Corticosteroid and corticosteroid metabolite levels in animals immunized against corticosteroids.
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Adrenal Cortex Hormones↗
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Inhaled corticosteroids compared with oral prednisone in patients starting long-term corticosteroid therapy for asthma. A controlled trial by the British Thoracic and Tuberculosis Association.
Inhaled beclomethasone dipropionate and inhaled betamethasone valerate have been compared with oral prednisone in the treatment of 75 patients with asthma who were starting long-term corticosteroids for the first time. Both of the inhaled corticosteroids controlled asthma as well as did oral prednisone in those who had responded to therapy in the initial period of the trial. A daily dose of 400 mug of inhaled drug was approximately equivalent to 7-5 mg daily of prednisone. Prednisone suppressed the adrenal response to tetracosactrin, whereas the mean responses in the groups receiving inhaled corticosteroids did not change significantly from pre-trial values. The 30% incidence of other systemic unwanted effects of prednisone contrasted sharply with the low incidence (5%) of symptomatic oropharyngeal candidiasis in the patients receiving inhaled corticosteroids. In a sample of 19 patients no change in exfoliative cytology was detected over the period of the trial nor was there any evidence of fungal colonisation of the bronchial tree. There was no difference between the three treatment groups in the number of antibiotic courses prescribed. The persistent production of sputum made no difference to the response to inhaled corticosteroids. Patients not on sodium cromoglycate did as well in the trial as those receiving sodium cromoglycate. Both inhaled beclomethasone dipropionate and inhaled betamethasone valerate have advantages over oral prednisone in the maintenance treatment of patients with asthma, but in the management of exacerbations systemic corticosteroids will usually be needed as a supplement to inhaled therapy.
Administration, Intranasal↗
Extremely high levels of corticosteroids and low levels of corticosteroid binding macromolecule in plasma of marmoset monkeys.
Marmoset monkeys were shown to have extremely high resting plasma corticosteroid levels compared to those of macaque monkeys and humans. A major component of corticosteroids seems to be cortisol. Levels of total 11-deoxy-17-KS in plasma of marmoset monkeys were very low (less than 0.01-0.04 microng/ml). Following the injection of ACTH, plasma corticosteroid levels of marmoset monkeys increased by 18-62% (at 1 h), and by 62-160% (at 2 h). Concentrations of plasma corticosteroid binding macromolecule in marmoset monkeys were extremely low (less than 10 nM). It was suggested that in these monkeys, the majority of plasma corticosteroids exists in non-protein bound forms.
Adrenal Cortex Hormones↗
[Treatment of acute asthma. Comparison of the effectiveness of corticosteroids and of a combination of corticosteroids and an adrenergic beta-stimulant (author's transl)].
Two comparable groups of patients hospitalised for acute asthma received an intravenous infusion for two hours, containing corticosteroids in the first group and corticosteroids combined with an adrenergic beta-stimulant in the second. Course was assessed by the hourly measurement of forced expiratory volumen in one second (FEV1), heart rate and blood pressure. It was found that corticosteroids alone had a modest action (5,1% improvement in FEV1). By contrast, the combination of corticosteroids with an adrenergic beta-stimulant resulted in a rapid and pronounced improvement in FEV1 (19,9%), without producing any undisrable side-effects. No changes in arterial blood gases were noted under the influence of treatment. Injectable adrenergic beta-stimulants are therefore worthy of use in the treatment of an asthma attack, in the absencd of any contraindication.
Adrenal Cortex Hormones↗
Studies of the diurnal pattern of plasma corticosteroids and gonadotropins in two cases of feminizing adrenal carcinoma: measurements of estrogen and corticosteroid production.
