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PubMed1973

Effect of cortisone administration on experimental nocardiosis.

Effect of cortisone administration on the pathogenicity of Nocardia asteroides, N. caviae, and N. brasiliensis for white mice has been investigated by using the intravenous route of inoculation. The observations indicated that the susceptibility of white mice to nocardiosis was enhanced by cortisone. Test strains of the three species of Nocardia caused a higher and more rapid mortality, as well as more extensive lesions, in the cortisone-treated than in the normal mice. The mean lethal dose (LD(50)) values of N. asteroides and N. caviae for the cortisonetreated group were found to be seven and eight times lower than their respective values for the normal group. N. asteroides and N. caviae were more virulent than N. brasiliensis, the LD(50) of N. brasiliensis for cortisone-treated mice being 30 and 26 times higher than that of the former two species, respectively. N. brasiliensis also differed from the other two species in its inability to infect the brain. In the untreated animals, N. asteroides and N. caviae showed a tendency to form conglomerate growth, in contrast to formation of freely dispersed growth in the lesions of cortisone-treated animals.

Animals↗
PubMed1985

Development of gastrointestinal mucosal barrier. VII. In utero maturation of microvillus surface by cortisone.

When studying mucosal barrier function of developing animals, we noted that intestinal microvillus membranes (MVM) of newborn animals differ in their fluidity and binding characteristics to lectins compared with adult MVM. To further investigate these differences and determine whether maturation of the microvillus surface could be accelerated in utero, pregnant rats were given intraperitoneal cortisone beginning on the 17th day of gestation. Control and cortisone-treated animals were allowed to deliver normally, and the small intestines from newborns were used to isolate MVM. Microvillus membrane surface characteristics were evaluated by employing an 125I-labeled fucose-specific lectin, Ulex europeus (UEA). Changes in MVM proteins were monitored by disaccharidase activities and sodium dodecyl sulfate-polyacrylamide electrophoresis. MVM fluidity was accessed using a 5-doxyl stearic acid label and electron-spin-resonance spectroscopy. Results from these studies indicate that the birth weights of newborn rats exposed to cortisone in utero were significantly reduced; sucrase activity was prematurely induced and specific activities of lactase and maltase were enhanced in the intestines of the cortisone-treated newborns as contrasted with control animals. Furthermore, binding of 125I-UEA to MVM was greatly increased in treated animals. MVM fluidity decreased (P less than 0.001) compared with control animals and resembled the structural characteristics of more mature MVM. These results suggest that cortisone exposure in utero accelerate maturation of the microvillus surface of enterocytes.

Animals↗
PubMed1992

Modulation of sleep by cortisone in normal and bacterially infected rabbits.

Infectious disease is known to alter both sleep patterns and hydrocortisone (cortisol) concentrations in rabbits. Moreover, the sleep-altering effects of microbial infections are likely to be mediated via endogenous immune modulators whose actions are attenuated by glucocorticoids. To evaluate the relationships between sleep and glucocorticoids during infectious disease, the effects of cortisone administration (20 mg/kg, im) on sleep were examined before and after inoculation of rabbits with Staphylococcus aureus or Escherichia coli. When administered alone, cortisone did not alter the amount of time spent in slow-wave sleep (SWS) but did reduce electroencephalographic (EEG) slow-wave amplitudes during SWS, the number of bouts of SWS and the amount of time spent in rapid-eye-movement sleep. The duration of individual bouts of SWS was increased after cortisone treatment. Bacterially infected rabbits developed biphasic changes in sleep patterns that were characterized by an initial increase and a subsequent decrease both in SWS time and in EEG slow-wave amplitudes during sleep. Cortisone treatment attenuated these effects in S. aureus-inoculated rabbits. In contrast, cortisone treatment did not alter the initial phase of enhanced sleep in E. coli-inoculated rabbits but did attenuate the subsequent sleep suppression. These data indicate that glucocorticoid administration is associated with an attenuated sleep response in bacterially inoculated rabbits.

