Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “corticosteroids”

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 37 records · Page 2Linked to original sources
PubMed2026

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↗
PubMed1977

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↗
PubMed2026

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↗
PubMed1978

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↗
PubMed1979

Comparison of chlorambucil, azathioprine or cyclophosphamide combined with corticosteroids in the treatment of lupus nephritis.

163 patients with diffuse lupus glomerulonephritis, proven by renal biopsy, were divided into four therapeutic trial groups: 67 were put on corticosteroids alone, 11 on corticosteroids and azathioprine, 32 on corticosteroids and cyclophosphamide, and 53 on corticosteroids and chlorambucil and were followed up for several years. The addition of azathioprine to corticosteroids did not increase the survival rate, improve the renal function or alter the grim prognosis of the patients. Cyclophosphamide appeared to influence favourably the pathological lesion and the renal function when added to corticosteroids, and the disease progressed at a slower rate. The fatal side effects nearly balanced the therapeutic value of cyclophosphamide. Patients on corticosteroids and chlorambucil had an excellent course. This therapeutic regimen resulted in resolution or regression of the renal pathology, marked improvement of the renal function and marked improvement of the survival rate. The authors believe that this therapeutic regimen holds the best chance of becoming the standard treatment for lupus nephritis, particularly since the side effects of chlorambucil were minimal.

Adolescent↗
PubMed1975

Reduction of blue tetrazolium by corticosteroids.

Pseudo-first-order rate constants were observed for the reaction of corticosteroid or corticosteroid esters with blue tetrazolium. The data indicate that the reactivity of corticosteroids is, in part, a function of their geometry in that corticosteroid reactivity toward blue tetrazolium increases with increasing planarity of the steroid molecule and that corticosteroid esters must be hydrolyzed as a necessary prerequisite to reaction with blue tetrazolium. Evidence is presented indicating that free radicals are not involved in the blue tetrazoliun reaction with corticosteroids. Certain pharmaceutically important compounds such as pyrocatechol derivatives and hydroquinone appear to reduce blue tetrazolium by the anion free radical mechanism proposed previously. A spectrophotometric method for determining the number of reduction units transferred to blue tetrazolium per molecule is described.

Adrenal Cortex Hormones↗
PubMed1975

Some aspects of corticosteroid-induced cleft palate: a review.

Since the discovery 25 years ago that cortisone can produce cleft palate in mouse embryos investigations into possible mechanisms of this corticosteroid-induced defect have been many and varied. However, the teratogenic mode of action remains not fully clarified. It is with this thought in mind that we have reflected upon what is known concerning corticosteroids and cleft palate. The major metabolic pathways upon which glucocorticoids act as well as their intracellular mode of action are well known. Differential sensitivity of various mouse strains to cortisone treatment as well as recent results from interstrain blastocyst transfer experiments demonstrate that corticosteroid action is influenced by both the fetal and maternal genomes. Labeling experiments indicate that corticosteroid-induced cleft palate is the result of direct action of the steroid molecule on the fetus, whose own sensitivity to insult, perhaps owing to differences in binding of corticosteroids to tissue proteins, determines the final effect. Possible mechanisms that have been proposed by which corticoids may produce cleft palate include: disruption of glycosaminoglycan or collagen synthesis or both, intracellular lysosomal membrane stabilization, myopathy, weakened midline fusion, and loss of amniotic fluid. Also discussed is the role of stress and stress-induced corticosteroids and their possible role in the production of cleft palate.

Adrenal Cortex Hormones↗
PubMed1978

Comparison of synchronization of circadian corticosteroid rhythms by photoperiod and food.

Under conditions of feeding at will and normal light-dark alternation, rats consume the major portion of their daily food intake during the dark period and the circadian peak of plasma corticosteroid concentrations and of body temperature levels occurs just prior to or subsequent to the time of light-dark transition. Both light-dark transition and time of food presentation have been implicated as "Zeitgebers" in determining the phase of these two circadian rhythms. THE PRESENT DATA INDICATE THE FOLLOWING: (i) The time of food presentation appears to be a more potent synchronizer of the phase of plasma corticosteroid levels than is the light-dark cycle. This has been demonstrated in rats under conditions in which light-dark phase shift has been dissociated from a concomitant shift of time of eating. In contrast, under such conditions, the rhythm of body temperature appears to be more tightly coupled to the light-dark cycle. This illustrates that the time of food ingestion and the peak of body temperature rhythms can be uncoupled and that the phasing effects of restricted food ingestion on corticosteroid rhythms does not extend to body temperature rhythms. It also suggests the presence of different control mechanisms and/or pathways for corticosteroid and body temperature rhythms as well as the use of different pathways by different Zeitgebers. (ii) Rats maintained in constant dim light with free access to food exhibit aperiodic feeding behavior; plasma corticosteroid concentrations and body temperature levels are also aperiodic. Imposition of a restricted period of food access under such constant light conditions is associated with the appearance of a circadian periodicity of both plasma corticosteroid concentrations and body temperature levels, with peaks, respectively, just before and after the time of food presentation. This represents an additional example of food entrainment of previously aperiodic functions, similar to the food entrainment we have described in animals rendered aperiodic by lesions of the suprachiasmatic nucleus.