Two adult men with feminizing adrenal cortical carcinoma had measurements of their 24-h plasma corticosteroid and gonadotropin patterns as well as 24-h mean hormone levels of estradiol, estetrol, 11-desoxycortisol, DHEA-S, DHEA and testosterone. Cortisol, 11-desoxycortisol and estrogen production rates were also measured. The 24-h corticosteroid patterns showed preservation of the normal 24-h episodic and circadian patterns, albeit at higher levels. The cortisol production rates were markedly elevated despite only moderate elevation of the 24-h mean cortisol level. There were elevated plasma 11-desoxycortisol levels and a markedly elevated 11-desoxycortisol production rate in one patient and THS excretion in the other. The plasma estradiol levels, urinary excretion and production rates were markedly elevated. In addition, there was a decrease in the specific activity of estriol compared with estrone and estradiol as well as measurable levels of estetrol in both patients. These latter observations coupled with the urinary immunoassayable hCG in one patient suggest that these tumors may be functioning like trophoblastic tissue. The possibility that estetrol may serve as an additional marker for tumors of trophoblastic origin is of additional interest.
Adrenal Cortex Hormones↗
Effect of corticosteroids on sciatic nerve-tibialis anterior muscle of rats treated with hemicholinium-3. An experimental approach to a possible mechanism of action of corticosteroids in myasthenia gravis.
We studied the effect of intraperitoneally administered corticosteroids on the neuromuscular transmission in the sciatic nerve-tibialis anterior muscle preparation of the anesthetized rat stimulated at a rate of 10 Hz. Administered simultaneously with hemicholinium-3 (HC-3), 80 mug per kilogram (that is, half the lethal dose for 50 percent survival), prednisolone and dexamethasone cause a marked reversal of the block of the neuromuscular transmission caused by HC-3. The effect of aldosterone is very small. The blocking action of d-tubocurarine is not antagonized by either prednisolone or dexamethasone. Choline provides total protection against the HC-3 blockade, whereas physostigmine, in a just sublethal dose, is ineffective. We tentatively conclude that in myasthenia gravis the carrier-mediated transport of choline into the nerve endings may be deficient and that the beneficial effect of corticosteroids in this condition is based on their ability to ameliorate the deficient choline transport.
Animals↗
Synthesis and secretion of corticosteroid-binding globulin by rat liver. A source of heterogeneity of hepatic corticosteroid-binders.
Classical glucocorticoid receptors (type II) have a high affinity for synthetic and natural glucocorticoids. We have previously demonstrated an additional binding site in kidney cytosol (type III) which has a high affinity for corticosterone but a low affinity for dexamethasone. In many ways, this binder resembles plasma corticosteroid-binding globulin (CBG). The first goal of this study was to determine the organ distribution of the type III binding sites. Cytosol was prepared from isolated cells to avoid plasma contamination. Of the tissues examined, type III sites were found only in liver and kidney; sites were absent from thymocytes, IM-9 lymphocytes, adipocytes, and bone cells. The second goal of this study was to ascertain whether CBG is synthesized in liver and kidney. Liver and kidney slices were incubated in vitro and the concentration of type III sites was seen to rise in hepatic cytosol and incubating medium but not kidney. To verify the impression that liver was synthesizing and secreting CBG, the following experiments were performed: (a) To demonstrate that type III sites were CBG, steroid-binding profiles and migration on polyacrylamide gel electrophoresis were shown to be identical for hepatic type III sites and serum. (b) To indicate that the rise in type III sites was dependent on protein synthesis, it was shown that cycloheximide blocked the appearance of new type III sites. (c) To establish that the type III sites were being secreted, in situ liver perfusion experiments showed time-dependent release of new sites into the perfusate. In conclusion, liver synthesizes and secretes type III sites, a finding previously suspected but never proved. The presence of type III sites in kidney remains to be explained.
Animals↗
Corticosteroids and the humoral immune response of mice. II. Enhancement of bone marrow antibody formation to lipopolysaccharide by high doses of corticosteroids.
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Animals↗
Polar corticosteroids in human neonatal urine; synthesis and gas chromatography-mass spectrometry of ring A reduced 6-hydroxylated corticosteroids.
