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At least 217 records · Page 12Linked to original sources
PubMed1995

A longitudinal study of the perimenopausal transition: altered profiles of steroid and pituitary hormones, SHBG and bone mineral density.

From a longitudinal prospective study, 160 women with spontaneous menopause and without steroid medication were followed during the transition from pre- to postmenopause. After 12 years 152 women were still participating in the study. Blood samples were drawn every 6 months until 1 year after the menopause and every 12 months thereafter. Measurements of bone mineral density (BMD) on the forearm were performed every second year. All women routinely completed a questionnaire concerning symptoms frequently attributed to the climacteric period. All data were grouped around the onset of the menopause, thereby allowing longitudinal evaluation of the changes in the variables from the premenopausal to the postmenopausal period. The beginning of the perimenopausal period was characterized by transitory elevations of follicle-stimulating hormone (FSH). A significant increase in serum levels of gonadotropins was observed for both FSH and luteinizing hormone (LH) from about 5 years before the menopause. Within the 6 month period around the menopause there was a further increase which culminated within the first postmenopausal year for LH and 2-3 years postmenopause for FSH. Thereafter, a continuous decrease in LH occurred over the following 8 years. With respect to FSH, there was a slight decline starting about 4 years postmenopause. During the premenopausal period an increasing frequency of inadequate luteal function or anovulation occurred and, in the postmenopausal years, the serum levels of progesterone (P) were invariably low. Gradually, the ratio between estrone (E1) and 17-beta-estradiol (E2) increased, reflecting the declining follicular steroidogenesis. A marked decrease in estrogen levels occurred during the 6 month period around the menopause, most pronounced in E2. During the next 3 years, the levels of E2 and E1 showed an essentially parallel, moderate decline. Around the menopause, serum levels of testosterone (T), delta 4-androstenedione (A) and sex hormone-binding globulin (SHBG) showed small but significant decreases. From about 3 years postmenopause, the levels were relatively constant over the following 5 years. A decrease in BMD was observed in the postmenopause, and from about 3 years postmenopause, estradiol correlated positively with BMD. Before, as well as after the menopause, body mass index (BMI) showed an inverse correlation with SHBG. Postmenopausal androstenedione correlated positively with E1, E2 and T. BMI correlated positively with E1 and E2. The concentrations of the free fraction of E2 and T are dependent on the levels of SHBG, which in turn has a negative correlation with BMI. The impact of this will influence the severity of symptoms, the degree of bone loss and the need for supplementary therapy.

Androstenedione↗
PubMed2001

Pre-parturition profile of steroids and prostaglandin in cows with or without foetal membrane retention.

Retained foetal membranes in cattle is one of the most common complications associated to the reduction in milk yield and impaired fertility in dairy cattle. In order to determine some endocrine mechanisms controlling parturition and delivery of foetal membranes, plasma concentrations of steroids and prostanoids were determined in 20 healthy Holstein cows. Samples were taken within the interval of 5 days pre-parturition to 12h after calving. Progesterone (P4) levels were similar in cows with (PR) and without (NPR) placental retention. While the estradiol-17beta (E2) peak at parturition was lower in PR than in NPR cows, cortisol levels were greater in PR cows 12 and 24h pre-parturition. The Prostaglandin F2alpha metabolite (PGFM) levels were higher at parturition in NPR compared with the PR group, but 12h later, these levels in the PR group increased so that concentrations were greater as compared with NPR cows. The Prostaglandin E2 metabolite (PGEM), 24, 48 and 72 h pre-parturition, were higher in PR cows. However, the PGFM:PGEM ratio was greater in cows up NPR at all time when included, indicating the importance of higher levels of Prostaglandin F2alpha (PGF2alpha) than Prostaglandin E2 (PGE2) for normal placental delivery. In conclusion, placental retention was related to both estrogen and PGF2alpha deficiency, which may be a consequence of metabolic stress leading to PGE2 and maternal cortisol synthesis before parturition.