Adrenal Cortex Hormones↗
PubMed1976

Corticotropin and corticosteroids in generalized myasthenia gravis: comparative studies and role in management.

The effect of 310 courses of corticotropin, methylprednisolone, prednisone, and dexamethasone were studied in 62 patients with generalized myasthenia gravis who were poorly responsive to anticholinesterase medication and most of whom required assisted respiration. Improvement in strength and response to anticholinesterase medication occurred in 91% of the courses, and was moderate or marked in 63%. The incidence, degree, and duration of improvement appeared to be dose related. High doses of dexamethasone (20 mg orally each day for 10 days, repeated if necessary), which had 75% more glucocorticoid effect than any other regimen studied, produced the highest incidence of both improvement (100%) and moderate-to-marked improvement (75%), and the greatest duration of improvement (more than 3 months after 40% of the courses). The duration of improvement following intensive courses of any of the corticosteroids was approximately doubled by the subsequent administration of smaller doses of dexamethasone or prednisone on alternate days. Most patients with severe disease relapsed after 3 to 6 months of corticosteroid treatment, but increase in the dose of corticosteroid, and daily administration, which was more effective than alternate-day administratin, almost always again resulted in improvement. Corticotropin and corticosteroids were equally effective before and after thymectomy. High doses of corticotropin and corticosteroid produced an initial exacerbation of the disease in 80% of the courses, which was moderate or marked in 57%. Reduction in dose reduced the incidence of severe exacerbation, but did not prevent it, and also resulted in slower and less marked improvement. Withholding anticholinesterase medication did not prevent exacerbation or increase improvement, and afforded no advantage, though it was usually helpful to reduce the dose of this medication. Because of the hazard of initial exacerbation and the occurrence of other serious side effects in 15% of the patients. (bleeding ulcer, vertebral compression, aseptic necrosis of the femoral head or tibia, and subcapsular cataracts), it is recommended that corticosteroid treatment be limited to myasthenic patients who are not responding satifactorily to anticholinesterase medication, that smaller doses be employed in patients whose disease is not life threatening, and that higher doses be reserved for patients who are critically ill and are being managed, at least initially, in an intensive care unit.

Adolescent↗
PubMed1978

Radiological study of cervical spine and hand in patients with rheumatoid arthritis of 15 years' duration: an assessment of the effects of corticosteroid treatment.

Radiological abnormalities in the cervical spine were assessed in detail in a group of 62 patients with rheumatoid arthritis of approximately 15 years' duration, of whom 33 had been treated with corticosteroids and 29 had not. The 10 criteria of damage described by Bland (1974), which include subluxation, correlated as a whole with the severity of the disease in general but not with the duration of corticosteroid treatment. Subluxation alone, whether assessed in the cervical spine as a whole or in the atlanto-axial joint alone, was less closely related to disease activity, was on average greater in patients treated with corticosteroids, and tended to increase in relation to the duration of treatment. Corticosteroid treatment thus tends to produce, over the course of years, a degree of subluxation in addition to that caused by the disease itself. Radiological signs of damage to the metacarpophalangeal (MCP) joints and carpal bones correlated with both the degree of damage and the degree of subluxation in the cervical spine as well as with corticosteroid treatment. Mutilans deformity at the MCP joints was associated with subluxation in the neck and with corticosteroid treatment.

Adrenal Cortex Hormones↗
PubMed1977

Intestinal calcium absorption in exogenous hypercortisonism. Role of 25-hydroxyvitamin D and corticosteroid dose.