This report describes the synthesis of 3alpha,6beta,11beta,17alpha,21-pentahydroxy-5beta-pregnane-20-one, 3alpha,6beta,11beta,17alpha,21-pentahydroxy-5beta-pregnane-20-one, 3alpha,6alpha,11beta,17alpha,21-pentahydroxy-5alpha-pregnane-20-one, 3alpha,6beta,17alpha,21-tetrahydroxy-5beta-pregnane-11,20-dione, 3alpha,6beta,17alpha,21-tetrahydroxy-5alpha-pregnane-11,20-dione, 3alpha,6alpha,17alpha,21-tetrahydroxy-5beta-pregnane-11,20-dione and 3alpha,6alpha,17alpha,21-tetrahydroxy-5alpha-pregnane-11,20-dione. The gas chromatographic-mass spectrometric properties of these compounds are given. Proof of structure was accomplished using gas chromatography-mass spectrometry, microchemical reactions, optical rotatory dispersion and nuclear magnetic resonance spectroscopy.
Chromatography, Gas↗
Corticosteroids and the humoral immune response of mice i. Differential effect of corticosteroids upon antibody formation to sheep red blood cells in spleen and bone marrow.
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Adrenal Cortex Hormones↗
[Study on suppression of the pituitary-adrenocortical function by the therapeutic use of corticosteroids and its spontaneous recovery (author's transl)].
The present study was undertaken to investigate suppression of the pituitary-adrenocortical function by long-term corticosteroid therapy and spontaneous recovery from such a suppressant drug effect. Sixty patients who were on corticosteroids (hereinafter their dosage is expressed as the equivalent of prednisolone) given at 10 to 40 mg initially and then on a gradually decreasing basis down to below 10 mg currently or who had already been withdrawn from such a drug regimen were involved in the study and analysed for baseline values for plasma cortisol. These patients were evaluated for the functional status of the pituitary-adrenocortical system in relation to varying combinations of such factors as the total dose of corticosteroids, the duration in days of medication, the duration in days of mecication at reduced dosage levels, and time in days elapsed from cessation of medication. The results led to the following conclusions: (1) In patients receiving corticosteroids at such daily dosage levels as are reduced gradually to 7.5 mg or below within the duration in days as defined by the inequality Y greater than or equal to 8.4X + 222 (where Y stands for total dose given and X stands for the duration in days of administration), the pituitary-adrenocortical function is assumed to be in a state of being suppressed. When corticosteroids have been given at daily dosages reduced gradually to 7.5 mg or below within the duration in days as determined by the inequality Y less than or equal to 6.8X + 140 (where Y and X, respectively, stand as mentioned above), the pituitary-adrenocortical function of the recipient patient is considered to be in a state either of being not suppressed or of being recovered from suppressant drug effect. (2) In cases where corticosteroid therapy is started with a moderate dosage, then reduced to a low dosage level or stopped within relatively short period of time, the recipient patient can be safely withdrawn from the drug therapy without suppression of the pituitary-adrenocortical function if the dosage schedule is in line with the inequality Y less than or equal to 5.9X + 331 (where X denotes the duration in days of medication and Y, total dose). These results led the author to formulate a model of a corticosteroid dosage schedule which is reasonable free from the risk of causing pituitary-adrenocortical insufficiency. More particularly, the dosage of corticosteroids is reduced by a 5 mg decrement at regular intervals of 5, 8, 13, 27 and 103 days, respectively, when the initial daily dose is 30, 25, 20, 15 and 10 mg. By following this dosage regimen one might expect safe withdrawal from corticosteroid therapy without risking suppression of the pituitary-adrenocortical function. (3) Corticosteroid therapy, when given at a dosage of 7.5 mg or less daily, is considered to have little suppressant effect on the pituitary-adrenocortical function...
Adolescent↗
Corticosteroid effect on immunoglobulins.