Animals↗
PubMed1995

Effects of cortisone and testosterone on diaphragmatic function and biochemistry in the rabbit.

The effects of cortisone and testosterone on in vivo diaphragmatic function and biochemistry were assessed in rabbits to determine whether androgens can prevent the effects of corticosteroids on diaphragmatic function and biochemistry and what mechanisms of muscle function may be altered. Cortisone altered respiratory muscle endurance and diaphragmatic glycogen and lactate levels but had little effect on diaphragmatic strength. Testosterone had no significant impact on diaphragmatic strength, endurance, or biochemistry. However, concomitant administration of testosterone with cortisone blunted the effect of cortisone on respiratory muscle endurance, even though it failed to block the effects of cortisone on diaphragmatic glycogen and lactate levels. Alterations in respiratory muscle endurance were not due to low- or high-frequency contractile fatigue of the diaphragm or diaphragmatic glycogen depletion or lactate accumulation in any of the treatment conditions. On the other hand, alterations in central drive played a dominant role, as evidenced by alterations in inspiratory duty cycle and a falloff in the intensity of central drive during loading. Although the exact mechanisms underlying the alterations in central drive remain unknown, concomitant administration of androgens with corticosteroids blunted the impact of corticosteroids on respiratory muscle function.

Animals↗
PubMed2003

The serum cortisol:cortisone ratio in the postoperative acute-phase response.

OBJECTIVE: In a previous cross-sectional pilot investigation, an increase in the ratio of active cortisol to inactive cortisone in serum has been found as a general phenomenon during the acute-phase response. The aim of the present study was to further characterize this alteration of cortisol metabolism in patients undergoing elective cardiac bypass surgery. METHODS: Cortisol and cortisone were quantified by use of liquid-chromatography tandem mass spectrometry in sera that were sampled preoperatively and on the first 4 postoperative days (POD) from 16 patients undergoing aortocoronary bypass grafting (7.00 a.m.). RESULTS: The median serum cortisol concentration peaked on the first POD and then decreased statistically significantly until the end of the observation period: preoperatively, 245 nmol/l (IQR 198-331); 1st POD, 532 nmol/l (IQR 409-678 ); 4th POD, 373 nmol/l (IQR 306-493); p for trend = 0.019. In contrast, the cortisol:cortisone ratio was constantly increased approximately twofold on all POD compared to preoperative sampling: preoperatively, 5.4 (IQR 5.0-7.2); 1st POD, 11.3 (IQR 9.2-13.6); 4th POD, 9.9 (IQR 7.7-11.0), with no significant trend of normalization. CONCLUSION: Following major surgery, the substantial increase in the serum cortisol:cortisone ratio - reflecting a shift in the overall set-point of 11beta-hydroxysteroid dehydrogenase activity - is more sustained than the increase in serum cortisol; the increase in the cortisol:cortisone ratio seems to be a long-term phenomenon of the activation of the hypothalamic-pituitary-adrenocortical system by surgical stress and systemic inflammation.

Acute-Phase Reaction↗
PubMed1993

Cortisone image and emotional support by key figures in patients with bronchial asthma. An empirical study.

In a subgroup of patients with bronchial asthma, irrational fears of steroid medication can be observed beyond justified worries about side-effects. A cortisone image which involves overemphasizing the threatening aspects of cortisone often underlies non-compliant illness behaviour. In the present study, cortisone image and the relationship with a key figure was investigated in 62 patients with bronchial asthma, all of whom had participated in a structured asthma treatment and teaching programme (ATTP). The data show that (1) perceiving cortisone as threatening predicts poor adherence to ATTP guidelines how to manage severe attacks, and (2) patients having a supportive relationship with their key figure are less likely to experience threatening aspects of cortisone.

Acute Disease↗
PubMed1969

Parotid fluid cortisol and cortisone.