Pharmacologic doses of corticosteroids impair intestinal calcium absorption and contribute to negative calcium balance. However, the relationship between the impaired calcium absorption and a possible defect in the conversion of vitamin D to its physiologically active form, 1,25-dihydroxyvitamin D, is unknown. We compared fractional calcium absorption (double-isotope method, 100-mg carrier) and serum 25-hydroxyvitamin D (25-OH-D) (Haddad method) in 27 patients receiving pharmacologic doses of prednisone with 27 age-, sex-, and season-matched normal subjects. In patients receiving high daily doses of prednisone (15-100 mg/day), calcium absorption (P < 0.02) and serum 25-OH-D (P < 0.001) were decreased. However, in patients receiving low doses (8-10 mg/day) or high doses (30-100 mg) of prednisone on an alternate-day schedule, both of these parameters were normal. Calcium absorption in the patients treated with daily prednisone correlated inversely with the dose of corticosteroids (r = -0.52, P < 0.025) and, in all steroid-treated patients, correlated directly with serum 25-OH-D (r = 0.58, P < 0.01). In four patients who received high-dose corticosteroid therapy for an average of 4 wk, serum 25-OH-D decreased by 35.5% from pretreatment values. Administration of a physiologic or near-physiologic dose of synthetic 1,25-dihydroxyvitamin D(3) (0.4 mug daily for 7 days) to patients receiving high-dose corticosteroids led to an increase in calcium absorption in all patients. These results suggest that calcium malabsorption in the corticosteroid-treated patients is due to a dose-related abnormality of vitamin D metabolism and not to a direct effect of corticosteroids on depressing transmucosal intestinal absorption of calcium.

Adrenocortical Hyperfunction↗
PubMed1977

Dynamics and mechanics of corticosteroid feedback at the hypothalamus and anterior pituitary gland.

Corticosteroid feedback mechanisms were investigated at the hypothalamic level using the rat hypothalamus in vitro and the pituitary level using basal hypthalamic-lesioned rats. Both fast and delayed corticosteroid feedback effects were demonstrated at the level of the hypothalamus and pituitary gland with doses of corticosteroids within or near the physiological range. These two phases of feedback were separated temporally by a 'silent period' during which no feedback was apparent. Studies on the mechanism of action of corticosteroids at the hypothalamic level showed that the fast feedback mechanism acts by inhibition of release whilst the delayed feedback mechanism acts by inhibition of both synthesis and release. The fast feedback action of corticosterone does not appear to act by excitation of neuroinhibitory pathways since neither picrotoxin nor phentolamine prevented the feedback action of corticosteroids in vitro. Corticosterone inhibition of corticotrophin releasing factor release was overcome by depolarization of the membrane with K+ suggesting that the mechanism of action of the fast feedback of corticosteroids is by membrane stabilization.

Acetylcholine↗
PubMed1979

Effects of oral and parenteral corticosteroids on intestinal villous morphology and brush border enzymes in the rat.

The effects of corticosteroid have been studied in rats submitted to oral administration of prednisone (5 mg. per kg. per day) during 8, 15, 30, and 90 days. The results were compared to those obtained after parenteral administration of hydrocortisone acetate (50 mg. per kg. per day intramuscularly). The morphometric changes of the villus-crypt axis and the brush border enzymic content of the mucosa (sucrase, enterokinase, alkaline phosphatase, and aminopeptidase) were the parameters investigated at the duodenal, jejunal, and ileal levels. Oral administration of prednisone resulted in a significant increase of the duodenal villous height at the 15th (+ 13 per cent, p less than 0.01), 30th (+ 33 per cent, p less than 0.001), and 90th day (+ 56 per cent, p less than 0.001), whereas in the jejunum a constant decrease of the villous height was noted. Parenteral hydrocortisone administration did not affect intestinal morphology. Effects of oral corticosteroids on the microvillous enzymic activities were related to both intestinal level and duration of corticoids administration: (1) in the duodenum increase of sucrase, alkaline phosphatase, and aminopeptidase during 30 days followed by normalization at the 90th day, (2) an initial increase of sucrase, alkaline phosphatase, and aminopeptidase limited to the first 8 days in the jejunum, and (3) a significant rise of alkaline phosphatase (greater than 100 per cent, p less than 0.001) and enterokinase (greater than 100 per cent, p less than 0.001) in the ileum at the 15th day of treatment. Parenteral corticosteroid administration was associated with a significant increase of both sucrase and enterokinase activities. The present study suggests that: (1) Corticosteroids exert a direct effect on the intestinal morphology varying with the intestinal level and duration of treatment. (2) No correlation could be established between anatomic and functional changes. (3) Oral corticosteroids exert an enhancing effect of the brush border enzymic activities, even in the adult mucosa and particularly at the ileal level where they stimulate significantly the enterokinase mucosal activity. (4) Parenteral corticosteroids exert a more specific effect limited to sucrase and enterokinase enhancement.

Administration, Oral↗
PubMed1978

Effect of corticosteroid therapy on the phagocytosis of antibody-coated platelets by human leukocytes.

