SEARCH · PubMed Health

Results for “ESTRIOL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

PubMed1980

An assay for urinary estriol-16 alpha-glucuronide based on antibody-enhanced chemiluminescence.

An immunoassay for estriol-16 alpha-glucuronide in pregnancy urine is described that utilizes antibody-enhanced chemiluminescence. The steroid glucuronide was covalently conjugated with the chemiluminescent marker aminobutyl-ethyl-isoluminol. The light yield of this conjugate upon oxidation was augmented by specific antibody, and this effect was inhibited by addition of the homologous steroid glucuronide (10-100 pg) in a dose-dependent manner. The assay does not require separation of bound and free ligand and proved satisfactory with respect to sensitivity, precision and accuracy. Assay results obtained by radioimmunoassay and chemiluminescence immunoassay were in good agreement (r = 0.98; n = 25).

Antibody Specificity↗

PubMed1976

Biliary metabolites of estriol in the rat.

Following the subcutaneous administration of estriol-6,7-3H to rats, biliary metabolites were identified and quantitated. Approximately 70% of the metabolites were excreted in the form of "glucosiduronate" conjugates. 3,17beta-Dihydroxy-2-methoxy-1,3,5(10)-estratrien-16-one was the major metabolite in this conjugate fraction. Significant amounts of 3,17beta-dihydroxy-1,3,5(10)-estratrien-16-one and 2,3,17beta-trihydroxy-1,3,5(10)-estratrien-16-one, as well as smaller quantities of 1,3,5(10)-estratriene-2,316alpha,17beta, tetrol and 2-methoxy-1,3,5(10)-estratriene-3, 16alpha, 17beta-triol, were also found. In 17alpha-ethinylestradiol-treated animals, the rate of excretion of radioactivity and the proportion of 16-oxo-17beta-ol metabolites found in the "glucosiduronate" fraction were reduced.

Animals↗

PubMedDate not supplied

Prenatal screening using maternal serum alpha-fetoprotein, human chorionic gonadotropin, and unconjugated estriol: two-year experience in a health maintenance organization.

The objective of this study was to evaluate a 2-year experience in a health maintenance organization with mid-trimester maternal serum screening with alpha-fetoprotein (AFP), human chorionic gonadotropin (HCG), and unconjugated estriol (UE) as a screen for fetal Down's syndrome. Women at 15-20 weeks gestation were offered triple marker screening. A patient-specific second trimester risk of 1:295 for Down's syndrome was used as a threshold for referral. Women at risk for trisomy 18 were identified by a protocol with fixed low cutoffs. The AFP threshold for referral for neural tube defects (NTD) was 2.0 multiples of the median (MoM). Patients at risk were offered ultrasonography, genetic counseling, and prenatal diagnosis. A total of 6,474 samples were drawn. The initial screen positive rate for Down's syndrome was 7.1%. After ultrasound evaluation, 351 (5.7%) of the remaining 6,197 women were still at risk for Down's syndrome. After genetic counseling, 292 (4.7%) women underwent prenatal diagnosis. Overall, 12 of 16 (75%) cases of Down's syndrome were detected antenatally by triple marker screening. Using AFP alone, only 3 of 14 (21%) cases of Down's syndrome in women under 35 years would have been detected. We detected 1 abnormal karyotype (including one 45, X) for every 22 amniocenteses performed for abnormal Down's syndrome screening. For trisomy 18, 13 women (0.2%) were at risk and, of these, 3 cases were diagnosed. All 6 cases of NTD during the study period were detected by AFP after identifying 3.8% of women as at risk. In conclusion, in the setting of a health maintenance organization where abnormal screening tests were managed by a single referral center, triple marker screening was effective not only for screening for fetal Down's syndrome, but also for trisomy 18 and NTD.

Amniocentesis↗

PubMedDate not supplied

Unexplained elevated midtrimester maternal serum levels of alpha fetoprotein, human chorionic gonadotropin, or low unconjugated estriol: recurrence risk and association with adverse perinatal outcome.

