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PubMed1977

Post-coital contraceptive activity and estrogen receptor binding affinity of phenolic steroids.

Estradiol, estradiol-16alpha, estriol and a series of positional isomers of estriol were tested for their post-coital contraceptive activity, and their ability to compete with estradiol for the cytosolic estrogen receptor protein of rat uteri. Estrogenicity was determined for each compound in immature rats with single injections and in mature castrated rats by injecting the lowest fully contraceptive dose for four consecutive days. All compounds were active anti-implantational agents, varying in required dosage from 4 mug to 2000 mug (total dosage over 4 days). The rank order or contraceptive activity was found to be: estradiol greater than estriol = epiestriol greater than 11beta - (OH) - estradiol greater than estradiol - 16alpha greater than 7alpha-(OH)-estradiol greater than 6beta-(OH)-estradiol, while the order of estrogenicity at levels of contraceptive activity in the ovariectomized mature rat was: epiestriol = estriol less than 7 alpha - (OH) - estradiol less than estradiol - 16alpha less than 6beta - (OH) - estradiol = 11beta - (OH)- estradiol less than estradiol-17beta. Reasonably good correlation between competition for estrogen receptor and anti-implantational activity was observed. The most active binding competitors were estradiol-16alpha, epiestriol, and estriol which showed an affinity from 50-20% that of estradiol, while the other compounds had 3% or less binding competition for estradiol.

Animals↗
PubMed1999

Regiospecific esterification of estrogens by lecithin:cholesterol acyltransferase.

Lecithin:cholesterol acyltransferase (LCAT), the enzyme that esterifies cholesterol in blood, also esterifies other steroids at the 3beta-hydroxyl. These steroids, like cholesterol, are delta5-3beta-hydroxysteroids, such as pregnenolone and dehydroepiandrosterone. One unusual LCAT substrate is the estrogen, estradiol, which is esterified at the 17beta-hydroxyl. The esterification of estradiol by LCAT has been reported to produce a powerful antioxidant that protects low density lipoprotein (LDL) from oxidation. We investigated the substrate specificity of LCAT, comparing the esterification of four different steroids (estradiol, estriol, testosterone, and 5-androstene-3beta, 17beta-diol) by human LCAT in blood and by acyl-coenzyme A:acyltransferase in tissue (placenta and fat). Estradiol was esterified only at the D ring 17beta-hydroxyl group in both blood and tissue. In contrast, although testosterone has a D ring structure identical to that of estradiol, and it was esterified at the 17beta-hydroxyl by acyl-coenzyme A:acyltransferase in tissue, it was not esterified by LCAT. When 5-androstenediol was the substrate in the tissues, both the 3beta- and 17beta-esters were synthesized, but the major product was the 17beta-ester. Conversely, although 5-androstenediol was an excellent substrate for LCAT, only the 3beta-hydroxyl was esterified. No 17beta-ester was formed. The comparison of the esterification of estriol by acyl-coenzyme A:acyltransferase and LCAT was also surprising. In the tissues, estriol is esterified at both D ring hydroxyls, and both are esterified about equally. Although estriol is an extremely polar estrogen, it is esterified by LCAT, albeit at a very slow rate. Although again both D ring hydroxyls were esterified, the LCAT esterification site was mainly at the 17beta-hydroxyl. Esterification of estriol at the 17beta-hydroxyl in preference to the 16alpha-hydroxyl is especially striking, because the 17beta-hydroxyl group is sterically shielded by the C-18 methyl group, making esterification at this position energetically much more difficult. Furthermore, these studies demonstrate that esterification of the 17beta-hydroxyl group by LCAT is unique to estrogens. It suggests that this unusual regiospecific esterification of C-17 of the estrogens underlies a distinct stereochemical requirement for the powerful antioxidant action that has reported for the estradiol esters formed by LCAT.

Acyl Coenzyme A↗
PubMedDate not supplied

[Climacteric syndrome: comparison of several secondary therapies].

During a first one year period a random treatment for climacteric symptoms with "Estriol vaginal cream" vs "Trazodone and Estriol vaginal cream" and, after it and only in patients not complaining of dyspareunia, with "Trazodone" vs "Veralipride" has been conducted. After the first year all women complaining of dyspareunia were treated with Estriol vaginal cream. Eighty women were enrolled in the five treatment groups. After three months of treatment, a good remission of symptoms was shown, with differences in relations to treatment schedules. Dyspareunia subsided for more than 70% in women treated with Estriol vaginal cream (either by itself or in association), and Estriol vaginal cream achieved the best response from the highest number of the considered symptoms, besides being the only active treatment in insomnia. A good answer on hot flushes and "irritability, anxiety, depression" was obtained by Trazodone, while Veralipride showed to be more active on all neurovegetative symptoms (hot flushes, sweatings, tinglings, palpitations, astenia).

