Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “STEROIDS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 343 records · Page 19Linked to original sources

[Results of the treatment of steroid-resistant and steroid-dependent nephrotic syndrome with pulsed doses of prednisolone].

In 12 children with steroid-resistant and 17 with steroid-sensitive nephrotic syndrome massive doses of prednisolone were used in intravenous infusions ("pulses"). In 8 children with steroid-resistant and 9 with steroid-sensitive nephrotic syndrome very good or good results were obtained. The authors suppose that in a part of the children previous ineffectiveness of this immunosuppressive treatment could have been due to insufficient dosage. Rosette tests before and after pulses demonstrated a reduction of the total number of T-cells after pulses. The change of the ratio of theophylline-resistant to theophylline-sensitive lymphocytes suggests that this reduction was caused mainly by a fall of the number of helper T-cells and non-specific cytotoxic cells.

Adolescent↗

Elemental diet in steroid-dependent and steroid-refractory Crohn's disease.

Sixteen patients with Crohn's disease who had symptoms uncontrolled by high-dose steroids (n = 11) or symptoms invariably appearing on reduction or withdrawal of immunosuppressive therapy (n = 5) were treated with elemental diet. After 4 wk of dietary treatment, 10 patients were in remission and off all medication. Seven continued to be well without treatment for a minimum of 6 months, and four for at least 1 yr. No patient who subsequently relapsed had further steroid-refractory symptoms. Of the six patients failing to respond to elemental diet, four with steroid-refractory disease required early resective surgery for symptom relief, and two continued with steroid therapy, one in much reduced dosage. Elemental diet can bring about a sustained remission in many patients with Crohn's disease dependent on or refractory to corticosteroids, and reduce the need for surgical intervention.

Adolescent↗

Cyclosporin in the treatment of steroid-responsive and steroid-resistant nephrotic syndrome in adults.

The effect of cyclosporin on proteinuria was studied in 11 patients with steroid-responsive nephrotic syndrome (10 minimal change nephropathy, one IgM nephropathy) and in four patients with steroid-resistant nephrotic syndrome from focal segmental glomerulosclerosis. Cyclosporin (mean initial dose 7.7 mg/kg per day) produced a complete remission of proteinuria in 15 nephrotic episodes in the ten patients with minimal-change nephropathy after a mean 14.3 days (range 7-23 days) of therapy. All patients remained in remission while receiving cyclosporin (mean duration of follow-up 147 days; range 40-230 days). However, when cyclosporin was discontinued on nine occasions in five patients, all relapsed after a mean 47.8 days (range 7-180 days). Four of the five patients were subsequently rechallenged with cyclosporin and all responded. Maintenance cyclosporin therapy to prevent relapse was not associated with any adverse effects, and there was no significant difference between the creatinine clearance before and after 30 days of therapy (86.9 +/- 19.3 and 81.7 +/- 23.5 ml/min respectively, P greater than 0.1). The patient with steroid-responsive IgM nephrotic syndrome did not respond to cyclosporin, and there was no significant effect of cyclosporin on proteinuria in the four patients with FSGS. Cyclosporin is an effective agent for the treatment of patients with frequently relapsing minimal-change nephropathy who became steroid dependent when cyclophosphamide is contraindicated. However, unlike cyclophosphamide, long-term remissions which persist after treatment is withdrawn are not obtained, and patients may be said to be cyclosporin dependent.

Adolescent↗

Steroids excreted by human skin. II. C19-steroid sulphates in human axillary sweat.

Beside dehydroepiandrosterone sulphate and androsterone sulphate, 5-androstene-3 beta, 17 beta-diol-3-sulphate and testosterone sulphate were isolated and identified from the axillary sweat of sexually mature women and men. The quantities of these four C19-steroid sulphates were determined individually in the sweat of eight healthy, sexually mature women and men: dehydroepiandrosterone sulphate was found in the highest amount, it was followed by 5-androstene-3 beta, 17 beta-diol-3-sulphate and androsterone sulphate. Testosterone sulphate occurred in the lowest quantity, its excretion amounting to about one-thousandth of that of dehydroepiandrosterone sulphate. Study of the C19-steroid sulphates excreted by the apocrine sweat glands permitted an insight into the steroid metabolism in human skin, which presumably is, closely connected with the steroid hormones of peripheral blood.