The corticosteroid (prednisone) effect on serum immunoglobulins in 9 atopic asthmatic patients who required corticosteroids for the control of asthma was evaluated. Serum immunoglobulins were determined before corticosteroids were administered, an average of 15 days while on corticosteroids, and again an average of 22 days after corticosteroids were discontinued. While on corticosteroids (averaging 16.8 mg prednisone daily) for 15 days, mean serum IgG was significantly decreased (-22%, p less than or equal to 0.01), mean serum IgA tended to be decreased (-10%), and mean serum IgM was essentially unchanged. Serum IgE was initially significantly increased (p less than 0.01) when compared to levels of other serum immunoglobulins (IgG,A,M). An average of 22 days after corticosteroids were discontinued, mean serum IgG was still significantly decreased (p less than 0.05), and mean serum IgA again tended to be decreased. Serum IgM remained unchanged and mean serum IgE now was significantly decreased (p less than 0.01). Corticosteroids appear to have a significant effect on levels of some serum immunoglobulins.
Adolescent↗
Single-nucleus profiling reveals hepatocyte identity and immune features associated with corticosteroid response in severe alcohol-related hepatitis.
BACKGROUND & AIMS: Severe alcohol-related hepatitis (sAH) is associated with high short-term mortality. However, 30-40% of patients fail to respond to corticosteroids, the only proven pharmacological treatment. The pathophysiological mechanisms underlying sAH and the marked heterogeneity in treatment response remain incompletely understood. We aimed to define cellular changes associated with corticosteroid response in sAH and to identify baseline markers predictive of treatment outcome. METHODS: Single-nucleus RNA sequencing was performed on liver biopsies from patients with biopsy-proven sAH (n = 17), including paired baseline and day 8 biopsies in a subset of patients (n = 8). Patients were classified as corticosteroid responders (sAH-R; Lille score <0.45) or non-responders (sAH-NR; Lille score ≥0.45). Liver biopsies from patients with acute decompensation of alcohol-related cirrhosis (AD; n = 5) and healthy controls (n = 4) were included for comparison. Findings were validated using immunohistochemistry and spatial proteomics in a large multicenter validation cohort (n = 172). RESULTS: At baseline, sAH-R exhibited a significantly higher proportion of liver-infiltrating S100A8+ monocytes compared to sAH-NR, a difference that persisted at day 8. sAH livers showed a marked reduction in mature hepatocytes and an expansion of stressed and intermediate hepatocyte populations, indicating progressive loss of mature hepatocyte identity. This loss was more pronounced in sAH-NR, who also exhibited fewer cycling hepatocytes at day 8, consistent with impaired regenerative capacity. Expression of SULT2A1, a marker of mature hepatocyte identity, was significantly reduced in sAH-NR at baseline. Finally, liver biopsies with ≥50% SULT2A1-positive hepatocytes at baseline were strongly predictive of corticosteroid response. CONCLUSIONS: This study delineates distinct immune and hepatocyte changes associated with corticosteroid response in sAH. Baseline SULT2A1 expression may facilitate stratified treatment approaches in sAH. IMPACT AND IMPLICATIONS: Severe alcohol-related hepatitis (sAH) represents one of the most devastating manifestations of alcohol-related disorders. sAH is characterized by acute hepatic inflammation and high short-term mortality. Clinical management remains challenging, as corticosteroids - the only pharmacological therapy currently applied - are ineffective in a substantial proportion of patients and are associated with significant adverse effects. These limitations highlight the need for a more detailed understanding of sAH pathophysiology and for approaches that enable improved patient stratification and therapeutic decision-making. In this study, we identify distinct pre-treatment differences between corticosteroid responders and non-responders at the level of both hepatocytes and myeloid cells, providing new insight into the cellular mechanisms underlying treatment heterogeneity in sAH. Furthermore, leveraging these findings, we developed a histology-based SULT2A1 scoring system using a commercially available antibody, which predicts corticosteroid response at baseline and may support stratified treatment approaches in clinical practice.
Humans↗
Corticosteroid-binding proteins in human colostrum and milk and rat milk.