Adult↗
PubMed1990

Combined histochemical and biochemical analysis of sex hormone dependence of ferric nitrilotriacetate-induced renal lipid peroxidation in ddY mice.

Ferric nitrilotriacetate (Fe-NTA) induces renal proximal tubular necrosis, a consequence of lipid peroxidation, that finally leads to a high incidence of renal adenocarcinoma in rats and mice. Male animals are much more susceptible than female animals to both effects. Moreover, the distribution of the susceptible proximal tubules is different between male and female animals. The present study investigated the effects of castration and sex hormones on Fe-NTA-induced renal lipid peroxidation. Male and female ddY mice were either left untreated, castrated, and/or treated with testosterone or estriol. Histochemical (reactivity to cold Schiff's reagent) and biochemical (thiobarbituric acid-reactive substance) evaluations were performed 1 h after the i.p. injection of Fe-NTA (5 mg iron/kg). Testosterone treatment and/or oophorectomy increased the Schiff positivity of the renal cortical proximal tubules and the amount of thiobarbituric acid-reactive substance (testosterone-treated female greater than intact female, P less than 0.005; castrated female greater than intact female, P less than 0.1; castrated and testosterone-treated female greater than intact female, P less than 0.005). In contrast, estriol treatment and/or orchiectomy decreased the Schiff positivity of the renal cortical proximal tubules and the amount of thiobarbituric acid-reactive substance (estriol-treated male less than intact male, P less than 0.01; castrated male less than intact male, P less than 0.01; castrated and estriol-treated male less than intact male, P less than 0.005). Estradiol treatment produced similar results to estriol treatment (estradiol-treated male less than intact male, P less than 0.005). Castration and/or administration of the opposite sex hormone reversed the sex difference in the distribution of proximal tubules susceptible to lipid peroxidation. However, the i.v. injection to male mice, 5 min prior to the Fe-NTA treatment, of conjugated estrogen that is promptly excreted via the urine produced no significant effect. Thus, altered metabolic pathways rather than the direct scavenging activity of estrogens seem to be involved in the sex hormone-dependent difference of lipid peroxidation. Genetically determined sex hormone status appears to have influenced the incidence of Fe-NTA-induced renal adenocarcinoma in intact animals.

Acetates↗
PubMed1982

What are the most suitable fetoplacental tests in the monitoring of the third trimester of pregnancy?

The case-series of the Institute of Obstetrics and Gynaecology were examined to evaluate the suitability of urinary estriol, total plasma estriol, unconjugated plasma estriol, unconjugated plasma estetrol, plasma placental lactogen, plasma S.P.-1 glycoprotein, plasma alphafetoprotein and biparietal diameter in correctly forecasting the perinatal risk, when performed after the 25th week of pregnancy. In high-risk pregnancies, according to our results, S.P.-1 glycoprotein and urinary estriol are the most sensitive tests, while S.P.-1 glycoprotein, placental lactogen and biparietal diameter are found to have the highest predictive value. The repetition of the considered tests increases their sensitivity, but not their predictive value. In pregnancy mass screening the most suitable tests, on the basis of the "relative risk" are S.P.-1 glycoprotein (or even placental lactogen), estriol and biparietal diameter. For the last one a single measurement seems to be enough during the third trimester.

Estetrol↗
PubMed1980

Endocrine assessment of high-risk pregnancies.

For critical obstetrical judgment, no single laboratory test or biophysical technique has proved completely effective in preventing fetal deaths. Endocrine assessment of high-risk pregnancies has proved helpful in managing pregnancies with diabetes, hypertension, third trimester bleeding, suspected IUGR, and postdate pregnancies. No single endocrine test has proved to be effective in all cases, and much research remains to be done. Of the current endocrine factors being evaluated when all factors are considered, serum unconjugated estriol would appear to be the best predictor of fetal distress or well-being. However, it must be remembered that interpretation of laboratory values is difficult, and that there are many false positives and false negatives. Perhaps the greatest problem with estriol interpretation is short-term and daily fluctuations. If the estriol values are used as the only indicator for following high-risk pregnancies, there is a very likely possibility of delivering a normal premature infant that was wrongly diagnosed as having fetal distress. In the following high-risk pregnancies with estriols, the delivery decision should not be based on a single factor. Rather, the decision to deliver should be based on the estriol values, monitoring of the fetal heart rate (rhythm strip or OCT), amniotic fluid evaluation for fetal lung maturity, and clinical judgment.