Adolescent↗

Comparison of alternate day steroids and daily steroids in renal transplant recipients.

This retrospective study examined whether alternate day steroid therapy decreased the incidence or severity of side effects of prednisone without decreasing renal function. We conclude that alternate day steroid therapy is indicated in adult renal transplant recipients to treat steroid-induced diabetes, hypertension and minor prednisone side effects, but is not useful for obesity. Further, alternate day steroid therapy can be used safely without compromising renal function or graft survival.

Blood Glucose↗

Physiology of steroid dependent and non-steroid dependent asthmatic youths.

This study was designed to compare physical findings, pulmonary function and pituitary-adrenal function in steroid dependent (SD) and non-steroid dependent (NSD) children and adolescents in order to clarify similarities and differences between these groups. Study patients included 20 steroid dependent and 14 non-steroid dependent subjects. Abnormalities confined to the SD group included growth suppression, bone age retardation and cataracts. Pulmonary function abnormalities were severe in both groups. While the SD group also showed a degree of pituitary-adrenal abnormality. This suggests that chronic pulmonary disease may have physiologic consequences extending beyond the pulmonary tree.

Adolescent↗

Effect of cortisol on percentage of non-sex-hormone-bound steroid: implications for distribution of steroids on binding proteins in serum.

We previously observed that in men concentrations of serum testosterone (T) not bound to sex-hormone-binding globulin (n-SHBGT) decreased as concentrations of cortisol increased in early morning. This led us to investigate in vitro the influence of several steroids on protein-bound T. Steroids were added to late-evening sera containing low concentrations of cortisol. Changes were measured in percent T or estradiol not bound to SHBG (%n-SHBGT or %n-SHBGE). Results were compared with computer simulations of a mass action model describing current understanding of steroid binding to serum proteins. In vitro measurements confirmed changes observed in vivo. Cortisol at 600 nmol/L reduced %n-SHBGT to 61% +/- 5% of basal, but this was reversed with cortisol at 2000 nmol/L. Progesterone reduced %n-SHGBT less, and dexamethasone had no effect. Free T rose with added cortisol. Increasing estradiol to 900 nmol/L caused an increase in %n-SHBGT. The %n-SHBGE rose with added cortisol (121% +/- 5% of basal with cortisol at 1000 nmol/L). Simulation predicted all behaviors except the marked initial decrease in %n-SHBGT as cortisol concentrations increased and the absolute values of %n-SHBGT and %n-SHBGE. A possible explanation for the former is that T is displaced from corticosteroid-binding globulin (CBG) by added cortisol, more T is bound to CBG than expected, and T displaced from CBG associates with SHBG rather than albumin. Alternatively, current understanding about steroid binding to serum proteins has other major deficiencies.

Binding, Competitive↗

[Comparison of addition of theophylline to inhaled steroid with doubling of the dose of inhaled steroid in asthma].

The anti-asthmatic effect of theophylline may supplement those of inhaled steroids in asthma. The aim of the present trial was to study how the addition of theophylline compares to doubling the dose of inhaled steroid in asthmatics who remain symptomatic on beclomethasone dipropionate (BDP) 400 micrograms/day. The trial was designed as a randomized, double-blind, parallel-group study in several European countries. 69 patients were treated for 6 weeks with theophylline plus BDP 400 micrograms/day, compared to 64 patients treated with BDP 800 micrograms/day. The mean +/- SD serum theophylline concentration was 10.1 +/- 4.2 mg/l. Lung function measurements were made throughout the study and patients kept daily records of peak expiratory flow rate (PEF), symptoms and salbutamol usage. Forced expiratory volume in one second and PEF at week 6 were significantly increased by both treatments (p < 0.01). PEF variability was reduced by about 30% in both groups. There were significant improvements in asthma symptoms and rescue medication use (p < 0.001). There were no significant differences between the treatment groups. The study demonstrated clinical equivalence of theophylline plus beclomethasone dipropionate 400 micrograms/day and beclomethasone dipropionate 800 micrograms/day in patients whose asthma is not controlled on beclomethasone dipropionate 400 micrograms/d. The results support the use of theophylline as steroid-sparing agent. The combination of low-dose inhaled steroid plus theophylline is a suitable treatment for moderate asthma.