A corticosteroid-binding protein was detected in the whey of human colostrum and milk which resembles serum corticosteroid-binding globulin in certain respects: the equilibrium association constants for cortisol and progesterone binding and the apparent molecular size, as determined by Sephadex G-200 chromatography, were similar, and cortisol andd progesterone competed strongly for binding to the same site in each instance. Dexamethasone-binding activity could not be detected. The concentration of corticosteroid-binding protein in the colostrum obtained before parturition is about 0.1 muM; the concentration declines rapidly after parturition to about 0.01 muM. A corticosteroid-binding protein was found, also, in the whey of mature rat milk at levels of about 0.3 muM. This protein resembles rat serum corticosteroid-binding globulin: the equilibrium association constants for cortisol, corticosterone, and progesterone binding, and the apparent molecular size, as determined by Sephadex G-200 chromatography, were similar; the elution behavior of the respective proteins on anion exchange chromatography with DEAE-Sephadex A-50 was similar, also. Identity of the corticosteroid-binding proteins in whey with corticosteroid-binding globulin in serum is not presumed, however. Rat and human whey exhibited very little testosterone- or 17 beta-estradiol-binding activity. It is suggested the corticosteroid-binding proteins may play a significant physiological role in regulating the concentration of the bound and unbound forms of progesterone and cortisol in the fluids bathing the epithelial cells lining the mammary ducts and acini.
Adrenal Cortex Hormones↗
Evaluation of early prophylactic corticosteroid administration on early safety and efficacy outcomes of adeno-associated virus gene therapy in the hemophilia dog model.
BACKGROUND: Prior to commercial withdrawal, adeno-associated virus (AAV) gene therapy was approved for the treatment of adults with severe hemophilia A. Mechanisms underlying variability, durability, and liver transaminitis are largely uncharacterized. OBJECTIVES: To evaluate the effects of prophylactic corticosteroid administration on AAV gene therapy outcomes in dogs with severe hemophilia A. METHODS: Seven dogs with hemophilia A received 6e13 vector genomes/kg of AAV5-canine factor (F)VIII. Four dogs received oral prednisolone (1 mg/kg/day) starting 3 hours preinfusion with dose-tapering over 6 weeks; three control dogs received no corticosteroids. Percutaneous liver biopsies were performed on detection of alanine aminotransferase (ALT) >2-fold the upper limit of normal. RESULTS: All dogs expressed therapeutic FVIII:C (8.7-56.1%), improved whole blood clot time, and decreased bleeding rates (pre = 6.11 vs post = 1.42 bleeds/year, P = .016) over 2 years post-AAV5-canine FVIII. Corticosteroid-treated dogs demonstrated a modest increase in mean FVIII:C at 2 years by chromogenic substrate assay (39.1%) compared with controls (29.5%), driven by one female with markedly elevated FVIII:C from day 54 onward. When analyzed by sex, all female dogs exhibited increased mean FVIII:C chromogenic substrate assay at 2 years (49.3%) compared with males (9.1%), regardless of prophylactic corticosteroid use. Prophylactic corticosteroids did not impact transient posttreatment elevations of proinflammatory cytokines, anti-AAV antibody formation, or ALT levels. One corticosteroid-treated dog experienced ALT > 4.3-fold the upper limit of normal at 18 weeks without impacting long-term FVIII:C expression. A liver biopsy showed diffuse, minimal periportal lymphocyte and neutrophil infiltration, consistent with nonspecific minimal hepatitis. CONCLUSIONS: Prophylactic corticosteroids were not clearly associated with increased transgene expression in dogs with hemophilia A.
adeno-associated virus↗
Metyrapone: a possible tool in investigating the role of endogenous corticosteroids in inflammation.