Parotid fluid corticosteroids, substantially comprised of cortisol and cortisone, were previously demonstrated to rise to far greater levels 4 hr after administration of ACTH than they did in the third trimester of pregnancy, although the plasma total corticosteroid concentrations were similar in these two states. It was therefore suggested that only nonproteinbound corticosteroid gains access to parotid fluid. In the present study parotid fluid cortisol and cortisone and plasma dialyzable cortisol concentrations have been measured in normal men before and 2 hr after 40 U ACTH, and, in another group, before and after 10 days of diethystilbestrol (5 mg daily). Total plasma cortisol rose from a mean of 6.3 to 17.9 mug/100 ml after ACTH and from 14.6 to 39.4 mg/100 ml after the estrogen. However parotid fluid cortisol plus cortisone rose from 0.8 to 2.6 mug/100 ml after ACTH and to only 2.2 after estrogen. This rise resembled that of the plasma dialyzable cortisol (control 0.4, ACTH 1.8, estrogen 1.2 mug/100 ml) rather than the increase in total plasma cortisol which was over twice as high after estrogen as after ACTH. Thus parotid fluid corticosteroids seem to be a good measure of nonprotein-bound corticosteroid, the cortisol available to the cell. The total amount of cortisol plus cortisone excreted is approximately constant, independent of parotid fluid flow rate. Cortisone exceeds cortisol in parotid fluid in the basal state, but after ACTH the situation is reversed.

Adrenocorticotropic Hormone↗
PubMed1988

Syndrome of apparent mineralocorticoid excess. A defect in the cortisol-cortisone shuttle.

The first adult case of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) deficiency is described. The impaired conversion of cortisol to cortisone (indicated by urinary cortisol and cortisone metabolites and failure to metabolize 11 alpha-[3H]cortisol to [3H]H2O), was associated with hypertension, hypokalemia, and suppression of the renin-angiotensin-aldosterone system. When established on a fixed Na+/K+ intake, dexamethasone, given orally, produced a natriuresis and potassium retention. Plasma renin activity became detectable. When hydrocortisone (10 mg daily s.c. for 4 d) was added, there was marked Na+ retention, a kaliuresis (urinary Na+/K+ falling from 1.2 to 0.15), with suppression of plasma renin activity and an increase in blood pressure. These changes were also seen with the subject on no treatment. Conversion of cortisone to cortisol was not affected. These results suggest that cortisol acts as a potent mineralocorticoid in 11 beta-OHSD deficiency. The major site for the oxidation of cortisol to cortisone is the kidney. In this patient congenital deficiency of 11 beta-OHSD results in high intrarenal cortisol levels which then act on renal type I mineralocorticoid receptors. This condition can be treated with dexamethasone, which suppresses cortisol secretion and binds to the type II glucocorticoid receptor. We suggest that 11 beta-OHSD exerts a critical paracrine role in determining the specificity of the type I receptor. In the normal state cortisol is converted by 11 beta-OHSD to cortisone which thus allows aldosterone to bind preferentially to the type I receptors in the kidney and gut. In this patient deficiency of 11 beta-OHSD results in high intrarenal cortisol concentrations that then bind to the type I receptor.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1980

Plasma cortisone in man: its determination, physiological variation, and significance.

In a method for the simultaneous determination of cortisone, cortisol, and corticosterone, the extracted steroids are separated using paper chromatography and assayed by competitive protein binding. Evidence of the reliability of the method, particularly with respect to the determination of cortisone, is presented. Only trivial changes in cortisone level were detected in response to exercise, surgery, and ACTH, even though marked changes in cortisol level were simultaneously recorded. It is suggested that the inertia in plasma cortisone level may be related to its lesser degree of binding to plasma proteins, relative to cortisol, which would permit more rapid hepatic uptake and possible accumulation of a large extravascular pool of cortisone.

Adrenocorticotropic Hormone↗
PubMed2005

Plantar fasciopathy and orthotripsy: the effect of prior cortisone injection.