Adrenal Glands↗
PubMed2005

Effects of sex hormones on costimulatory molecule expression in multiple sclerosis.

Sex hormones play a central role as modulators of immune responses and autoimmune diseases. We hypothesized that suppression of MS disease during pregnancy may be mediated by sex steroid hormones via regulation of costimulatory molecules such as CD40L or CD80/CD86 (B7-1/B7-2). We tested two sex hormones that are implicated in immune suppression during pregnancy: estriol and progesterone. We also examined whether this regulation is gender-specific or disease-related. PBMC from untreated relapsing remitting multiple sclerosis (RR MS) patients and controls were examined for expression of T cell and monocyte costimulatory molecules following mitogen stimulation in the presence or absence of sex hormones. In the absence of hormones, we confirmed that mitogen stimulation induced significantly more CD40L on the surface of CD4(+)T cells in MS patients compared to controls, and we extend these findings by showing there were no gender differences in induction of CD40L. Although supra-physiologic doses of hormones mildly suppressed CD40L expression on activated T cells, in vitro exposure to typical pregnancy-related physiologic doses of estriol or progesterone showed very little or no suppression of CD40L. On monocytes, neither estriol nor progesterone significantly altered the expression of CD80/CD86. These results suggest that physiologic doses of estriol or progesterone cannot alter CD40L on T cells or CD80/CD86 on monocytes sufficiently to explain the improvement observed in MS during pregnancy. Thus, although amelioration of MS and other autoimmune diseases during pregnancy is thought to be due to increased sex hormones, the present results do not support a role for suppression of costimulation via estriol or progesterone.

Adult↗
PubMed1976

Intestinal metabolism of estrogens.

Estrogen metabolism in the human intestine was studied in two ways. Firstly, by measuring the excretion of 12 estrogens in pooled human late pregnancy feces before and during the administration of ampicillin (2 g/day). Secondly, by administering 5.4 and 20 mg of 16alpha-hydroxyestrone orally to two postmenopausal women and analyzing the estrogens in simultaneously drawn portal and peripheral venous blood samples at time intervals from 0 to 150 min after steroid administration. The majority of the estrogens in normal pregnancy feces were unconjugated. The amounts of estradiol, estreon and 16-epiestriol excreted, relative to the principal estrogen estriol, were greater than in pregnancy bile or urine and 16alpha-hydroxyestrone, an important biliary estrogen, was only present in trace amounts. Considerable quantities of 15alpha-hydroxyestradiol-17beta were also found. Ampicillin administration, which decreases intestinal bacterial steroid metabolism, caused a huge increase in the fecal excretion of conjugated estrogens. In particular it caused very striking increases in the excretion of both unconjugated and conjugated, estriol, 15alpha-hydroxyestrone, 15alpha-hydroxyestradiol and 2-methoxyestrone. These findings emphasize the active role played by the intestinal microflora in estrogen metabolism under normal conditions. Administration of 16alpha-hydroxyestrone resulted in increases in portal venous unconjugated and conjugated 16alpha-hydroxyestrone, 16-oxoestradiol-17beta, 15alpha-hydroxyestrone, 16-epiestriol and conjugated estriol levels. The most significant finding in both subjects was the large increase in portal venous unconjugated 15alpha-hydroxyestrone. This would suggest that the human intestine (or intestinal contents) has the ability to carry out the transformation, 16alpha-hydroxyestrone leads to 15alpha-hydroxyestrone. Increases in the same estrogens were found in peripheral plasma, with the increase in conjugated estriol occurring in peripheral blood before it was seen in portal blood. The largest elevations in peripheral plasma values were seen in unconjugated estriol and conjugated 16alpha-hydroxyestrone in the subject who received the 20 mg dose and in unconjugated 16alpha-hydroxyestrone and 16-oxoestradiol-17beta in the subject who had the 5.4 mg dose. The intestinal and enterohepatic metabolism of estrogens is discussed in relation to these findings.