Despite much early work on corticosteroid levels in the blood and urine of patients with rheumatic diseases, little strong evidence is available concerning the role of endogenous corticosteroids in inflammation. Nevertheless, the modulating role of adrenal corticosteroids in inflammation seems to be taken for granted even though the small amount of evidence in laboratory animals is, in some cases, contradictory. In the light of the immunological aetiology of some chronic inflammatory diseases and the immunosuppressive properties of corticosteroids, investigations into the role of endogenous corticosteroids in these conditions seem particularly worthwhile. Adrenalectomy has been used widely in studies on the physiological roles of adrenal corticosteroids but the operation requires care to avoid mortality. The adrenal corticosteroid synthesis inhibitor, metyrapone, could be used quite profitably in such investigations. However, it has been shown to exert differential effects on prostaglandin (PG) production in uterine tissue and may produce non-selective antagonism of the actions of PGs. Because PGs are probably involved in inflammation, care should be exercised in the doses of metyrapone used in any studies on inflammatory models to avoid interactions with the PG system.
Adrenal Cortex Hormones↗
Corticosteroids as adjunctive therapy to standard treatment in Kawasaki disease: a GRADE-assessed systematic review and meta-analysis of randomized controlled trials.
UNLABELLED: Kawasaki disease (KD) is an acute systemic vasculitis and the leading cause of acquired heart disease in children in developed countries. While IVIG plus aspirin remains standard treatment, 10-20% of patients are IVIG-resistant and face an elevated risk of coronary artery abnormalities. Corticosteroids have been explored as adjunctive therapy, though evidence on their benefit remains inconsistent. To assess the efficacy and safety of adjunctive corticosteroids in Kawasaki disease across key clinical outcomes. This PRISMA 2020-compliant systematic review and meta-analysis included RCTs identified through database searches up to April 2026. Risk of bias was assessed using Cochrane RoB 2.0. Data were pooled using random-effects models to estimate risk ratios (RRs) and mean differences (MDs) with 95% CIs. Subgroup analyses, leave-one-out sensitivity analyses, and GRADE certainty appraisal were also performed. Eight studies (n = 4106) were included. No significant differences were found in coronary artery abnormalities (CAA) within 1 month (RR 0.49, 95% CI 0.17-1.42), after 1 month (RR 0.81, 95% CI 0.43-1.55), fever duration (MD - 1.75, 95% CI - 3.71 to 0.21), or adverse events (RR 1.08, 95% CI 0.57-2.07). Hospital stay was modestly shorter with corticosteroids (MD - 0.99, 95% CI - 1.86 to - 0.11). Exploratory subgroup analyses suggested potential benefits with prednisolone-based and prolonged corticosteroid regimens for selected outcomes; however, these findings should be interpreted cautiously given multiple subgroup comparisons. Overall certainty of evidence was very low. CONCLUSION:  Adjunctive corticosteroids did not significantly improve major outcomes in KD. Prednisolone-based regimens showed some promise, but high-quality trials are still needed before any firm conclusions can be drawn. WHAT IS KNOWN: • Corticosteroids have been studied as adjunctive therapy for Kawasaki disease, but their effects on coronary outcomes and other clinical outcomes remain inconsistent. WHAT IS NEW: • This meta-analysis found no significant improvement in major outcomes with adjunctive corticosteroids, although prednisolone-based and prolonged regimens may provide benefits for selected outcomes.
Humans↗
The effects of acute corticosteroid therapy for asthma on serum immunoglobulin levels.
Immunoglobulin levels were followed in 21 nonsteroid-dependent asthmatics who required corticosteroids for an exacerbation of asthma. Twenty subjects who did not receive corticosteroids were used as controls. Baseline IgM and IgE levels were significantly higher in the corticosteroid-treated group. A fall in IgG level, maximal at 2 to 4 wk, was observed in the corticosteroid group, but not in control patients. Similarly, a significant fall in IgA was observed only in the corticosteroid group, maximal at 6 to 8 wk. There was no significant change in IgM levels in either group. Total IgE levels increased dramatically 1 wk after institution of corticosteroids. This was followed by a decrease to baseline or below at 6 to 8 wk. Changes in specific IgE antibody titers as measured by RAST technique revealed similar changes to those seen with total IgE. The results of the study indicate that asthma therapy with short-term corticosteroids can be associated with prolonged depressions of serum IgG, IgA levels and transient elevations of IgE levels, without apparent alterations of IgM levels.
Adolescent↗