Adolescent↗

Relations between steroid-cell contact, steroid-binding and induction of tyrosine aminotransferase.

The induction of tyrosine aminotransferase by a variety of steroids was studied in cells from a hepatoma tissue culture (HTC). We have defined a class of steroids that induce TAT synthesis to a higher level than optimal inducers described earlier; these are called supra-inducers. When TAT induction is compared with the binding of the steroids to the cytoplasmic receptor or to their binding in the whole cell, a good correlation between binding in vivo of the hormone and its induction capacity can be established, whereas such a correlation was not systematically observed in vitro. A very short exposure of HTC cells to either dexamethasone or corticosterone is sufficient to induce TAT. When the inducer is removed from the culture medium a few minutes after its administration, the intracellular hormone concentration decreases very rapidly but TAT will be synthesized at its maximal rate. Thus the hormones behave as a starting signal for the optimal synthesis of the enzyme, and their presence in the culture medium is not necessary throughout the entire induction period.

Animals↗

New advances in the understanding of the role of steroids and steroid receptors in disease.

Steroids and related compounds are important in disease development and prevention, via steroid receptor-mediated and receptor-independent mechanisms. Interaction of endogenous oestrogens with the oestrogen receptor has unfortunate mitogenic effects in breast cancer. However, dietary consumption of non-steroidal weak oestrogens, such as the soy isoflavone phytoestrogens genistein and diadzein, is associated with a decreased breast cancer risk. This may arise in part from the suboptimal configuration induced in the transactivation helix of oestrogen receptor-beta.

Animals↗

Influence of the position of the double bond in steroid substrates on the efficiency of the proton-transfer reaction by Pseudomonas testosteroni 3-oxo-steroid delta 4-delta 5-isomerase.

Studies of the proton-transfer reaction by Pseudomonas testosteroni 3-oxo steroid Delta(4)-Delta(5)-isomerase with Delta(5(6))- and Delta(5(10))-steroid substrates demonstrate the importance of the position of the double bond for the efficiency of the isomerization process. Thus 3-oxo-Delta(5(6))-substrates have markedly high k(cat.) values, whereas those of 3-oxo-Delta(5(10))-substrates are very low and their apparent K(m) values approach equilibrium dissociation constants. The first step in the isomerization process is: [Formula: see text] which is governed by the k(-1)/k(+1) ratio and is shown to be very similar for the two classes of substrates (3-oxo-Delta(5(6))- and -Delta(5(10))-steroids). They therefore differ in the steps distal to the initial formation of the Michaelis-Menten complex. The use of the deuterated androst-5(6)-ene-3,17-dione substrate enabled us to calculate individual rate constants k(+1) and k(-1) as well as to determine the apparent rate-limiting step in the isomerization process. With the deuterated oestr-5(10)-ene-3,17-dione substrate, no significant isotope effect was observed suggesting that a different rate-limiting step may be operative in this isomerization process. Data are presented that indicate that under optimal concentrations of the efficient androst-5(6)-ene-3,17-dione substrate, the forward reaction for ES complex formation (as defined by k(+1)) is limited only by diffusion and the apparent K(m) does not approach the equilibrium constant, suggesting that the evolution of this enzyme has proceeded close to ;catalytic perfection'.

Androstenedione↗

Steroid and non-steroid anti-inflammatory agents in asthma.

Anti-inflammatory steroids are the principal agents for the treatment of asthma. Systemic corticosteroids are recommended for the treatment of acute episodes of asthma, whereas inhaled steroids should be used in the long-term prophylaxis of asthma. Because of their side-effects, there is a need for additional research and development of steroids without systemic activity, and/or other anti-inflammatory agents for use in the long-term prophylaxis of asthma.

