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Results for “Steroid profiling”

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PubMed2005

Novel insertion frameshift mutation of the LH receptor gene: problematic clinical distinction of Leydig cell hypoplasia from enzyme defects primarily affecting testosterone biosynthesis.

Leydig cell hypoplasia (LCH) is a rare autosomal recessive condition that interferes with normal development of male external genitalia in 46,XY individuals and is caused by inactivating mutations of the LH receptor gene. The clinical and biochemical diagnostic parameters of LCH are not always specific and may therefore show significant overlap with other causes of insufficient testicular steroid biosynthesis. We have studied a 46,XY newborn with completely female external genitalia and palpable testes. Due to an increased basal serum ratio of androstenedione/testosterone, 17 beta-hydroxysteroid dehydrogenase type 3 (17 beta-HSD 3) deficiency was initially suspected. DNA analysis of the corresponding HSD17B3 gene, however, showed no abnormalities in the entire coding region. In contrast, direct sequencing of the LH receptor gene revealed a novel homozygous single nucleotide insertion in exon 11 (codon A589fs) producing a frame shift in the open reading frame predicting for premature termination of translation 17 amino acids downstream. From the genetic perspective, this mutation represents the first frame shift mutation in the LH receptor gene ever reported to date. From the clinical standpoint, LCH should always be considered in the differential diagnosis as steroid profiles may not be informative. Therefore, molecular genetic analysis should be warranted for androgen biosynthesis defects in all cases.

Amino Acid Sequence↗

PubMed2006

GH effect on enzyme activity of 11betaHSD in abdominal obesity is dependent on treatment duration.

OBJECTIVE: In the past years the interaction of GH and 11beta hydroxysteroid dehydrogenase (11betaHSD) in the pathogenesis of central obesity has been suggested. DESIGN: We studied the effects of 9 months of GH treatment on 11betaHSD activity and its relationship with body composition and insulin sensitivity in 30 men with abdominal obesity, aged 48-66 years, in a randomised, double-blind, placebo-controlled trial. METHODS: Urinary steroid profile was used to estimate 11betaHSD type 1 and 2 (11betaHSD1 and 11betaHSD2) activities. Abdominal s.c. and visceral adipose tissues were measured using computed tomography. Glucose disposal rate (GDR) obtained during a euglycaemic-hyperinsulinaemic glucose clamp was used to assess insulin sensitivity. RESULTS: In the GH-treated group the 11betaHSD1 activity decreased transiently after 6 weeks (P < 0.01) whereas 11betaHSD2 increased after 9 months of treatment (P < 0.05). Between 6 weeks and 9 months, GDR increased and visceral fat mass decreased. Changes in 11betaHSD1 correlated with changes in visceral fat mass between baseline and 6 weeks. There were no significant correlations between 11betaHSD1 and 11betaHSD 2 and changes in GDR. DISCUSSION: The study demonstrates that short- and long-term GH treatment has different effects on 11betaHSD1 and 11betaHSD2 activity. Moreover, the data do not support that long-term metabolic effects of GH are mediated through its action on 11betaHSD.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗

PubMed1983

Development of some male characteristics supported by oestrone but not dehydroepiandrosterone in the boar.

Prepubertally castrated boars received subcutaneous injections twice weekly, from 13 to 35 weeks of age, of dehydroepiandrosterone (2 mg/5 kg) or oestrone (1 mg/5 kg). Dehydroepiandrosterone did not support the growth and secretory activity of the accessory organs, or induce copulatory behaviour. However, oestrone caused hypertrophy of the prostate, seminal vesicles and bulbourethral glands which was due to an increase in fibrous stromal tissue and not to the secretory epithelium. Oestrone also induced some male mating behaviour patterns in the presence of an oestrous gilt, although penile extrusion and ejaculation did not occur. The morphological and behavioural effects of the steroid treatments were supported by steroid profiles in blood plasma as seen in comparison with androgen and oestrogen values of intact and untreated castrated boars. It is concluded that oestrogen in the intact boar might enhance the secretion of the accessory organs by affecting the neural control of the secretory processes rather than by increasing the amount of secretory epithelium in the glands.

Androgens↗

PubMed1989

Relationship between pre-partum relaxin concentrations and farrowing intervals in the pig.

