to (1) identification of women at increased risk for preterm birth and (2) development and controlled testing of etiology-based strategies to prevent preterm birth. STUDY DESIGN: Five hundred forty-two women were enrolled at five study sites in a prospective evaluation of salivary estriol in samples obtained weekly beginning at 22 weeks' gestation (Salest, Biex, Inc., Boulder, Colo.). Estriol concentrations were determined with a well-characterized enzyme-linked immunoassay. Women adjudged at either high risk or low risk for prematurity were evaluated through to delivery. RESULTS: A total of 267 women submitted serial samples that were analyzed; 241 women with singleton pregnancies submitted sufficient samples. Twenty-three women with singleton fetuses went into idiopathic preterm labor (without prior rupture of membranes) and were delivered preterm (mean 35 weeks' gestation); 182 were delivered at term (> or = 37 weeks' gestation). Mean (geometric) estriol concentrations were higher from 24 to 34 weeks in women with singleton pregnancies delivering preterm (p < 0.05). A surge in estriol concentrations occurred approximately 3 weeks before the onset of labor in both women delivering at term and those delivering preterm. This increase occurred approximately 4 weeks earlier in women delivered preterm versus term. Receiver-operator curve analyses showed that exceeding a 2.3 ng/ml saliva estriol level was associated with occurrence of preterm labor (71% sensitivity, 77% specificity, 23% false-positive rate). CONCLUSION: Detection of an early estriol surge or increased level (> or = 2.3 ng/ml) may be clinically helpful in identifying women at elevated risk for preterm labor and birth, allowing for evaluation of biologically based interventions in controlled trials.

Adult↗

PubMed1981

Effects of prostaglandin F2 alpha or oxytocin on serum estriol and its conjugates during induced labor.

Twelve patients underwent induction of labor at term, seven by prostaglandin F2 alpha (PGF) and five by oxytocin infusion. Serum samples were drawn before induction and at two hour intervals after infusion was started, throughout labor. The samples were analyzed for estriol (E3) and its principal conjugates, estriol-3-sulfate (E3-3S), estriol-16-glucosiduronate (E3-16G), estriol-3-glucosiduronate (E3-3G), and estriol-3-sulfate-16-glucosiduronate (E3-SG). No significant changes occurred before eight hours of infusion. Two pre-eclamptic patients showed a 100% increase in serum E3 while receiving PGF. The increases correlated best with rising levels of E3-SG. None of the five pre-eclamptic patients given oxytocin showed this striking changes. These observations raise the possibility that PGF may alter the metabolism of estriol in pre-eclamptic patients, during labor.

Estriol↗

PubMed1991

Estrogenic action of estriol fatty acid esters.

Recent studies suggest that, estriol, like estradiol, is biosynthetically esterified with fatty acids. We have synthesized the stearate estriol, at C-16 alpha, C-17 beta and the diester, C-16 alpha,17 beta and tested these D-ring esters for their estrogenic action both in vivo and in vitro, comparing them to estradiol, estriol and estradiol-17-stearate. None of the estriol esters bind to the estrogen receptor. They are only weakly estrogenic in a microtiter plate estrogen bioassay: stimulation of alkaline phosphatase in the Ishikawa endometrial cells. However, both estriol monoesters are extremely potent estrogens when injected subcutaneously (in aqueous alcohol) into ovariectomized mice. Compared to the free steroids, they produced a dramatically increased uterine weight with a greatly prolonged duration of stimulation. The 16 alpha,17 beta-diester also induced a protracted uterotrophic response, but the stimulation of uterine weight was comparatively low. Since the esters of estradiol and estriol do not bind to the estrogen receptor, their estrogenic signal must be generated through the action of esterase enzymes. These naturally occurring esters have the potential of being extremely useful pharmacological agents for long-lived estrogenic stimulation.

Alkaline Phosphatase↗

PubMed1984

ELISA for salivary and plasma estriol in pregnancy.