Administration, Inhalation↗

Characteristics of steroid hormone receptors in cultured MC3T3-E1 osteoblastic cells and effect of steroid hormones on cell proliferation.

We examined the binding characteristics of three kinds of steroid hormones--estrogen, androgen, and glucocorticoid--in cultured MC3T3-E1 mouse osteoblastic cells by whole-cell binding assay. The binding studies revealed the presence of a single class of high-affinity binding sites for [3H]17 beta-estradiol, [3H]mibolerone (a synthetic androgen), and [3H]triamcinolone acetonide (a synthetic glucocorticoid). The numbers of binding sites for these steroid hormones were found to be 4534 +/- 819, 14312 +/- 1884, and 24898 +/- 655 sites/cell; and the Kd values were 8.57 +/- 0.62 x 10(-10) M, 1.12 +/- 0.19 x 10(-9) M, and 6.08 +/- 1.24 x 10(-10) M, respectively. We also examined the effects of steroid hormones on the proliferation of MC3T3-E1 cells. 17 beta-estradiol significantly stimulated the proliferation of the cells (130-150% of control). Dihydrotestosterone also significantly stimulated the proliferation of the cells (115% of control); the effect was, however, much less potent than that of 17 beta-estradiol, although the number of binding sites was approximately three times more than that of 17 beta estradiol. Triamcinolone acetonide and dexamethasone had no effect on cell proliferation. These results suggest that estrogen and androgen act directly on osteoblastic cells through a receptor-mediated mechanism, and that androgen is much less potent than estrogen in stimulating the proliferation of MC3T3-E1 osteoblastic cells.

Animals↗

Possible mechanism of steroid action of the plant herb extracts glycyrrhizin, glycyrrhetinic acid, and paeoniflorin: inhibition by plant herb extracts of steroid protein binding in the rabbit.

To assess the action of some components of herbal medicine, glycyrrhizin, glycyrrhetinic acid, and paeoniflorin, on steroids, their binding to several classes of intracellular and serum steroid-binding proteins were studied in the rabbit. The affinity (inhibitor constant) for binding of dihydrotestosterone-sex hormone binding globulin in the serum (dissociation constant of 2.0 nmol/L for dihydrotestosterone) was approximately 520 nmol/L, and that for the binding of cortisol-corticosteroid-binding globulin in the serum (dissociation constant of 2.0 nmol/L for cortisol) was approximately 10 mumol/L. In the uterine cytosol, the inhibitor constant value for estradiol receptor binding (dissociation constant of 1.0 nmol/L) was 0.9 mumol/L, and these compounds did not influence progestin receptor binding (dissociation constant of 1.4 nmol/L). The inhibitor constant values for glucocorticoid receptor binding (dissociation constant of 1.0 nmol/L) in the liver cytosol were 3.0 nmol/L for paeoniflorin, 2.0 nmol/L for glycyrrhizin, and 1.7 nmol/L for glycyrrhetinic acid, and those for mineralocorticoid receptor binding (dissociation constant = 1.1 nmol/L) in the kidney cytosol were 3.5 nmol/L for paeoniflorin and glycyrrhetinic acid and 3.0 nmol/L for glycyrrhizin. These results suggest that herbal extracts such as the above compounds influence steroid effects by glucocorticoid and mineralocorticoid receptors and to a lesser extent by estrogen receptors or serum sex hormone-binding globulin and corticosteroid-binding globulin.

Animals↗

Adrenal steroid type I and type II receptor binding: estimates of in vivo receptor number, occupancy, and activation with varying level of steroid.