Gilts were treated on Day 112 of gestation with saline or a prostaglandin (PG) F-2 alpha analogue. In control gilts there was a rise in the relaxin concentration from 48 h before the onset of delivery, peaking between 12 and 28 h pre partum followed by a steep fall. The relaxin concentrations at each 1-h time interval were analysed in relation to the farrowing interval for each gilt using correlation analysis. There was a significant (at least P less than 0.05) positive correlation between the relaxin concentration and the farrowing interval at every time period from 14 to 2 h before delivery. In contrast there was little relationship between concentrations of progesterone, oestrone and oestradiol-17 beta and farrowing intervals. The gilts treated with PGF-2 alpha analogues had steroid profiles indistinguishable from those in controls but differing relaxin secretion patterns. Relaxin concentrations peaked at 1-2 h after PGF-2 alpha injection and this was followed by a second smaller increase closer to the time of delivery in 7 out of 12 gilts. The 'two-peak' gilts had significantly higher relaxin concentrations at farrowing and took significantly longer to farrow than did the 'one-peak' gilts (P less than 0.005). These results suggest that high relaxin concentrations during the last 14 h before the onset of parturition are associated with increased farrowing times, but are not associated with any increase in neonatal mortality.

Animals↗

PubMed1985

Control of zona glomerulosa function in the isolated perfused rat adrenal gland in situ.

The extent to which results obtained using in-vitro techniques can be taken to reflect in-vivo physiological responses in the study of adrenocortical function has not been subjected to systematic study. Some evidence suggests that in-vitro preparative methods may affect the secreted steroid profile. For this reason it seemed desirable to study adrenal function using an isolated perfused whole gland technique, and this study reports results obtained with known aldosterone stimulants. Angiotensin II, ACTH and potassium ions all stimulated aldosterone secretion in a dose-dependent manner. The stimulation thresholds of these substances were compatible with their normal circulating concentrations. For angiotensin II stimulation this preparation was two orders of magnitude more sensitive than any in-vitro preparation. Most importantly, the specific glomerulosa effectors, angiotensin II and potassium, selectively stimulated aldosterone output, and had no consistent effect on corticosterone secretion at any dose used. On the other hand, ACTH stimulated both corticosterone and aldosterone output at all effective concentrations. The actions of alpha-MSH were also studied using this preparation. Low doses of alpha-MSH selectively stimulated aldosterone secretion, while higher doses were needed to stimulate corticosterone. The onset of response to all stimulants was invariably seen within the first 10 min after administration of stimulants. Maximal aldosterone output was achieved within the first 10 min whereas corticosterone secretion usually peaked 10-20 min later. The amount of aldosterone produced by this preparation was much higher than the amount produced by dispersed cell preparations, and closely approximated to the levels of aldosterone obtained in adrenal vein blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1997

Lactogenic hormones of the placenta and pituitary inhibit suckling-induced prolactin (PRL) release but not the ante-partum PRL surge.

Prolactin (PRL) and other lactogenic hormones feed back at the hypothalamus to inhibit PRL release. At midpregnancy, high circulating levels of placental lactogens (PL) terminate the mating-induced biphasic PRL surges in female rats. In the dark period preceding parturition, however, an ante-partum PRL surge occurs despite continuously high levels of PL. This study examined whether the lactogenic hormone negative feedback loop is altered during the ante-partum surge using two models: (i) pregnant rats given a hypothalamic implant of albumin, ovine PRL, or recombinant rat PL-I on Day 19 or 20 of pregnancy; and (ii) pregnant rats bearing a transplant of a rat choriocarcinoma cell line, Rcho-1 (PL-secreting), or HRP-1 (non-PL-secreting). Serial blood samples were taken via carotid cannula from all rats. Although lactogenic hormones placed in the hypothalamus reduced suckling-induced PRL release by 89%, hypothalamic implants of oPRL or recombinant rPL-I did not attenuate the ante-partum PRL surge. Rcho-transplanted rats also did not have a significantly reduced ante-partum PRL surge (peak PRL level, 131 ng/ml) compared with HRP-bearing rats (peak PRL level, 107 ng/ml). Northern blot analysis revealed that the Rcho-1 tumors expressed both PL-I and PL-II, while the HRP-1 tumors did not express either PL. The inability of the Rcho-1 transplants to inhibit the ante-partum PRL surge suggests that lactogenic hormone negative feedback is disrupted during the ante-partum period, possibly by the changing steroid profile associated with parturition.

Animals↗

PubMedDate not supplied

[Low-renin hypertension and inherited mineralocorticoid diseases].