Animals↗
PubMed1993

Cardiff puerperal mood and hormone study. 1. Saliva steroid hormone profiles in late pregnancy and the puerperium: endocrine factors and parturition.

Participants were 120 primiparous women who had vaginal delivery of a non-handicapped child. Saliva was collected twice daily through parturition to day 35 post-partum. In the prepartum, a highly significant circadian rhythm was seen in cortisol, with a lower-amplitude rhythm in progesterone (AM/PM = 1.12). Evening samples showed a rise in cortisol, with a highly significant rise on day -1. The rise was small. The fall in progesterone in the 3 days before parturition was also small (approximately 6%). Neither change provides an obvious trigger for parturition.

Adolescent↗
PubMed1979

Gas-liquid chromatographic analysis of urinary steroids.

A method for gas-liquid chromatographic separation and quantitation of urinary steroid metabolites is described. A normal reference range has been established and classic examples of urinary steroid profiles of the major steroid disorders are given.

17-Ketosteroids↗
PubMed1988

DNA profile and steroid receptor content of human ovarian cancer.

The cellular DNA content was measured in 37 biopsy specimens from human malignant ovarian tumours by flow cytometric analysis. The same specimens were processed for measurement of steroid receptor content. In 14 cases both parameters were investigated in different parts of the same tumour. The results showed that 54% of the tumours contained aneuploid cell populations. Approximately half of the specimens were oestrogen receptor positive whereas 43% contained progesterone receptors. Both ploidy level and steroid receptor content proved constant throughout the tumour, but no relation between the two parameters was demonstrated.

Biomarkers, Tumor↗
PubMed1987

Alteration in the histochemical profile of steroid dehydrogenases in the uropygial gland of male domestic pigeons following androgen deprivation and testosterone supplement.

Activities of delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSDH)) were histochemically demonstrated in the alveoli of the uropygial glands of male domestic pigeons (Columba livia Gmelin). The level of 3 beta-HSDH (Substrates: pregnenolone and dehydroepiandrosterone) was very low. On the other hand, an intense activity of 17 beta-HSDH was observed in the glandular alveoli of both sexually immature and adult pigeons when testosterone was used as the substrate. In the adult specimens, bilateral castration resulted in a moderate increase of the level of 17 beta-HSDH indicating a faster rate of conversion of testosterone into the weaker androgen, namely, delta 4-androstene-3,17-dione. On the other hand, administration of testosterone propionate (TP), 500 micrograms/bird/day for 15 days in the intact prepubertal and castrated adult pigeons caused a perceptible depletion of 17 beta-HSDH, which may be correlated with the increase in the local concentration of testosterone. Low dose of TP (100 micrograms/day) had no effect. When estradiol-17 beta was used as the substrate for 17 beta-HSDH, there was only a feeble response within the alveoli.

17-Hydroxysteroid Dehydrogenases↗
PubMed2001

Clinical measurement of steroid metabolism.

Analysis of steroids in biological samples is used routinely in the diagnosis of endocrine disorders. Binding assays (radioimmunoassays, immunosorbant immunoassays and non-radioactive immunoassays) are reported often for the analysis of single steroids in plasma and urine. Chromatographic methods (high-performance liquid chromatography and gas chromatography) are used for steroid profiling where complex mixtures of steroids are analysed and the activity of biosynthetic and metabolic pathways deduced. Mass spectrometry is the ideal reference technique for detection of steroids, allowing high specificity and sensitivity. This review describes the practical issues concerning the quality of the assays performed and the potential pitfalls facing the analyst in the design of such methods. Novel approaches for the quantification of steroids, including microarrays and stable-isotope tracers are described, with these being applied in the research environment as opposed to routine biochemical laboratories.

Adrenal Cortex Hormones↗
PubMed2006

P450 oxidoreductase deficiency: a new form of congenital adrenal hyperplasia.