A competitive, sensitive, and rapid enzyme-linked immunoadsorbent assay (ELISA) was developed for the determination of estriol in saliva and in plasma. Horseradish peroxidase (HRP) was used as the label enzyme; separation between free and bound steroid was carried out by insolubilized antibody prepared by adsorbing purified IgG of rabbit anti-6-oxoestriol-6-(O-carboxymethyl)oxime-BSA on polystyrene balls. The enzyme activity was measured by a colorimetric reaction using o-phenylenediamine dihydrochloride and hydrogen peroxide as substrate. The sensitivity of the assay was 12 pg/tube. In order to compare ELISA to RIA estriol estimations in different biological fluids, we selected six women during normal pregnancy, from the 30th to the 40th week of gestation. Salivary estriol was assayed by direct and extraction methods, while the corresponding plasma samples of the same subjects were analyzed only for unconjugated estriol by an extraction method. A good agreement was found between the results obtained by RIA and ELISA: r = 0.897, p less than 0.001 between direct RIA and direct ELISA in saliva; r = 0.909, p less than 0.001 between extraction RIA and direct ELISA in saliva; and r = 0.916, p less than 0.001 between extraction RIA and extraction ELISA in plasma. A good correlation (r = 0.793, p less than 0.001) was present between plasma samples by RIA and saliva samples by ELISA (direct method). These results indicate that: ELISA is a reliable method for the determination of estriol in plasma and saliva. Saliva samples can be used for the assay of estriol and therefore for the assessment of fetal conditions during pregnancy.

Enzyme-Linked Immunosorbent Assay↗

PubMed2002

Regulatory effects of estriol on T cell migration and cytokine profile: inhibition of transcription factor NF-kappa B.

The protective role of pregnancy in autoimmune conditions, such as multiple sclerosis (MS), is potentially associated with immune regulation by sex hormones produced during pregnancy. This study was undertaken to examine the regulatory effects of estriol on the T cell functions, including transmigration and the cytokine production. The results revealed for the first time that estriol significantly inhibited T cell transmigration at a concentration range typical of pregnancy, which correlated with decreased T cell expression of matrix metalloproteinase-9. Estriol was also found to alter the cytokine profile of T cells toward Th2 phenotype by up-regulating the production of IL-10 and inhibiting TNFalpha secretion of T cells. However, the inhibitory effects of estriol on T cells were not antigen-dependent. Further characterization indicated that estriol inhibited nuclear transcription factor kappa B (NF-kappa B), which controls a variety of immune-related genes. This study provides new evidence that estriol is a potent regulator for the T cell functions potentially through its interaction with the NF-kappa B signaling pathway.

Adult↗

PubMed2002

The effects of oral estriol on the endometrium in postmenopausal women.

OBJECTIVES: To study the long-term effects of oral estriol tablets on the endometrium of postmenopausal women by TVS and histology. METHOD: This was a cross sectional, parallel-group, multicenter trial of 241 postmenopausal women, out of whom 125 were treated with oral estriol and 116 were untreated controls. Endometrial histology using Pipelle biopsies and/or dilatation and curettage (D&C) was taken, endometrial thickness was assessed by use of transvaginal ultrasound (TVS), and the relation between endometrial thickness and histology was calculated. RESULTS: No statistically significant differences between the two groups were found in endometrial histology. There were found more polyps in the oral estriol group (14.0%) as compared with the control group (2.9%). The mean endometrial thickness in the oral estriol group was 3.0 mm compared with a mean value of 2.4 mm in the control group: P=0.01. CONCLUSIONS: No clinically relevant difference was found between the endometrium status (assessed by histology and TVS) of postmenopausal women on long-term oral estriol therapy and untreated controls. This trial supports the endometrial safety of maintenance treatment with oral estriol tablets. However, there are signs, not statistically significant, that may be associated with more endometrial polyps in postmenopausal women than if therapy is not given and that TVS is a useful instrument for the diagnosis.

Administration, Oral↗

PubMed1985

Daily variation of serum unconjugated estriol and estetrol in normal pregnancy.

Serum unconjugated estriol and estetrol were assayed daily in seven nondiabetic, uncomplicated third-trimester pregnancies to define the daily variation of these compounds. When compared to the mean of the three preceding days' values, or to the highest mean of three consecutive daily values previously obtained in a pregnancy, daily estriol and estetrol values fell greater than or equal to 40% on 1.2 and 0% of occasions, respectively. Isolated estriol values represented falls of greater than or equal to 40% from previously obtained single estriol values on 2% of occasions, and no isolated estetrol values fell greater than or equal to 40% from any other isolated values obtained in a given pregnancy. These results define the stability of daily serum estriol and estetrol in late-gestation normal pregnancy, although they emphasize the large variability encountered when comparing isolated estriol values.

Circadian Rhythm↗

PubMed1977

Clinical and experimental aspects of the anti-mammary carinogenic activity of estriol.