Ampicillin↗
PubMed1990

Steroid hormones modulate the release of immunoreactive gonadotropin-releasing hormone from cultured human placental cells.

The aim of the present study was to evaluate whether steroid hormones or opiate receptor agonists participate in the mechanisms regulating the release of immunoreactive GnRH (irGnRH) from cultured human placental cells. No significant changes in irGnRH concentrations were found in the culture medium after 48-h incubation of estradiol, estriol, or progesterone. Both estriol and estradiol augmented, while progesterone decreased, the irGnRH release induced by 8-bromo-cAMP. The stimulatory effect of estriol or estradiol was reversed by the concomitant addition of progesterone. The secretagogue effect of activin on irGnRH release from cultured placental cells was increased by the presence of estriol and reduced by the addition of progesterone. The action of estriol was counteracted by both tamoxifen, an estrogen antagonist, and progesterone. The inhibitory effect of progesterone was completely reversed by RU 486, a specific receptor antagonist. The addition of morphine, methionine-enkephalin, or UP50, 488H which preferentially bind mu-, delta-, and kappa-opiate receptors, respectively, did not decrease basal irGnRH release from cultured human placental cells. However, both morphine and UP50, 488H significantly inhibited 8-bromo-cAMP-induced GnRH release. The present results showed that steroid hormones and opiate receptor agonists influence irGnRH release from human cultured cells, suggesting that local interaction between steroids and peptides modulates irGnRH release from human placenta.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Gas chromatography-mass spectrometric determination of activity of human placental aromatase using 16alpha-hydroxyandrostenedione as a substrate.

Aromatization of 16alpha-hydroxyandrostenedione (16alpha-OH AD) with aromatase in human placental microsomes was studied by gas chromatography-mass spectrometry (GC-MS) using 12,4,6,6,9alpha,16beta,17alpha-2H7]estriol as an internal standard. 16alpha-OH AD was incubated with the microsomes in the presence of NADPH in air. The metabolite was extracted with ethyl acetate and treated with NaBH4. The reduced product, estriol, was isolated by Sep-Pak C18 cartridge and then analyzed as the tris(trimethylsilyl)ether by a GC-MS (EI mode). The production of estriol was dependent upon protein concentration and incubation time. Apparent Km and Vmax values of the microsomal aromatase for 16alpha-OH AD were 568 nM and 25.5 pmol/min/mg protein, respectively. In this assay, aromatase activity, estriol formation, could be determined at a level as low as 1 pmol/min/mg protein. Aromatase inhibitors, 4-hydroxy- and 6-oxo-androstenediones, prevented the estriol formation in a competitive manner with 25 and 30 nM of apparent Ki values, respectively.

Androstenedione↗
PubMed1989

[Blood lipids and the clinical state of hormone-treated women during menopause].

The aim of the work was to investigate the influence on lipids and lipoproteins in blood serum exerted by smallest, preventing hot flushes, doses of mestranol and diethylstilbestrol administered with chlormadinon by sequential method as well as estriol by cyclic method. In the studied women, prior to treatment, after 1, 3 and 6 months of therapy, the made evaluation also covered the intensity of climacteric symptoms according to Kupermann scale, and the concentration of FSH, LH, estadiol as well as testosterone in blood serum. Moreover the arterial blood pressure and the body mass were measured. The treatment involved 82 women, and was carried out by resorting to: mestranol in a dose from 0.025 mg to 0.1 mg in 29 females, diethylstilbestrol in a dose ranging from 0.125 mg to 0.5 mg in 30 females, and estriol in a dose from 1 mg to 3 mg in 25 women. Estrogenic drugs were given from the 5th to 25th day of the cycle and chlormadinon (2 mg) from the 16th to 25th day of the cycle. Lipids and lipoproteins were determined in 65 females. The respective climacteric symptoms decreased equally significantly and at a similar pace in consequence of the treatment provided by three methods. The values of Kupermann's index decreased from the compartment 15-50 to 0-15 points. Concentration of FSH and testosterone would not change in the course of the treatment. On the other hand, diminution was recorded in LH concentration after 3 month-long administration of mestranol and after 6 months-long use of estriol. There is also an increase after the first month, and subsequently a significant decrease of estradiol concentration in women treated with mestranol. In the same group of women, lowering of arterial, systolic and diastolic blood pressure was recorded after 6 months of therapy. Systolic pressure decreased also in 6 women receiving estriol, under the influence of diethylstilbestrol and chlormadinon arterial blood pressure did not change. No change in the body mass of the treated women took place. Evaluating the changes in concentration of lipids and lipoproteins in the blood serum, during the treatment, it was stated that as compared with initial values there was a significant rise in the concentration of HDL cholesterol in the group of females treated with mestranol and diethylstilbestrol with chlormadinon; as well as of HDL phospholipids in women being given estriol, and also in women taking diethylostilbestrol with chlormadinon. An increase in concentration of total phospholipids was also revealed in the latter two groups of women.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Pressure↗
PubMed1978

Estrogen profiles in young women: effect of maternal history of breast cancer.

