Low Urinary Oestrogen Excretion Research Articles

A case of turner syndrome with the karyotype of 45,X/46,X,i(Xq) associated with acute monocytic leukemia.

An infertile 37-year-old woman was diagnosed as having acute monocytic leukemia (AMoL) (FAB classification; M5b). In addition, a diagnosis of infertile Turner syndrome was made, based on the presence of the ovarian dysplasia, abnormal physical features (short stature, lack of pubic hair, shield-like chest, etc.), and low urinary estrogen excretion with high plasma gonadotropin level. Karyotypes in the peripheral blood and bone marrow cells were mosaic 45,X and 46,X,i(Xq): isochromosome Xq, which were consistent with infertile Turner syndrome. No further chromosomal abnormalities were found during the course of her treatment for leukemia. This is the first report of the combination of Turner syndrome and AMoL. However, this patient did not have any of the other autosomal chromosomal abnormalities which are common in acute non-lymphocytic leukemias.

Low urinary oestrogen excretion during pregnancy, due to an impairment of fetal adrenocorticotrophic hormone secretion

Four cases of newborn infants whose mothers had a low urinary oestrogen excretion during pregnancy are reported. Placental sulphatase deficiency and placental insufficiency were excluded by a dehydroepiandrosterone sulphate loading test. Postnatally, they developed a clinical picture characterized by an inappropriate secretion of cortisol which, by the results of an adrenocorticotrophic hormone stimulation test, appeared to be due to an impairment of adrenocorticotrophic hormone secretion. The prenatal and postnatal steroid metabolism is discussed.

Endocrine aspects of bovine dystocia with special reference to estrogens

Little information is available concerning the role of hormones in dystocia. Data regarding the variability in estrogen production by the feto-placental unit are reviewed. Evidence is presented that the sire, or the breed of sire influences the amount of estrogens produced by the feto-placental unit, estimated as estrogen/creatinine ratio in the maternal urine during late pregnancy. The greatest differences were found in Zebu cows bred to Friesian bulls as compared to pure bred Zebus. Urinary estrogen excretion in late gestation was shown to be relatively low in Dutch Friesian cows bred to Charolais bulls and in MRI (Maas Rhine JIsel; Red and white) cows bred to bulls, known to cause a high incidence of dystocia in their offspring. These findings suggested a possible association of low urinary estrogen excretion, from day 260 of gestation to parturition, with a high incidence of dystocia. In a study of over 500 cows during late gestation over a period of 26 months, a seasonal influence on urinary estrogen excretion proved to be significant. The influence of season on dystocia is discussed. Because of a heritability of about .30 and a large variability between cows in urinary estrogen excretion, sire selection for urinary estrogen excretion is suggested as a tool in decreasing the incidence of dystocia.

Plasma prolactin levels during pregnancy.

Plasma prolactin levels in women who were between 8 and 40 weeks pregnant were determined by a homologous double antibody radioimmunoassay method. There were 980 samples from 839 uncomplicated and 213 samples from 116 complicated pregnancies. Prolactin levels in normal pregnancies varied from 6 ng/ml during early pregnancy to 210 ng/ml near term. A few values beyond the normal range were found in various groups of complicated pregnancies. About 14 per cent of samples from patients with threatened abortion and 7 per cent from patients with hypertension were above the upper normal range. The proportion of values below the 10th centile in patients with a low urinary oestrogen excretion was significantly higher than that in the normal population. Plasma prolactin levels did not seem to be a valuable guide to maternal or fetal well-being.

Hypogonadism and parathyroid adenoma in congenital poikiloderma (Rothmund-Thomson syndrome).

In two adult patients with congenital poikiloderma (Rothmund-Thomson syndrome) the following endocrine abnormalities were found: Patient 1, female, with short stature had primary amenorrhoea and did not develop secondary sexual characteristics. Despite lacking an oestrogen effect on the vaginal smear and the low urinary oestrogen excretion, basal LH and FSH and their response to LH-RH were normal. At age 36 a parathyroid adenoma was diagnosed because of increased immunoreactive plasma parathyroid hormone and persistent hypercalcaemia. After removal of the tumour the patient remained normocalcaemic. The result of growth hormone response to insulin in the intermediate range was suggestive of partial deficiency. In patient 2, male, hypergonadotrophic hypogonadism with small testes and high basal LH and FSH levels as well as increased LH and FSH response to LH-RH were found. Plasma testosterone was normal. Endocrine abnormalities in previously published cases are summarized.

Galactorrhea-amenorrhea due to primary hypothyroidism

Two women, aged 23 and 33, with primary hypothyroidism, galactorrhea, and amenorrhea are described. Elevated serum prolactin and TSH levels, normal serum gonadotropin levels, and normal to low urinary estrogen excretion were observed. Following thyroxine replacement therapy, normal menses returned in two and four months, the galactorrhea resolved in two and three months, and the serum prolactin and TSH levels fell to within normal limits. It is postulated that the prolactin excess and galactorrhea observed in primary hypothyroidism are mediated by an elevated level and/or an enhanced biologic effect of TRH.

Neutral C 19-steroids and steroid sulfates in human pregnancy II. Dehydroepiandrosterone sulfate, 16α-hydroxyderhydroepiandrosterone, and 16α-hydrosydehydroepiandrosterone sulfate in cord blood and blood of pregnant women with and without treatment with corticoids

Dehydroepiandrosterone sulfate (DS), 16α-hydroxydehydroepiandrosterone sulfate (16α-OH-DS) and 16α-hydroxydehydroepiandrosterone (16α-OH-D) were measured in mixed cord plasma and maternal plasma of 6 pregnant women who were treated with prednisone and hydrocortisone succinate during pregnancy and labor. All three steroid hormones were markedly lowered in the fetal blood. (DS: M = 53 μ%, 16α-OH-DS: M = 45 μg%, 16α-OH-D = < 6 μg%). The level of these steroids appears to vary inversely with the amount of corticoids given to the mother. In the maternal blood DS was either not measurable or very low (range < 8–29 μg%) as compared with normal values for untreated pregnant women. No 16α-OH-D or 16α-OH-DS could be detected in the p lasma of these patients. Maternal urinary estriol, estrone, and estradiol were also decreased in three of the cases studied. It is hypothesized that the decrease of urinary estrogens in these patients is mainly due to a suppression of the release of C 19-steroid hormones by the maternal and fetal adrenal; the suppression of the fetal adrenal by exogenous corticoids being of major importance. It is pointed out that in cases with corticoid treatment during pregnency a low urinary estrogen excretion does not need to interfere with the development of pregnancy and does not reflect a hazard to the fetus.