PURPOSE OF REVIEW: P450 oxidoreductase deficiency--a newly described form of congenital adrenal hyperplasia--typically presents a steroid profile suggesting combined deficiencies of steroid 21-hydroxylase and 17alpha-hydroxylase/17,20-lyase activities. These and other enzymes require electron donation from P450 oxidoreductase. The clinical spectrum of P450 oxidoreductase deficiency ranges from severely affected children with ambiguous genitalia, adrenal insufficiency and the Antley-Bixler skeletal malformation syndrome to mildly affected individuals with polycystic ovary syndrome. We review current knowledge of P450 oxidoreductase deficiency and its broader implications. RECENT FINDINGS: Since the first report in 2004, at least 21 P450 oxidoreductase mutations have been reported in over 40 patients. The often subtle manifestations of P450 oxidoreductase deficiency suggest it may be relatively common. P450 oxidoreductase deficiency, with or without Antley-Bixler syndrome, is autosomal recessive, whereas Antley-Bixler syndrome without disordered steroidogenesis is caused by autosomal dominant fibroblast growth factor receptor 2 mutations. In-vitro assays of P450 oxidoreductase missense mutations based on P450 oxidoreductase-supported P450c17 activities provide excellent genotype/phenotype correlations. The causal connection between P450 oxidoreductase deficiency and disordered bone formation remains unclear. SUMMARY: P450 oxidoreductase mutations cause combined partial deficiency of 17alpha-hydroxylase and 21-hydroxylase. Individuals with an Antley-Bixler syndrome-like phenotype presenting with sexual ambiguity or other abnormalities in steroidogenesis should be analyzed for P450 oxidoreductase deficiency.

Adrenal Hyperplasia, Congenital↗
PubMed1996

Inhibin and activin differentially regulate androgen production and 17 alpha-hydroxylase expression in human ovarian thecal-like tumor cells.

Activin and inhibin are structurally related dimeric glycoproteins belonging to the transforming growth factor-beta superfamily of proteins which are synthesized and secreted by the granulosa cells of the ovary. Although initially characterized by their ability to influence FSH secretion from pituitary cells, paracrine regulatory roles of these factors on neighboring ovarian theca interna have been suggested. While inhibin has been shown to increase and activin to decrease the production of androgens, the mechanisms of action are not well defined, partly due to difficulties in obtaining adequate numbers of thecal cells from individual patients or animal models. Using a unique human ovarian thecal-like tumor (HOTT) cell culture model system we investigated the biochemical and molecular mechanisms controlling C19 steroidogenesis and the effects of activin and inhibin on the activity and expression of key ovarian thecal steroidogenic enzymes, cholesterol side-chain cleavage cytochrome P450 (P450scc), 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) and 17 alpha-hydroxylase/17,20 lyase cytochrome P450 (P450c17). Steroid production, level of steroidogenic enzyme mRNA expression, and enzyme activity following treatment with forskolin, inhibin-A and activin-A were examined. Basal steroid production, enzyme activities, and steroidogenic enzyme mRNA levels were not markedly different following treatment with activin (25 ng/ml) or inhibin (25 ng/ml) alone. Forskolin (10 microM) markedly increased production of both androstenedione (fivefold) and progesterone (threefold) as well as the activity of 3 beta HSD (sevenfold), and P450c17 (sevenfold) over basal. Forskolin stimulated the expression of mRNA for P450scc (fourfold), 3 beta HSD (threefold), and P450c17 (eightfold) over basal. Androstenedione accumulation was decreased by 60% in the forskolin plus activin group compared with forskolin alone, while progesterone production was maintained. This was attributed to a reduction of P450c17 mRNA (45% of forskolin alone) and activity (45% of forskolin alone). In contrast, co-treatment with forskolin and inhibin increased androstenedione production by 40% while decreasing progesterone by 40% compared with forskolin alone. Concomitantly, this was associated with a higher P450c17 mRNA expression (1.5-fold) and activity (twofold) but with minimal effects on the mRNA for 3 beta HSD and P450scc. HOTT cell responses to activin (0.05-50 ng/ml) and inhibin (0.05-50 ng/ml) in the presence of forskolin demonstrated dose-dependent effects on the steroid accumulation, enzymatic activity and mRNA expression of P450c17. Additionally, the differences seen on mRNA expression of steroidogenic enzymes in response to these factors were time-dependent. In summary, forskolin stimulated C19 steroid production from HOTT cells by increasing the expression of all steroidogenic enzymes examined. Inhibin and activin exerted differential effects on the expression of these enzymes which resulted in alterations in the steroid profile toward production of C19 steroids in the case of inhibin and away from C19 steroids in the case of activin. The influence of these important intraovarian factors on the expression of P450c17, a pivotal enzyme in thecal cell production of C19 steroids, could impact greatly on the follicular milieu of a normal developing follicle as well as in pathophysiological disorders such as polycystic ovarian syndrome.