To examine the hypothesis that familial breast cancer risk is related to estrogen metabolism, we analyzed urines of daughters of breast cancer patients and their matched controls for estrone (E1), estradiol (E2), and estriol (E3). From this, we computed estriol proportions (E3/E1 + E2 + E3). "Patient-daughters" and the matched controls showed no differences in estriol proportions. Our results failed to support the hypothesis that high-risk women (those with a family history of breast cancer) have relatively lower estriol proportions, and we concluded that whatever family history contributes to breast cancer risk, that risk is not likely to be transmitted by the estrogen profile.

Adolescent↗
PubMed1980

Socioeconomic status, urine estrogens, and breast cancer risk.

Urine estrogens were measured in 46 women students, ages 15-18, at a middle-class high school in Athens and in 40 women of the same age residing at one of three orphanages in the same city. The lower socioeconomic status (SES) of the latter group was documented by their lower mean height (by 5.2 cm) and weight (by 5.3 kg) relative to the high school students. Both in follicular and luteal phases of the menstrual cycle, the women with lower SES had 50% higher estriol ratios (ratio of the concentration of estriol to the sum of the concentrations of estrone and estradiol). In luteal specimens the concentration of all three major estrogens was higher in the group with low SES than in the women in the other group, but the concentration of estriol was most increased. There was also an indication of less frequent anovular cycles among the women with low SES. These findings are consistent with hypotheses linking either the estriol ratio or the frequency of anovular cycles to breast cancer risk.

Adolescent↗
PubMed1976

[Penetrations kinetics and distribution of topically applied estrogens (author's transl)].

The penetration into the single layers of human skin in vitro of 17 alpha-estradiol, 17 beta-estradiol and estriol was investigated. The radiolabeled substances were incorporated into 4 standard ointments and into an alcoholic solution mixture. After application to the skin and after different penetration periods, the horny layer was taken off by adhesive tape stripping. The epidermis and the dermis were separated by slicing them down parallel to the skin surface in a freeze microtome. In each single layer, the amount of substance was determined and calculated relative to the applied quantity and in absolute concentrations (mug per tissue weight and molarity). Besides the expected dependence of the penetration on the type of ointment, there is a distinct dependence on the chemical structure: estriol penetrates considerably slower and in less concentrations into the living layers of the human skin than the estradiols. Furthermore, estriol reaches the dermis only in low concentrations so that this substance may be termed epidermotropic. 17 alpha-estriol which has only weak sexhormone properties in humans penetrates as well as the sexhormone 17 beta-estradiol.

Administration, Topical↗
PubMed1976

Prenatal diagnosis of placental steroid sulfatase deficiency.

Placental steroid sulfatase deficiency is an unusual cause of low estriol production during pregnancy. Its importance lies in the differentiation of this disorder from the more ominous fetal defects that result in low estriol levels. Serum free estriol levels were found to be low or absent in a 25-year-old gravida 3, para 2 woman, while placental lactogen and chorionic gonadotropin levels were normal. An abdominal x-ray revealed no apparent congenital abnormalities and an oxytocin challenge test was negative. The dehydroepiandrosterone sulfate (DHEA-S) level in the patient's amniotic fluid was 6.8 to 18.4 times greater than those found in control amniotic fluids. The patient's amniotic fluid cortisol level was normal. Twenty-four hours following a normal, spontaneous labor and delivery at 39 weeks, the male infant underwent a synthetic ACTH1-24 stimulation test, with serum cortisols rising from 3.7 to 46 mug/dl at 1 hour. The placenta was morphologically normal on gross, light, and electron microscopic examinations. Steroid 3-alcohol sulfatase and arylsulfatase activities in the patient's placenta were virtually absent. These data indicate that this benign cause of low serum estriol levels may be diagnosed prenatally by elevated amniotic fluid DHEA-S levels.