Liddle's syndrome, apparent mineralocorticoid excess (AME) and glucocorticoid remediable aldosteronism (GRA) are inherited diseases characterized by hypertension and low plasma renin activity. Constitutive activation of distal renal epithelial sodium channel (Liddle's syndrome), defect in 11 beta-hydroxysteroid dehydrogenase activity (AME) and unequal crossing over, fusing regulatory sequences of 11 beta-hydroxylase gene to coding sequences of aldosterone synthase gene and forming a new chimeric gene (GRA), cause apparent or real mineralocorticoid excess. This diseases are often being unrecognized and classified as essential hypertension, especially in patients with normal serum potassium level. Family history of hypertension and characteristic serum and urine++ steroid profile direct us to diagnosis, and genetic analysis will confirm it.

Humans↗

PubMedDate not supplied

[Sex differences in the level of lipid peroxidation in white rats in a normal state and change in it after gonadectomy and administration of alpha-tocopherol].

The patterns of plasma lipid peroxidation (LPO) in normal male and female rats, after gonadectomy and alpha-tocopherol treatment were investigated. Sexual LPO differences were established and confirmed by the dispersion analysis. It is suggested that alpha-tocopherol participates in the regulation of steroid profile by regulating and adrenokynetic of the hypophysis.

Animals↗

PubMedDate not supplied

An unusual case of Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia.

We report a case of Cushing's syndrome due to ACTH-independent macro-nodular adrenal hyperplasia (AIMAH). The patient, a 51-year-old man, had been suffering from poorly controlled arterial hypertension for the previous 6 years and he complained of progressive weight gain, gynecomastia and impotence. Physical examination revealed classic cushingoid features. Endocrine basal assessment showed increased urinary free cortisol (264-600 micrograms/24 hr). Urinary steroid profile showed an increase of total 17-hydroxycorticosteroids (17-OHCS: 23 mg/24 hr), with a threefold increase of tetrahydrocortisol (THF:9.66 mg/24 hr) and of tetrahydrocorticosterone (THB: 1.35 mg/24 hr). Tetrahydrodesossicortisol was only slightly elevated (THS:0.67 mg/24 hr) and tetrahydrodesossicorticosterone was at the inferior limit of the normal range (THDOC: 0.03 mg/24 hr). Total 17-ketosteroids were decreased (17-KS: 3 mg/24 hr). Plasma cortisol level was elevated and without circadian rhythm (26-29 micrograms/dl in the morning, 26-28 micrograms/dl at 24:00 h). DHEAs and free testosterone levels were significantly reduced (106 ng/dl and 3.9 pg/ml respectively). ACTH was undetectable and unresponsive to CRH. Both dexamethasone and octreotide failed to suppress plasma cortisol levels. Abdomen computed tomography scan demonstrated bilaterally enlarged multinodular adrenal glands. Cerebral magnetic resonance revealed no alteration of the pituitary gland. The patient underwent bilateral adrenalectomy. On macroscopic examination, adrenal glands were occupied by multiple yellow nodules and their compressive weight was 190 g, with left adrenal heavier than the right one (120 g and 70 g respectively). Histologically, nodular lesions were predominantly composed of large clear cells, with small foci of "hybrid" cells and adipose tissue metaplasia. Reticularis zone was atrophic. In the immediate post-operatory course pulmonary embolism occurred, despite prophylaxis with low molecular weight heparin. After having recovered from this complication, the patient showed progressive regression of cushingoid status. The findings of increased THF/THS and THB/THDOC ratios were in agreement with a relative hyperfunction of 11-beta-hydroxylase "in vivo", which might have contributed to the hypercortisolism, in addition to the marked increase of secernent adrenal mass.

Adrenal Gland Diseases↗

PubMed1992

Mineralocorticoid excess due to precursors only in a patient with adrenal cortical carcinoma.

A patient with carcinoma of the adrenal cortex presented with mineralocorticoid excess due to hypersecretion of deoxycorticosterone, which is exceedingly rare. Backache was the only symptom and an unexplained hypokalaemia was the only sign. Because of the abnormal synthesis of steroid precursors in these tumours a urinary steroid profile may be helpful as a diagnostic tool in such cases.

Adrenal Cortex Neoplasms↗

PubMed1990

Adrenocortical carcinoma. A retrospective study of a rare tumor with a poor prognosis.