Adrenal steroid (AS) receptors differ from other steroid receptors in the inability of the activated form of the cytosolic receptor to exchange ligand in an in vitro binding assay. We extended this finding by demonstrating that AS receptors extracted from isolated brain nuclei also failed to exchange ligand. Taking advantage of this unique feature of AS receptors, we measured type I and type II AS binding level in rats with varying amounts of endogenous glucocorticoids or exogenous dexamethasone (DEX). We estimated the degree of receptor occupation/activation in various brain areas and the pituitary during basal glucocorticoid conditions and after acute stress. There was a variable proportion of type I receptors in the hippocampus which were unactivated during basal conditions (0-35%). The proportion of unactivated type I receptors increased (55-65%) after DEX treatment. The hippocampus was especially sensitive to the ability of low basal corticosterone (CORT) levels to activate both type I and type II receptors, whereas the pituitary was very insensitive, evidenced by a failure of acute stress levels of endogenous glucocorticoids to occupy/activate type II receptors in the pituitary. Comparison of estimates of the degree of in vivo hippocampal type I and type II receptor activation for the various treatment groups with estimates of in vitro type I and type II receptor occupation by steroid suggested that DEX was more efficient than CORT in producing or maintaining the activated form of the type II receptor in vivo, whereas CORT was more efficient than DEX in activating the type I receptor. These studies suggest that AS receptors in the brain, and especially the hippocampus, are more sensitive to circulating levels of glucocorticoids than the pituitary. There also may be a greater capacity for physiological variations in type I receptor occupation in vivo than had previously been suggested. Finally, discrepancies between CORT and DEX affinity in vitro for type I and type II sites and their in vivo potency may be accounted for by differences in the ability of these compounds to activate type I and type II AS receptors.

Animals↗

Quantitative assessment of endogenous testicular and adrenal sex steroids and of steroid metabolizing enzymes in untreated human prostatic cancerous tissue.

Total tissue content and subcellular distribution of DHEA sulfate, DHEA, androst-5-ene-3 beta,17 beta-diol, androst-4-ene-3,17-dione, testosterone, 5 alpha-DHT, and 5 alpha-androstane-3 alpha,17 beta-diol as well as the activities of steroid sulfate-sulfatase, 17 beta-hydroxysteroid dehydrogenase, 5 alpha-reductase, 3 alpha/beta-hydroxysteroid dehydrogenase, and creatine kinase were quantified in 12 untreated primary tumors of prostatic cancer. Samples were obtained by radical prostatectomy and serial sections, and were alternately used for either biochemical or morphological evaluation. The results were compared with values determined in benign parts of the same prostates. Qualitatively, all enzymes and steroids found in the benign tissues could also be demonstrated in the cancers. Steroid patterns showed individual quantitative variation but no general differences between the carcinomas and the benign tissues. Enzymes showed a tendency to lower activities in the cancers, particularly when expressed per DNA. Substantial diminutions of creatine kinase and 5 alpha-reductase activity, the latter being often accompanied by an increased testosterone/DHT ratio, were the most striking differences seen in most of the cases between malignant and nonmalignant tissues. Some interesting individual parallels of morphological and biochemical aspects were seen, but there was no obvious general parallelism between the histological picture and endocrinological characteristics.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

Interaction between rat prostatic steroid 5 alpha-reductase and 3-carboxy-17 beta-substituted steroids: novel mechanism of enzyme inhibition.

Efforts to identify novel compounds capable of blocking the steroid 5 alpha-reductase (SR) catalyzed conversion of testosterone (T) to 5 alpha-dihydrotestosterone have resulted in the development of 17 beta-substituted-3-androstene-3-carboxylic acids as potent inhibitors of the rat prostatic enzyme. The dead-end inhibition patterns of one of these steroidal acrylates, 17 beta-N-(2-methyl-2-propyl)-carbamoyl-androst-3,5-diene-3-carboxylic acid were best evaluated with a linear uncompetitive kinetic model vs both T (Kii = 11 +/- 1 nM) and NADPH (Kii = 22 +/- 2 nM). To interpret these observations, the kinetic mechanism of the rat prostatic SR was shown to involve the binding of NADPH prior to that of T through a series of dead-end and product inhibition experiments. Within the context of this preferentially ordered kinetic mechanism, it is proposed that the uncompetitive inhibition patterns result from the association of the steroidal acrylate to an enzyme complex containing NADP+ in formation of a dead-end ternary complex of enzyme, NADP+, and inhibitor.

5-alpha Reductase Inhibitors↗