Adult↗
PubMed1977

Effect of ampicillin administration on plasma conjugated and unconjugated estrogen and progesterone levels in pregnancy.

The administration of ampicillin to three women in the last trimester of pregnancy caused a transient reduction in the plasma concentration of total conjugated estriol and of estriol-16alpha-glucuronide, as measured by a specific radioimmunoassay. Similar changes were seen in plasma conjugated estrone and estradiol levels, but the effect seemed to be more prolonged. In most cases, the reduction in plasma conjugated estrogens was greatest on the second and third day of ampicillin administration, the pattern being similar to that described previously for urinary estriol and other estrogens. There were no obvious differences in the ampicillin effect between the morning and afternoon plasma levels. Ampicillin caused no consistent change in the plasma levels of unconjugated estrone, estradiol, and estriol or in plasma progesterone. These results are discussed with consideration of our present understanding of the effect of ampicillin on the intestinal metabolism and enterohepatic circulation of steroids.

Administration, Oral↗
PubMed1995

The advantages of using triple-marker screening for chromosomal abnormalities.

OBJECTIVE: Our purpose was to assess the utility of triple-marker serum screening for chromosomal abnormalities. STUDY DESIGN: Our laboratory received 10,605 samples that were between 15 and 22 weeks' gestation for maternal serum screening of chromosomal abnormalities. Triple-marker maternal serum screening consisted of alpha-fetoprotein, human chorionic gonadotropin, and unconjugated estriol in conjunction with maternal age. Women > or = 35 years old were first offered amniocentesis. If they refused amniocentesis, they were offered the screening test. A second-trimester risk for trisomy 21 > or = 1:270 was considered screen positive. Patients were screen positive for trisomy 18 if all three markers were low: alpha-fetoprotein < or = 0.75 multiples of the median, unconjugated estriol < or = 0.60 multiples of the median, and human chorionic gonadotropin < or = 0.55 multiples of the median. RESULTS: The initial screen-positive rate was 8.3% (880 women); amniocentesis was offered to 766 (7.2%). Twelve of 16 ascertained cases of trisomy 21 (75%), two of three cases of trisomy 18 (67%), five cases of 45,X karyotype, and one case each of 45,X/46,XX, 47,XXY, 47,XYY, 46,XX,ins(2)(q21p13p15)mat, and 69,XXX karyotypes were identified in the screen-positive patients. All four known cases of trisomy 21 in the 886 women > or = 35 years old who were screened were detected, with a 21% false-positive rate. Omitting unconjugated estriol from our screening program would have resulted in detecting nine of 16 trisomy 21 and six of 12 other chromosomal abnormalities. The false-positive rate would have remained the same. CONCLUSION: In our sample cohort addition of unconjugated estriol to the screening program resulted in an increased detection rate of chromosomal abnormalities with no change in the false-positive rate. Considering the advancement in screening for chromosomal abnormalities, maternal age alone as an indication for amniocentesis should be reevaluated.

Adolescent↗
PubMed1995

Corticotropin-releasing hormone and pituitary-adrenal hormones in pregnancies complicated by chronic hypertension.

OBJECTIVE: We hypothesized that maternal plasma corticotropin-releasing hormone levels are elevated in chronic hypertension and that elevations modulate maternal and fetal pituitary-adrenal function. STUDY DESIGN: Venous blood samples and 24-hour urine specimens were obtained in normal and hypertensive pregnancies at 21 to 40 weeks of gestation. Corticotropin-releasing hormone, corticotropin, cortisol, dehydroepiandrosterone sulfate, and total estriol levels were measured by radioimmunoassay. Mean hormone levels were compared by unpaired t test or two-way analysis of variance. RESULTS: Plasma corticotropin-releasing hormone levels were elevated early in hypertensive pregnancies but did not increase after 36 weeks. Levels of pituitary and adrenal hormones were not different in normal and hypertensive women. However, maternal plasma estriol levels were lower in hypertensive pregnancies compared with normal pregnancies. CONCLUSIONS: Fetal 16-hydroxy dehydroepiandrosterone sulfate, the major precursor to placental estriol production, has been reported to be lower than normal in hypertensive pregnancies, possibly explaining the decreased plasma estriol levels reported here. Early stimulation of placental corticotropin-releasing hormone production or secretion may be related to accelerated maturation of placental endocrine function in pregnancies complicated by chronic hypertension.

Adrenocorticotropic Hormone↗