A retrospective study was performed on 54 patients diagnosed as having adrenocortical carcinoma during 1974-1983. The initial symptoms were often diffuse: abdominal pain, weight loss, or fever, and more than 60% of the patients showed no evidence of overproduction of hormone. The median tumor diameter was 13 cm and almost half of the tumors had metastasized at diagnosis. A radical tumor resection could be performed in less than 50% of the patients, and at histopathological re-examination some tumors were not conclusively verified as malignant. Capsular invasion, nuclear pleomorphism and mitoses were found more commonly in patients who succumbed to the disease. Seven of 29 patients treated with chemotherapy showed an objective response and two of them are still alive and free of disease. The overall 5-year-survival rate was 19%, compared with 45% for patients with radically resected tumors. Patients with no biochemical signs of overproduction of adrenocortical hormone appeared to have a better prognosis than those with hormone excess. Together with increased use of ultrasound and computed tomography, a urinary steroid profile might hopefully contribute to earlier discovery of these often clinically silent tumors. However, it remains to be determined whether these diagnostic improvements, together with more aggressive surgery and adrenolytic chemotherapy, can improve the poor prognosis.

Adolescent↗

PubMed1987

Modification of steroidogenesis in rat adrenocortical cells transformed by Kirsten murine sarcoma virus.

Adrenal fibroblasts from adult rats acquire some adrenocortical parenchymal characteristics as a consequence of transformation in early passage with Kirsten murine sarcoma virus. To further define the effects of Kirsten murine sarcoma virus-induced transformation on the steroid enzymes of these cells, we investigated the capacity of Kirsten murine sarcoma virus-transformed and untransformed adrenocortical fibroblasts to convert progesterone to C19 and C21 steroid metabolites. Over 95% of metabolites produced were identified and quantitated, and rates of enzyme activities over 24 h were calculated. The transformed and untransformed cells exhibited 5 alpha- and 5 beta-reductase, 3 alpha-, 3 beta-, and 20 alpha-hydroxysteroid dehydrogenase; 11 beta-, 17-, and 21-hydroxylase (HY); and C17-20-lyase activities. Viral transformation resulted in several metabolites not found in untransformed cells, significantly increased 5 beta-reductase, 3 beta-hydroxysteroid dehydrogenase, and C17-20-lyase activities, and significantly decreased 5 alpha-reductase, 3 alpha- and 20 alpha-hydroxysteroid dehydrogenase, and 21-HY activities. The 11 beta-HY and 17-HY activities remained unchanged. The results support previous data suggesting that adrenocortical fibroblasts express some characteristics of adrenocortical parenchymal stem cells. In contrast to other experimental systems, viral transformation of adrenocortical fibroblasts did not cause a generalized reduction of differentiated functions. Instead, specific increases and decreases in individual enzyme activities, with persisting synthesis of fetal and adult adrenocortico-specific steroids, resulted in an altered steroid profile that may have unique effects on the biology of the malignant cells.

Adrenal Cortex↗

PubMed1987

Steroid secretion by different cell types of the horse conceptus.

Horse conceptuses were recovered non-surgically at Day 12-Day 15 and were dissociated with collagenase. Separation of the cells on a 31.8% Percoll gradient gave two bands of cells and indirect evidence suggests that the low density cells (LDC) are endoderm and the higher density cells (HDC) are trophectoderm. Each band was incubated for 24 h in Minimum Essential Medium and concentrations of oestradiol and progesterone in the medium were measured by radioimmunoassay (RIA). The LDC secreted predominately progesterone (log oestradiol/progesterone = -0.994 +/- 0.141; N = 15) whereas the HDC secreted mainly oestradiol (log oestradiol/progesterone = 0.522 +/- 0.135). When incubated for a further 24 h in fresh medium the oestradiol production decreased by 85% and 84% whereas the progesterone production decreased by 57% and 50% for LDC and HDC respectively. When cells from each band were incubated for 24 h with [3H]pregnenolone, separation of the radiolabelled metabolites by reversed-phase high-pressure liquid chromatography revealed a different steroid profile for each cell type. Therefore, in the intact embryo, an interaction between cells may be important for oestrogen synthesis and thus the maintenance of pregnancy.

Androstenedione↗

PubMed1987

Simultaneous measurement of eight corticosteroids by liquid chromatography, and application of the procedure to diagnosis of congenital adrenal hyperplasia.