Intermittent implantation of 600--1,300 microgram estriol subcutaneously beginning 48 h before oral administration of 7,12-dimethylbenz(a)anthracene or procarbazine prevents development of 80--90% of carcinomas of the breast occurring during the natural life span of the intact female Sprague-Dawley rat. Some estriol precursors were less inhibitory of breast cancer development among 23 other estrogens and androgens, progestins and glucocorticoids tested. More frequent or lower estriol doses than 100--200 microgram/kg/24 h every 2 months were less inhibitory of breast carcinogenesis. No other types of neoplasms were reduced in incidence by estriol implants, which also reduced uterine weights by 20--25%. Intermittent substitution of estriol for estrone or estradiol in the nuclear receptor complexes of target cells probably accounts for these observations, which resemble the effect of castration in reducing breast cancer incidence. Human studies indicate excellent tolerance for oral estriol doses of 10--200 microgram/kg/24 h, which may correct subnormal estriol/estrone + estradiol urinary quotients associated with elevated risk of breast carcinogenesis in epidemiologic investigations.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1976

Temporal relationships between hormone receptor binding and biological responses in the uterus: studies with short- and long-acting derivatives of estriol.

The temporal relationships between hormone receptor binding and early and late biological responses in the uterus were examined using estriol (E3), a weak estrogen, and several more long-acting estriol derivatives, namely ethinyl estriol (EE3), estriol cyclopentyl ether (E3CPE), and ethinyl estriol cyclopentyl ether (EE3CPE). Dose-response curves of 3-day uterotrophic assays indicate that biological potency follows the order EE3CPE greater than EE3 or estradiol greater than E3CPE greater than E3. After a single injection of 5 mug of compound, E3 elicits the early uterotrophic responses (increased uterine wet weight and 2-deoxyglucose phosphorylation at 2-6 h) but gives only weak stimulation of later uterotrophic responses (enhanced rates of 2-deoxyglucose phosphorylation at 20-24 h and increased DNA synthesis rate and uterine weight over a 72 h period). E3, EE3, and estradiol all elicit a rapid (maximal by 1/2-1 h) uptake of receptor into the nucleus and show an equivalent wet weight response at 3 h. After E3, nuclear receptor levels and uterine weight decline rapidly; however, after EE3 or estradiol, nuclear receptor levels decline less rapidly remaining at least two-fold above the control until 24-48 hr, and uterine weight also remains elevated for at least 48-72 h. EE3CPE elicits both the early (4 h) and later (20-24 h) waves of glucose metabolism, shows a prolonged effect on DNA synthesis rate, and shows the most dramatic and prolonged (beyond 72 h) maintenance of elevated uterine weight and high nuclear receptor (beyond 24 h). Thus, chemical modifications of the estriol molecule which result in a prolonged stimulation of uterine growth and metabolism also result in a long-term maintenance of hormone-receptor complex in the uterine nucleus. These studies give strong support to the concept that true uterine growth requires the direct and prolonged influence of the nuclear estrogen-receptor complex.

Animals↗

PubMed1977

Estriol conjugates in human breast cyst fluid and in serum of premenopausal women.

A sensitive method was developed for the assay of the four major estriol (E3) conjugates in human breast cyst fluid and in serum during the menstrual cycle. In the cyst fluid, estriol-3-sulfate (E3-3S) was found in each of ten samples, the concentrations ranging from 240-4310 pg/ml. Estriol-16-glucosiduronate (E3-16G) was detected in six samples at levels of 19-153 pg/ml; estriol-3-glucosiduronate (E3-3G) in five samples, 13-79 pg/ml and estriol-3-sulfate-16-glucosiduronate (E3-3S-16G) in four samples, 28-152 pg/ml. Unconjugated estriol was found in three of the ten cases (12-30 pg/ml). Serum samples obtained in the follicular and luteal phases of the cycle from eight different subjects were assayed in the same way. There was considerable variation between subjects and many values were indistinguishable from zero. But preliminary data suggest that E3-3G is the predominant E3 conjugate in the serum and E3-3S-16G is quantitatively least important. It appears that E3 conjugates in the cyst fluid are not derived from the blood directly, but are produced locally from precursors which have not been identified.

Adult↗

PubMed1979

Human chorionic somatomammotropin, estriol and oxytocinase as indexes of fetal growth.