Patients with idiopathic thrombocytopenic purpura (ITP), a disorder in which antibody coated platelets are cleared from the circulation by phagocytic cells, are often treated with glucocorticoids. The effect of corticosteroids on the recognition and ingestion of sensitized platelets by phagocytes can be quantified in these patients and compared to changes in platelet levels. Six patients with ITP were treated with 96 mg daily of methylprednisolone for 5 days. This treatment raised their platelet count and simultaneously decreased the ability of their granulocytes to phagocytize antibody-coated platelets and C3-coated paraffin oil droplets. Corticosteroid treatment did not affect the binding of antibody to platelets or the quantity of antibody in the patients' serum. The ingestion defect was present in isolated, washed leukocytes and persisted for 3-5 days after the corticosteroids were discontinued. Granulocytes and purified monocytes obtained from patients with other medical disorders receiving corticosteroids also ingested paraffin oil droplets and opsonized platelets at a slower rate. These studies provide direct evidence that corticosteroids induce a generalized phagocytic defect and that this may be the mechanism by which corticosteroids raise the platelet count in patients with ITP.

Adrenal Cortex Hormones↗
PubMed2026

Corticosteroids in ARDS: old controversies, new insights, and future directions.

Corticosteroids modulate key inflammatory and fibroproliferative pathways involved in ARDS through genomic and non-genomic glucocorticoid receptor signaling. Advances in ARDS pathophysiology have highlighted the importance of timing, inflammatory burden, and host response in determining treatment efficacy. Clinical evidence supports corticosteroid use in moderate-to-severe ARDS, particularly in COVID-19 ARDS and severe community-acquired pneumonia, with reductions in mortality and duration of mechanical ventilation. However, treatment effects remain heterogeneous across etiologies and biological subphenotypes. Recent identification of hyperinflammatory and hypoinflammatory ARDS phenotypes suggests that corticosteroid responsiveness is not uniform. Hyperinflammatory phenotypes and septic ARDS appear more likely to benefit, whereas evidence remains limited or conflicting in influenza-associated and non-septic ARDS. Long-term effects and adverse outcomes, including metabolic complications and ICU-acquired weakness, remain insufficiently characterized. Future research is increasingly focused on precision medicine approaches integrating biomarkers, adaptive platform trials, and phenotype-guided strategies. Emerging developments include lung-targeted corticosteroid delivery systems and selective glucocorticoid receptor modulators designed to improve efficacy while reducing systemic toxicity. Corticosteroids should therefore be considered a context-dependent therapy whose benefit is influenced by etiology, disease stage, inflammatory phenotype, and timing of administration.

Humans↗
PubMed1977

Dissolution rates of corticosteroids utilizing sugar glass dispersions.

A method of increasing the dissolution rates of some orally administered corticosteroids was investigated. This method involved glass dispersions using dextrose, galactose, and sucrose as the carriers. These dispersions were prepared by the fusion process and were subjected to a modified NF XIII dissolution rate determination. The results revealed a marked increase in the dissolution rate of the corticosteroids contained in the solid dispersions when compared to the dissolution rate of the plan corticosteroid powder. The increase in dissolution rates was attributed to the presence of the corticosteroid in a very fine state of subdivision and to the increased wettability of the corticosteroid powder.

Betamethasone↗
PubMed1979

Penetration of various corticosteroids through epidermis in vitro.

The penetration through the epidermis in vitro of various topically used corticosteroids was compared. The amount penetrating through the epidermis from an ethanolic solution showed good correlation with the polarity of the corticosteroids under study. Hydrocortisone, the most polar corticosteroid, penetrates the epidermis the most rapidly; clobetasone butyrate, the least polar, the slowest. Other corticosteroids, i.e., hydrocortisone-17-butyrate, triamcinolone acetonide, and clobetasol-17-propionate, form an intermediate group whose penetration rates and polarities decrease in the indicated sequence. The corticosteroid generally accepted as having greater clinical efficacy in creams or ointments did not permeate better from an ethanolic solution in vitro.

Administration, Topical↗
PubMed1979

Influence of haemoglobin type and selenium status on peripheral plasma progesterone and corticosteroid concentration in ewes grazing oestrogenic pastures.

Peripheral plasma progesterone and corticosteroid concentrations were studied in ewes grazing oestrogenic pastures during oestrus, pregnancy and parturition in 1974 and during pregnancy in 1975. Haemoglobin (Hb) type A ewes had significantly higher mean corticosteroid concentrations than HbB ewes in both years. In 1974 the concentration of progesterone did not differ significantly between Hb types whilst in 1975 the concentration was significantly (P less than 0.001) higher in HbA ewes. The mean corticosteroid concentrations were higher in selenium-supplemented ewes of both Hb types than in unsupplemented ewes in 1974 but lower in 1975. Selenium treatment did not significantly influence the progesterone concentration in ewes of both Hb types in 1974 but significantly (P less than 0.01) increased in 1975. It is concluded that the higher concentration of plasma corticosteroids or factors regulating the relationship between corticosteroids and progesterone could be responsible for the higher estimates of embryonic mortality reported in HbA ewes.

Adrenal Cortex Hormones↗