3-Hydroxysteroid Dehydrogenases↗
PubMed2005

Elevated and similar urinary testosterone/epitestosterone ratio in all samples of a competition testing: suspicion of a manipulation.

The case of seven urine samples collected for anti-doping purposes during a cycling stage race with moderately elevated testosterone and epitestosterone ratio (T/E) is reported. The very low probability of having all seven urine samples with such similar elevated T/E ratio (from 3.2 to 4.7) was very suspicious. Different pattern classification tools were tested to categorize the most similar steroid profiles, but none of the models enabled a clear classification of the different urine samples. Subsequently, genetic profiling of all urine samples was performed and demonstrated that three of the seven samples were collected from the same cyclist. Finally, the International Federation confirmed DNA profiling results. This suggests that urinary steroid data using several methodologies are not appropriate for identification purposes and to an extent not unique to individuals.

Bicycling↗
PubMed1988

Detection of late onset steroid 21-hydroxylase deficiency by capillary gas chromatographic profiling of urinary steroids in children and adolescents.

Patients suffering from late onset 21-hydroxylase deficiency (LO-CAH) excreted only slightly higher amounts of 17-hydroxypregnanolone (17-OH-PO), pregnanetriol (PT) and 11-oxo-pregnanetriol (11-O-PT) than age-matched healthy controls. To discriminate between LO-CAH and virilization of unknown origin and precocious pubarche, we calculated the following ratios: (1) pregnanetriol to tetrahydrocortisone (PT/THE), (2) the sum of 17-OH-PO, PT and 11-O-PT (OHP-M) to the sum of THE, tetrahydrocortisol (THF) and allotetrahydrocortisol (a-THF) (C-M) and (3) 11-O-PT to C-M. The following patients were studied: 9 patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency-non-salt losing (CAH-NSL), never treated; 8 patients with CAH (NSL/SL: 3/5) off treatment; 10 patients with LO-CAH; 11 patients with virilization of unknown origin (prepubertal/pubertal: 5/6) and 9 patients with precocious pubarche. Healthy individuals and obligatory heterozygote carriers of comparable ages served as controls. LO-CAH showed increased ratios (median (range] of PT/THE: 2.27, (1.15-9.09), OHP-M/C-M: 2.30, (1.24-8.15), and 11-O-PT/C-M: 0.24, (0.13-1.23) compared to healthy individuals and heterozygous carriers: PT/THE 0.28, (0.03-0.57), OHP-M/C-M 0.23, (0.06-0.46) and 11-O-PT/C-M less than 0.01, (less than 0.01-0.06), respectively. The calculation of ratios, rather than absolute amounts seems to allow the detection of LO-CAH in a single spontaneously voided urine specimen. The clinical and measurable hormonal manifestations of LO-CAH occur at the same time.

Adolescent↗