A group of 56 women with high risk pregnancies were studied since the 32nd week of gestation. With the aim of obtaining reliable fetal growth indicators, maternal serum hCS, estriol and oxytocinase levels were determined. hCS and estriol were determined by specific radioimmunoassays and oxytocinase with a colorimetric method. Mean values obtained the week before delivery of both hormones and the enzyme were correlated with the weight of the newborns. The correlation coefficients were 0.30, 0.33 and 0.30 for hCS, estriol and oxytocinase respectively (Figs. 2, 3 and 4). The newborns were classified into two groups, small for date and adequate weight for gestational age. Maternal hCS level corresponding to newborns with adequate birthweight for their gestational age was 7.94 ug/ml. This value was statistically higher than that corresponding to the group of small-for-date newborns, which was 5.15 ug/ml (Fig. 5). Similar results were obtained when the maternal estriol levels were considered according to the birthweight (Fig. 7). The same analysis applied to oxytocinase values did not show statistically significant differences. Arbitrary critical levels were established for hCS and estriol at 7 ug/ml and 35 ng/ml respectively. When values were below these levels, newborns would have greater possibility of being small for dates (Figs. 6 and 8). The predictive value was best when both hormones were considered concomitantly (77%) (Fig. 9). These results indicate the suitability of considering hCS and estriol levels in order to assess fetal growth.

Aminopeptidases↗

PubMed1995

Effects of danazol and medroxyprogesterone acetate on estrogen-(estradiol and estriol) specific binding sites in rabbit uterus.

In rabbit uterus, the presence of separate specific binding sites for not only estradiol but also estriol has been proposed. These sites may be correlated with an antiestradiol effect. Therefore, this study was designed to investigate the effect of antiestrogenic agents such as danazol and medroxyprogesterone acetate (MPA), especially on the estriol binding sites. Danazol and MPA in combination with estradiol were administered subcutaneously to immature female rabbits daily for 10 days, and resulted in a significant (p < 0.05) decrease in uterine weight and estradiol binding sites in the uterus. Treatment with MPA significantly (p < 0.05) decreased the level of estriol binding sites, but treatment with danazol resulted in this to a minimal extent in the uterus primed by estradiol. MPA did not bind to estradiol and estriol binding sites, while danazol at a high concentration bound to estriol binding sites with some affinity, but not to estradiol binding sites in the uterine cytosol of estrogen-primed rabbits. These results suggest that within the antiproliferative effect of danazol and MPA (an antiestrogenic action on estrogen-stimulated uterine growth) there are likely to be specific differences between some of the possible mechanisms of danazol and MPA in their action at the estriol binding site.

Animals↗

PubMed1997

Biochemical and histological effects of vaginal estriol and estradiol applications on the endometrium, myometrium and vagina of postmenopausal women.

Estrogen and progesterone receptors in the cytosol (ERc, PRc) and estrogen receptors in the nuclear compartment (ERn) were measured in the endometrium, myometrium and vagina of 29 postmenopausal women who underwent hysterectomy. The effects of vaginal estriol (0.5 mg daily) compared to 17 beta-estradiol (0.05 mg daily) therapy on these receptor levels were studied. In addition, the endometrium was examined by light microscopy for estrogenic stimulation. We found biochemical and histological signs of estrogenic stimulation in all three tissues after estradiol as well as estriol therapy. In the vagina the effect of both estrogens on the ERc concentration was different from that in the endometrium and myometrium. The effects of estradiol and estriol on the ERn were comparable in all three tissues. The PRc levels increased significantly in all tissues after estrogen therapy; in the myometrium it was significantly higher after estriol than after estradiol applications. In conclusion, there were no clear differences between vaginal estradiol and estriol medication with regard to the effects on receptor levels in vaginal and uterine tissues. In the histological studies at the light microscopy level similar signs of estrogen stimulation of the endometrium were found following estradiol and estriol medication.

Administration, Intravaginal↗

PubMed1999

The metabolic effects of estriol in female rat liver.

The effects of estriol on oxygen uptake, glucose release, lactate and pyruvate production, beta-hydroxybutyrate and acetoacetate production in perfused rat liver as well as, carbon uptake in rat liver and intracellular calcium in isolated Kupffer cells were investigated. Basal oxygen consumption of perfused liver increased significantly in estriol or ethanol-treated rats. But these increased effects were blocked by gadolinium chloride pretreatment. In a metabolic study, pretreatment with estriol resulted in a decrease in glucose production and in glycolysis while an increase in ketogenesis. A more oxidized redox state of the mitochondria was indicated by increased ratios of perfusate [lactate]/[pyruvate] and decreased ratios of perfusate [beta-hydroxybutyrate]/[acetoacetate]. Carbon uptake of Kupffer-cell increased significantly in estriol-treated rats. But these increased uptake were not shown in rats pre-treated by gadolinium chloride blocking phagocytosis. In isolated Kupffer cells from estriol-treated rats, intracellular calcium was more significantly increased after addition of lipopolysaccharide (LPS) than in controls. These findings suggest that the metabolic effects of estriol (two mg per 100 mg body wt) can be summarized to be highly toxic in rat liver, and these findings suggest that oral administration of estrogens may induce hepatic dysfunctions and play a role in the development of liver disease.