OBJECTIVE: To determine if women experiencing an unexplained elevated maternal serum alpha fetoprotein (MSAFP; > or =2.0 MoM) or human chorionic gonadotropin (hCG; > or =2.0 MoM), or low unconjugated estriol (E3; < or =0.5 MoM) in one pregnancy are at increased risk for similar results in a subsequent pregnancy, and to determine if recurrence of these analyte extremes is associated with adverse perinatal outcome. METHODS: We identified all women delivering two consecutive singleton pregnancies at one hospital between 1992-1997 for whom second trimester trisomy 21 serum screen was performed in each pregnancy. All screens were performed in a single laboratory. Each pregnancy delivered after 20 weeks and had gestational age confirmed by ultrasound prior to 24 weeks. Subjects were excluded if a fetal anomaly or aneuploidy was present. Adverse outcomes included abruption, oligohydramnios, preeclampsia, preterm membrane rupture, preterm delivery, stillbirth, birthweight <10th centile, and admission to neonatal intensive care unit (NICU). RESULTS: A total of 538 women had 1,076 pregnancies meeting inclusion criteria; 12/515 (2.3%) of women with a normal MSAFP, 28/470 (6.0%) with a normal hCG, and 11/504 (2.2%) with a normal E3 in the first pregnancy had an anomalous result for the respective analyte in the second pregnancy. In contrast, only 4/23 (17.4%) patients with an elevated MSAFP (P = 0.003), 14/44 (31.8%) with an elevated hCG (P < 0.001), and 2/10 (20.0%) with a low E3 (P < 0.025) in the first pregnancy had the same analyte anomaly recur in the second pregnancy. The odds ratios for recurrent elevated MSAFP, hCG, and low E3 were 7.5, 5.3, and 9.2, respectively. Adverse perinatal outcomes occurred with similar frequency, regardless of MSAFP, hCG, or E3 results in consecutive pregnancies, using women with normal MSAFP, hCG, and E3 results in one or both pregnancies as controls. CONCLUSIONS: Women experiencing an anomalous serum analyte in one pregnancy are at significant risk to experience the same analyte result in a subsequent pregnancy.

Biomarkers↗

PubMedDate not supplied

Elevated maternal serum alpha-fetoprotein with low unconjugated estriol and the risk for lethal perinatal outcome.

OBJECTIVE: To determine whether a combination of elevated maternal serum alpha-fetoprotein (MSAFP) and low unconjugated estriol (E3) concentration identifies pregnancies at particularly high risk for fetal abnormality or poor outcome. METHODS: Pregnancy outcomes were reviewed for women with elevated MSAFP (> or =2.0 MoM) from our database of 50,315 women who had received triple marker testing from 1993-1998. Outcomes for those with low E3 (< or =0.7 MoM) were compared with those with normal E3 (>0.7 MoM). The incidences of fetal death, neural tube defects, chromosome abnormalities, congenital abnormalities, preterm birth, small-for-gestational age (SGA), twins, and inaccurate dates were compared in the two groups using Fisher's exact test with P < 0.05 considered significant. RESULTS: Of the 50,315 women screened, 1,435 (2.85%) had an elevated MSAFP. Pregnancy outcomes were obtained in 94% of those with elevated MSAFP and 70% of all patients screened. Neural tube defects were present in 57 fetuses/infants (21 anencephalic, 29 spina bifida, 7 encephalocele) of which 46 (81%) had an elevated MSAFP. Of the 1,435 women with an elevated MSAFP, 199 (14%) had a low E3. Compared to those women with elevated MSAFP but normal E3, women with elevated MSAFP and low E3 were at significantly increased risk for fetal death (20.6% vs. 2.8%, relative risk (RR) 8.9), anencephaly (9.0% vs. 0.1%, RR 122.8) and chromosome abnormality (2.5% vs. 0.6%, RR 4.0). CONCLUSIONS: Pregnancies complicated by elevated second trimester MSAFP and low E3 are at a particularly high risk (32%) for lethal perinatal outcomes. Twins, while a common cause of elevated MSAFP, are rarely found when an elevated MSAFP is associated with low E3.