BACKGROUND: Corticoid steroid injection into the heel is a popular treatment method for painful heel syndromes. However, the positive results usually are short term. Extracorporeal shock wave treatment (ESW) has been shown to have a more permanent effect. We evaluated 555 patients who received ESW using the device Ossa Tron Orthotripsy (Health Tronics, Surgical Services, Marietta, GA) relative to antecedent cortisone heel injection. METHODS: Before ESW, 312 patients (56%) received one or more cortisone injections into the heel, and 243 patients (44%) had never received a cortisone injection. RESULTS: Two hundred and thirty-four patients (75%) who had antecedent injection or injections had positive outcomes after ESW. One hundred sixty-eight patients (69%) without prior heel injection had positive responses after ESW. CONCLUSION: The prior injection of cortisone did not affect the likelihood of a positive response to ESW. Similarly, the absence of prior injection of cortisone did not affect the outcome.

Animals↗
PubMed1982

Direct effect of cortisol and cortisone on insulin and glucagon secretion.

The direct effects of cortisol and cortisone on insulin and glucagon secretion by the isolated perfused rat pancreas were examined. Cortisone, but not cortisol, in a final concentration of 10(-4) M acutely and strongly inhibited both phases of glucose- and arginine-induced insulin secretion. In repeated pulse administrations, the second infusion of cortisone elicited an inhibition of insulin release equal to the first response. Glucagon output was slightly suppressed by cortisol and more significantly by cortisone in a glucose-free medium. The blockade of alpha-adrenergic receptors by phentolamine attenuated, but did not prevent, the strong inhibitory action of cortisone on insulin secretion.

Animals↗
PubMed1990

The influence of glycyrrhetinic acid on plasma cortisol and cortisone in healthy young volunteers.

Based on studies in laboratory animals and on measurements of the urinary metabolites (allo)tetrahydrocortisol and tetrahydrocortisone in human volunteers it has been claimed that liquorice-induced mineralocorticoid excess is caused by a unique defect in the conversion of cortisol to cortisone. To further evaluate this hypothesis we have investigated the influence of glycyrrhetinic acid (GA), the mineralocorticoid-active constituent of liquorice, on plasma cortisol and cortisone in 10 healthy young normotensive volunteers. Pure GA (500 mg/day), administered orally from days 3-10 of the study, exerted pronounced mineralocorticoid activity. Ingestion of GA resulted in an elevated urinary excretion of free cortisol and virtually unchanged plasma cortisol levels in the presence of markedly decreased levels of both plasma cortisone and urinary free cortisone. These results provide direct clinical support for the hypothesis that GA induces an inhibition of the activity of 11 beta-dehydrogenase, resulting in a blockade in the conversion of cortisol to cortisone.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2002

Absence of Cushingoid phenotype in a patient with Cushing's disease due to defective cortisone to cortisol conversion.

Cushing's syndrome invariably presents with a classical phenotype comprising central adiposity, prominence of dorsal, supraclavicular and temporal fat pads, bruising, abdominal striae, proximal myopathy, and hypertension. We report the case of a 20-yr-old student with pituitary-dependent Cushing's syndrome who was spared this classical phenotype because of a defect in the peripheral conversion of cortisone to cortisol. She presented to her general practitioner with secondary amenorrhea. Clinical examination revealed normal fat distribution (body mass index, 20.9 kg/m(2)), absence of hirsutism, myopathy, or bruising; her blood pressure ranged from 115/70 to 122/82 mm Hg. She was investigated for biochemical hypercortisolemia because of a mildly elevated random circulating cortisol (serum cortisol, 661 nmol/liter). Cushing's syndrome was confirmed on the basis of repeatedly elevated urinary free cortisols (831-1049; reference range, <350 nmol/24 h), failure of low-dose dexamethasone suppression (611 nmol/liter) and loss of circadian cortisol secretion. Investigations suggested Cushing's disease; there was suppression after high-dose dexamethasone (<20 nmol/liter) and a 950% increase in ACTH after stimulation with CRH. Pituitary magnetic resonance imaging revealed a 3-mm adenoma within the pituitary gland. Urinary corticosteroid metabolites were analyzed by gas chromatography-mass spectrometry and demonstrated a decreased THF+allo-THF/THE ratio of 0.66 (mean +/- SE in Cushing's disease, 1.74 +/- 0.24) suggesting a defect in 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), an enzyme that converts the inactive glucocorticoid cortisone to active cortisol. Transphenoidal microadenomectomy was performed, and histology confirmed the diagnosis of a corticotroph adenoma. Postoperatively, serum cortisol was undetectable and replacement therapy was commenced. Subsequent investigations revealed a significantly impaired ability to convert an oral dose of cortisone acetate (25 mg) to cortisol, reduced serum cortisol to cortisone ratios, and a reduced serum half-life for cortisol (57.3 min). These results provide strong evidence for a partial defect in 11beta-HSD1 activity and concomitant increase in cortisol clearance rate. We have described a case of Cushing's disease that failed to present with a classical phenotype, and we postulate that this is due to a partial defect of 11beta-HSD1 activity, the defect in cortisone to cortisol conversion increasing cortisol clearance and thus protecting the patient from the effects of cortisol excess. This observation may help to explain individual susceptibility to the adverse effects of glucocorticoids.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2003