3-Hydroxybutyric Acid↗

PubMed1986

Salivary estriol as an index to fetal wellbeing.

We adapted two commercially available kits for measuring serum estriol to use in assaying salivary estriol in the third trimester of pregnancy. Salivary estriol increases during gestation, as does unconjugated estriol in serum. With a meticulous collection protocol, fetal wellbeing can be monitored as successfully with saliva samples as with serum. A fetal demise was charted similarly by the salivary and the serum estriol assay. Inter- and intra-assay reproducibility (CV) of the saliva assay was 6.2%. Day-to-day CV, based on a fasting sample before breakfast but obtained 1 to 3 h after rising, was 14.8% (SD 5.8%). Values for salivary estriol obtained immediately after ingestion of food or drink dropped by 19.0% (SD 17.9%) and 32.1% (SD 21.9%), respectively, as compared with values determined immediately before intake of food or water.

Adolescent↗

PubMed1983

Preliminary isolation of urinary placental estriol before gas or liquid chromatography.

We describe a rapid, simple assay for placental estriol in urine, involving a small sample volume (250 microL) and, correspondingly, a small amount of enzyme reagent. After hydrolysis, estriol is adsorbed from urine onto graphitized carbon black (Carbopack B). After some washing steps, estriol is desorbed with a small volume of a suitable mobile phase. This single-step purification technique is rapid (about 15 min), with minimal sample manipulation. Analytical recoveries for estriol-supplemented urine ranged from 95.9 to 101.0%. Ten replicate analyses of urines containing typical concentrations of estriol gave CVs of 3.3, 2.6, and 2.4% for low, medium, and high concentrations, respectively. The specificity of our extraction technique was good, as assessed by treating 35 urine samples and quantifying estriol by gas chromatography with packed and capillary columns and by liquid chromatography with ultraviolet and fluorometric detection.

Chromatography, Gas↗

PubMed1983

Plasma unconjugated estriol as an indicator of fetal dysmaturity in postterm pregnancy.

The role of twice-weekly plasma unconjugated estriol determinations in the prediction of fetal dysmaturity was studied in 663 patients seen at the Postdates Clinic of the Los Angeles County/University of Southern California Medical Center. The correlation between estriol and gestational age was - 0.055. According to the criteria of the Postdates Clinic protocol, sensitivity, specificity, predictive values of positive results, and those of negative results of estriol determinations in predicting fetal dysmaturity were 44.4, 80.6, 32.9, and 87.1%, respectively. The major deficiency of this test for the detection of fetal dysmaturity was in the less-than-ideal predictive value of a negative result: 13% of patients who had normal estriol values had dysmature infants. When estriol was less than 12 ng/ml and the value fell more than 20% from the previous level, the predictive value of fetal dysmaturity was 56%. In these circumstances, the termination of pregnancy is a reasonable consideration. Until a more sensitive test for fetal dysmaturity is developed, plasma unconjugated estriol determination will retain its role as a screening test in managing postterm pregnancies in a large obstetric population.

Estriol↗

PubMed1978

Plasma estriol vs. estrogen assays in 24-h urines as an index to fetal status.

Conventionally, urinary estrogens are measured to monitor fetal well-being in the third trimester of pregnancy. There are many theoretical and practical advantages to the use of recently introduced plasma estriol assays; consequently, we undertook to compare the results of a spectrophotometric assay for total urinary estrogen with values for plasma total and free (unconjugated) estriol obtained by radioimmunoassay with commercially available kits. The data correlate well, r = 0.70 for plasma total estriol with urinary estrogen (expressed as milligrams of estrogens per gram of creatinine [E/C]), r = 0.79 for plasma free estriol with E/C, and r = 0.71 between the two plasma values. Minute-to-minute fluctuations during 90 min and day-to-day fluctuations followed during five days suggest that fluctuations of up to +/- 45% are within the normal range (means +/- SD of the day-to-day fluctuations were 16.9 +/- 7.7% and 15.6+/- 8.2%). Turn-around time is a minimum of 29 h for the urinary estrogen assay, 4.5 h for the plasma total estriol, and 3 h for the plasma free estriol.

Estriol↗