Biomarkers↗

PubMed2005

Recognition of Smith-Lemli-Opitz syndrome (RSH) in the fetus: utility of ultrasonography and biochemical analysis in pregnancies with low maternal serum estriol.

Smith-Lemli-Opitz syndrome (SLOS), or RSH, is an autosomal recessive disorder caused by mutations of the gene encoding 7-dehydrocholesterol reductase (DHCR7). The utility of maternal serum screens and ultrasound as prenatal screening methods for SLOS is presently undetermined. We report the clinical, cytogenetic, biochemical, and molecular findings of a stillborn with SLOS. The diagnosis was made postnatally on the basis of physical findings and confirmed by biochemical and DNA analyses of fetal tissue. Although abnormalities were detected by maternal serum triple screen and prenatal ultrasonography, a diagnosis of SLOS was not suspected before delivery. This study demonstrates that patients with SLOS may escape prenatal diagnosis despite the presence of multiple anomalies and abnormal maternal serum screen results, and lends support for consideration of prenatal biochemical testing for SLOS in pregnancies with these findings. As SLOS is a severe autosomal recessive disorder with a recurrence risk of 25%, ultrasonographic, cytogenetic, and biochemical analyses in the second trimester should be considered if abnormal maternal serum screening results, specifically low levels of unconjugated estriol, are detected.

DNA Mutational Analysis↗

PubMed1989

Determination of estriol and creatinine in urine by high performance liquid chromatography.

A quantitative method for the determination of estriol (E3) and creatinine (C) in random urine by high performance liquid chromatography is described. The mobile phase was a mixed solution of methanol and phosphate buffer (0.025 M, pH 6.5) and the detection wavelength was at 205 nm. The method was simple, rapid and accurate. The OCV for E3 and C using this method were 1.7-3.4% and 2.2-2.5%, respectively. The RCV for E3 and C were 6.2-7.0% and 4.5-6.9%, respectively. The recoveries were 87-104% for E3 and 98-103% for C, respectively. The method has been used for clinical determinations.

Chromatography, High Pressure Liquid↗

PubMedDate not supplied

The contribution of hepatic steroid metabolism to serum estradiol and estriol concentrations in nonylphenol treated MMTVneu mice and its potential effects on breast cancer incidence and latency.

The two major pathways for the metabolism of estradiol-17beta (E2) are the 2- and 16-hydroxylase pathways. Research has suggested that the increased production of the estrogenically active 16-hydroxy products such as estriol (E3) may be involved in increased susceptibility to breast cancer. 4-Nonylphenol (4-NP) is an environmental estrogen that also can activate the pregnane-X receptor (PXR) and induce P-450 enzymes responsible for the production of E3. It is hypothesized that 4-NP may act in part as an environmental estrogen by increasing E3 production. Based on its affinity for the estrogen receptor (ER) alone, 4-NP may be more potent than predicted at increasing mammary cancer incidence in the MMTVneu mouse. Female mice were treated per os for 7 days at 0, 25, 50 or 75 mg kg(-1) day(-1) 4-NP to investigate the effects of 4-NP on hepatic estrogen metabolism after an acute treatment. 4-Nonylphenol increased the hepatic formation of E3 in a dose-dependent manner. However, serum E3 concentrations were only increased at 25 mg kg(-1) day(-1) presumably due to direct inhibition of E3 formation by 4-NP. MMTVneu mice were then treated for 32 weeks at 0, 30 or 45 mg kg(-1) day(-1) 4-NP to determine its effects on mammary cancer formation and estrogen metabolism. 4-Nonylphenol increased mammary cancer formation in the MMTVneu mice at 45 mg kg(-1) day(-1) but not at 30 mg kg(-1) day(-1). Mice treated with an equipotent dose of E2, 10 microg kg(-1) day(-1), based on the relative binding affinities of nonylphenol and estradiol for ER alpha, did not develop mammary cancer. This suggests that nonylphenol is more potent than predicted based on its affinity for the estrogen receptor. However, no changes in serum E3 concentrations or hepatic E3 production were measured after the chronic treatment. Changes in E3 formation were correlated with increased CYP2B levels after the 7 day 4-NP treatment, and repression of CYP2B and CYP3A after 32 weeks of 4-NP treatment. Microarray analysis and Q-PCR of liver mRNA from the mice treated for 32 weeks demonstrated a decrease in RXR alpha, the heterodimeric partner of the PXR, which may in part explain the repressed transcription of the P450s measured. In conclusion, 4-NP treatment for 32 weeks increased mammary cancer formation at a dose of 45 mg kg(-1) day(-1). However, chronic treatment with 4-NP did not increase hepatic E3 formation or serum E3 concentrations. The transient induction by 4-NP of hepatic E3 formation and serum concentrations is most likely not involved in the increased incidence of mammary cancer in MMTVneu mice since E3 serum concentrations were only increased at 25 mg kg(-1) day(-1), a dose that was not sufficient to induce mammary tumor formation. Nevertheless, the induced hepatic E3 production in the acute exposures to 4-NP was indicative of an increase in mammary cancer incidence after the chronic exposure.