We describe a liquid-chromatographic procedure for simultaneously determining eight steroids in serum. We used a Zorbax ODS column and a mobile phase of methanol/isopropanol/water (44/10/46, by vol), which well resolves the steroids cortisone, cortisol, corticosterone, 11-deoxycortisol, 11-deoxycorticosterone, androstenedione, 17-hydroxyprogesterone, and progesterone, but not 11-deoxycorticosterone and androstenedione. Analytical recoveries of the steroids ranged from 89.27% to 99.58%. CVs were less than 10%. Prednisone and dexamethasone do not interfere. Using this method, we studied the serum steroid profiles of six patients with congenital adrenal hyperplasia (CAH) due to deficiency of 21-hydroxylase or 17-hydroxylase. Not only could we make a clearcut diagnosis and distinguish the subtle types of CAH, but also we could investigate clinical and biochemical variants of CAH. For example, we confirmed 17-hydroxylase deficiency in a patient who was normotensive with primary amenorrhea and streak gonads.

Adrenal Cortex Hormones↗

PubMed1993

Adrenocortical carcinoma--diagnostic and therapeutical implications.

OBJECTIVE: To evaluate the results of treatment of a consecutive series of patients with adrenocortical carcinoma who presented during the six year period 1985 to 1991. DESIGN: Open study. SETTING: Departments of Surgery, Pathology, Endocrinology, and Clinical Chemistry, Sahlgren Hospital, Göteborg, Sweden. SUBJECTS: 10 consecutive patients, two with recurrent and eight with primary adrenocortical carcinoma. INTERVENTIONS: All patients were treated surgically. Two required preoperative embolisation of the tumour vessels to facilitate excision of particularly large tumours, and eight were given adjuvant treatment with mitotane (o,p'-DDD). RESULTS: At a median follow up of 1.5 years (range 3 months, to 21 years) 6 patients were alive with no radiological or biochemical signs of disease; 2 were alive, but with signs of recurrence (at 3 months and 6 years, respectively); and two had died of their disease (at 4 and 8 months, respectively). For the past two years all patients have had their urinary steroid profiles monitored by gas chromatography and mass spectrometry to detect recurrence of the tumour at the earliest possible stage. CONCLUSION: Operation is the treatment of choice for patients with adrenocortical carcinoma, particularly stages I-III. The role of mitotane as adjuvant treatment can be evaluated only in multicentre studies.

Adrenal Gland Neoplasms↗

PubMed2003

Steroid hormone concentration profiles in healthy intact and neutered dogs before and after cosyntropin administration.

The purpose of this study was to determine steroid hormone concentration profiles in healthy intact and neutered male and female dogs. Seventeen intact female dogs, 20 intact male dogs, 30 spayed female dogs, and 30 castrated male dogs were used in this study. Serum samples were collected before and 1h after cosyntropin administration, and serum concentrations were determined for cortisol, progesterone, 17-OH progesterone (17-OHP), dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone, and estradiol. Intact male dogs had greater concentrations of DHEAS, androstenedione, and testosterone. Intact female dogs had greater concentrations of progesterone. There was no significant difference in estradiol concentration among the four groups. Intact male dogs had lower concentrations of cortisol post-stimulation. DHEAS and testosterone did not increase in response to ACTH in intact males, and estradiol concentrations did not increase in response to ACTH in any group. Results from this study will enhance interpretation of suspected adrenal and/or gonadal disorders of dogs. Because estradiol concentrations were similar in all groups of dogs, measuring estradiol may not be a useful diagnostic test. Cortisol concentrations for intact male dogs with hyperadrenocorticism may be lower than those of female or neutered dogs.

17-alpha-Hydroxyprogesterone↗

PubMed1989

Annual profiles of sex steroids in blood plasma and ovarian tissue of wild female musk shrew, Suncus murinus.

Relative ovarian weights with bursa and annual profiles of sex steroids have been described in the female musk shrew, Suncus murinus, collected in the vicinity of Rawalpindi, Pakistan. The relative gonadal weight was basal (23.20 +/- 1.20 mg/100 g) during anoestrus but enhanced (39.93 +/- 2.73 mg/100 g) abruptly at the onset of the breeding season. Plasma progesterone concentrations, measured during different parts of the year, indicated elevated levels during the late pregnant stage (p less than 0.01). The ovarian progesterone was also comparatively higher in late pregnant animals. No significant difference was observed in plasma and ovarian oestradiol.

Anestrus↗

PubMed1980

Steroid and gonadotropin profiles in menopausal women on three different oral replacement regimens.

Three different estrogen-progestin regimens were studied in the treatment of menopausal symptoms. Plasma steroid and gonadotropin profiles were determined. As judged by the increase of plasma FSH concentrations, as well as by the decrease of plasma estrone and estradiol concentrations, one treatment-free week during a four week cycle was too long. This FSH increase could not even be eliminated by administering estrogen at half the treatment dose.

Adult↗