Animals↗

PubMed1990

Measurement of serum unconjugated estriol and estradiol by high-performance liquid chromatography.

Measurement of Estriol (E3) and estradiol (E2) within 22 min by high-performance liquid chromatography (HPLC) was achieved in this study, and the values were compared with those of a radioimmunoassay (RIA). A totally computerized HPLC method was developed for measuring unconjugated E3 (u-E3) and E2 (u-E2) in the sera of pregnant women. The serum samples were injected directly into the apparatus and transferred to a pretreatment column where the estrogens were absorbed while hydrophilic components such as proteins and carbohydrates were excluded. The estrogens were then passed through another separation column containing a new type of polymer gel. The mobile phase consisted of an acetonitrile-water mixture, and separation was achieved by means of a reversed-phase procedure. The eluate was monitored for fluorescence. All procedures were monitored and controlled with a built-in microcomputer. Serum samples from 97 normal pregnant women at 20-41 wk gestation were simultaneously assayed by HPLC and RIA. The correlations obtained by HPLC and RIA were as follows: u-E3, y = 0.905x - 0.385, with a coefficient of correlation of r = 0.912; for u-E2, y = 0.964x + 5.024, with a coefficient of correlation of r = 0.841 (y, RIA value; x, HPLC value). The quick measurement of u-E3 and u-E2 by HPLC can be a useful method for evaluating fetoplacental function.

Chromatography, High Pressure Liquid↗

PubMed1979

Development of an estriol-releasing intrauterine device.

Estriol-releasing intrauterine devices were developed for experimental use in animals and humans. The devices consist of a reservior containing the steroid surrounded by a rate-limiting polyurethane membrane. After an initial transient, the drug is released from the device at a constant rate for 1 year or more; devices with a much longer release period can be fabricated readily. A constant release rate is achieved by maintaining solid drug in the reservoir and good physical contact between the drug and the inside wall of the device. The methods used to fabricate the devices are described along with release rate and stability data.

Chemistry, Pharmaceutical↗

PubMed2002

Low or absent unconjugated estriol in pregnancy: an indicator for steroid sulfatase deficiency detectable by fluorescence in situ hybridization and biochemical analysis.

It has been previously reported that a low or absent maternal serum unconjugated estriol (uE3) level is associated with placental steroid sulfatase (STS) deficiency. Here we report a correlation between patients who present with a very low or absent maternal serum uE3 and a deletion of the STS gene as assessed by fluorescence in situ hybridization (FISH). We studied nine prenatal cases that presented to the clinical laboratory with an abnormal triple screen, specifically low or absent maternal serum uE3 and a 46,XY karyotype. FISH analysis showed complete deletion of a probe containing the STS gene in six cases and one case had a partial deletion (reduced but not absent signal). The remaining two cases were not deleted for the STS probe. All mothers tested whose fetus showed a deletion were shown to be STS deletion carriers using FISH. Biochemical analysis was performed on 7/9 prenatal specimens. All fetuses deleted for the STS probe were also found to be deficient for STS by biochemical analysis of cultured amniotic fluid (5/5). Of the two fetuses not deleted for the STS probe, one was deficient for STS activity, while the other had a normal result. The abnormal result of enzyme deficiency by biochemical analysis in a non-deletion case likely represents a mutation in the STS gene, not detectable by this FISH assay. Postnatal FISH confirmation of the STS deletion was performed in 1/7 cases. Clinical follow-up was available for 4/9 cases following birth.

Adult↗

PubMed1978

Preparation and purification of estriol, estradiol, and progesterone labeled with radioactive iodine.

Steroids labeled with radioactive isotopes are useful tracers for radio-immunoassay and for in vivo nuclear medecine purposes. We here report and discuss methods for direct labeling of the steroids estriol, estradiol, and progesterone with radioiodine-125 or -131. The purification procedure and some chemical and physical properties of the purified labeled materials are referred to and discussed.

Chloramines↗

PubMed1984

The effect of 2 mg estradiol-17 beta plus 1 mg estriol, sequentially combined with 1 mg norethisteroneacetate, on LH, FSH, estradiol-17 beta, progesterone, testosterone and prolactin after ovariectomy.

The object of the study was to see whether maintenance of serum estradiol levels corresponding to the early and mid-follicular phase can prevent the gonadotrophin increase following ovariectomy. We also wanted to study the effect on LH and FSH of an additional dose of 1 mg dose of 1 mg norethisterone acetate administered for 10 days during each month. In 22 women with normal cycles 1 mg of estradiol benzoate was injected i.m. at the time of ovariectomy. From the first post-operative day onwards they received daily doses of 2 mg estradiol and 1 mg estriol in the form of micronized tablets. From the 41st to the 50th day and again from the 69th to the 78th day the patients received additional daily doses of 1 mg norethisterone acetate. LH, FSH, estradiol-17 beta, (E2) progesterone (P), testosterone (T), and prolactin (PRL) were measured in intervals of 2-17 days. Even though the estradiol mean values remained constant in the range of 65-115 pg throughout the period under observation, the LH mean levels increased continuously from 8 to a maximum of 23.9 mU/ml, and the FSH mean level from a pre-operative value of 6-48.0 mU/ml on the 85th day. On the 7th day after the last administration of norethisterone acetate LH was slightly depressed while FSH continued to rise slightly. Both FSH and LH are negatively correlated with E2 and this inverse correlation becomes even more pronounced the more time has elapsed after surgery. These findings suggest that not only the estrogens inhibit FSH and LH but also other steroids and/or nonsteroidal ovarian inhibiting factors.

Adult↗

PubMed1987

The effect of estriol on the production of alpha-fetoprotein by the liver in adult mice.

A single intraperitoneal injection with a 10 mg estriol (E3) in aqueous suspension induced a large and prolonged elevation of serum alpha-fetoprotein (AFP) in adult mice. E3 also raised the mitotic activity of hepatocytes in the absence of liver injury. Although both the AFP concentration and hepatocyte proliferation reached the peak on day 5 after E3 administration, a high level (about 12,500 ng/ml) of serum AFP persisted for a long period after hepatocyte proliferation declined. Five mg E3 showed a remarkable threshold effect on AFP elevation and 3 mg E3 on hepatocyte proliferation. Immunohistochemical studies indicated AFP production by hepatocytes in adult mice after the E3 administration.

Animals↗

PubMed1976

Plasma concentrations of unconjugated estrone, estradiol-17beta and estriol, and HCS throughout pregnancy in diabetics and gestational diabetics.

Plasma unconjugated estrone (E1), estradiol-17beta (E2) and estriol (E3), and HCS were measured in the same plasma samples collected throughout pregnancy in 19 gestational diabetics (GD) and 21 diabetics (D). When compared to the results obtained in 22 normal subjects, plasma levels of E1 and E2 were significantly elevated in D in the second half of gestation. The results were intermediate although closer to the normals, in GD. E3 values were not different from the normals in both D and GD. HCS values were lower than normal in early pregnancy in both D and GD. In late pregnancy HCS levels were not different from normal in either D or GD, although some individual values were much above the upper limit in some diabetic patients. The hormonal ratios in D and GD parallel those in normals, although E3/E2 and HCS/E2 were lower in D. These results are discussed with respect to the different behaviour of E2 and E3, taking into account the difference in their respective biosynthetic pathways. Besides a possible quantitative modification of the placental function in D, the results could tentatively be explained by a qualitative change in the fetal estrogen precursors to placental aromatization, in favour of the 16 non-hydroxylated compound. However, maternal modifications in precursor production or in estrogen metabolism can be an alternative hypothesis. Finally, the present work does not support the hypothetical estrogen deficiency in diabetic pregnancy. Estrogen treatment appears to have no objective justification.

Adult↗

PubMed1990

Conversion to estriol in "normal", benign and malignant human breast tissues.

Since there are controversial reports in the literature on 16 alpha-hydroxylase activity in human breast tumors, we have studied this enzyme activity in "normal", benign and malignant breast tissues by measuring the conversion of estradiol to estriol. Whereas 8 out of 14 (58%) malignant tumors showed positive activity, none of the other tissues had any detectable 16 alpha-hydroxylase activity. These preliminary results, when combined with reports in the literature on animal and human tissues, appear to indicate that more extensive studies on this enzyme could be useful as it could be an additional metabolic marker in human breast cancer.

Adult↗

PubMed1989

The occurrence of estrone and estriol in Trichostrongylus colubriformis (Nematoda).

Mammalian sex steroids and cholesterol were isolated from the lipid extract of the zooparasitic nematode Trichostrongylus colubriformis. In addition to the previously identified sex steroids progesterone and testosterone, estrone and estriol were detected and isolated from the mixture. The steroids were analyzed by thin-layer, gas-liquid and high-performance liquid chromatography, and their structures confirmed by proton nuclear magnetic resonance and mass spectroscopy.

Animals↗

PubMedDate not supplied

Prolactin, estriol and progesterone levels in frequent blood samples throughout normal pregnancy (lack of prolactin pulsatile secretion).

The aim of this paper was to study the episodic fluctuations of circulating prolactin (PRL), estriol (E3) and progesterone (P4) concentrations throughout pregnancy. We examined 24 pregnant women; 21 were between the 28th and 40th week of gestation, and the other 3 in the 12th, 16th and 20th week of gestation. Blood samples were drawn every 5 min for half an hour, and every 15 min for one and a half hour. Blood samples were taken in two and three different weeks of gestation in 11 and 2 of the cases, respectively. Two normal non-pregnant women were also studied and used as controls. PRL, E3 and P4 were determined by radioimmunoassay in all the samples. The coefficients of variation of PRL values were 40 and 22.6%, respectively, in the two control women, 8, 12 and 9.8% in the pregnant women studied at the 12th, 16th and 20th week of gestation, respectively, while in the 21 cases studied during the third trimester the coefficient of variation was 8 +/- 3% (mean +/- SD). The coefficients of variation of the values obtained for E3 and P4 in women studied in he third trimester were 26 +/- 15 and 16 +/- 6% (Mean +/- SD), respectively. There was an increase in the average concentration of the three hormones in all the cases at two or three different weeks. We can conclude that E3 and P4 have a pulsatile secretion pattern throughout pregnancy, and that PRL looses its pulsatile secretion as from an early gestational age. Our results suggested that central mechanisms regulating PRL episodic fluctuations were altered during pregnancy.

Estriol↗