Comparative effect of intra-articular administration of hyaluronan and/or cortisone with evaluation of malondialdehyde on degenerative osteoarthritis of the rabbit's knee.

Hyaluronan and cortisone have controversial and an important role in the healing of degenerative osteoarthritis. The purpose of the research was to compare individual and combined effects of hyaluronan and cortisone on the healing of degenerative osteoarthritis and to determine the serum malondialdehyde level as a lipid peroxidation marker. A rabbit model was used in which a degenerative osteoarthritis was created in the articular cartilage by resection of anterior cruciate ligament. The rabbits divided into three groups namely were injected with hyaluronan (group A) and cortisone (group B) at days 31, 38 and 45. Cortisone at day 31 and hyaluronan at days 38 and 45 were injected to the third group (group C). We obtained blood samples from each rabbit to determine the malondialdehyde levels at days 1, 30, and 52. At day 52, 21 rabbits were sacrificed. In biopsies obtained from treated and untreated knees articular cartilage degeneration was examined by light microscopy. Histopathologically the healing rate was significantly higher in group C than the other groups. Degeneration decreased 72% in group A, 52% in group B and 88% in group C at day 22. Malondialdehyde levels were 2.056 +/- 0.37 in the control group, 1.94 +/- 0.54 in group A, 1.98 +/- 0.37 in group B and 1.55 +/- 0.41 in goup C. The malondialdehyde levels of group A and B were less than the control group (statistically insignificant, p > 0.05). But, there were statistically significant values between control group and group C (p < 0.05). The results showed that the combination of cortisone and hyaluronan is the most effective in the treatment of cartilage degeneration in the course of the ostearthritis and the malondialdehyde levels are correlated with the severity of degeneration.

Adjuvants, Immunologic↗
PubMed1981

Maintenance of unimplanted fertilized ova in spayed rats: effects of cortisone acetate therapy during the period of embryonic diapause.

Rat dams were ovariectomized on day 3 of pregnancy and treated with corn oil (0.25 ml/day), progesterone (4 mg/day), cortisone acetate (2 or 10 mg/day), cortisone acetate (10 mg/day) plus progesterone (4 mg/day) or progesterone (4 mg/day) plus oestrone (1 microgram/day) from days 2 to 8 or 14, followed by 6 to 11 days of treatment with progesterone (4 mg/day) plus oestrone (1 microgram/day). Implantation of ova at the normal time was realized in the animals treated from day 2 with progesterone plus oestrone. Implantation of ova was only realized subsequent to progesterone plus oestrone in the dams treated with progesterone alone, cortisone acetate alone, or progesterone plus cortisone acetate, except for one animal in the latter group. Implantation of ova was not usually realized even after progesterone plus oestrone treatment in the dams treated with corn oil. Even though cortisone acetate maintained unimplanted ova in spayed rats in much the same manner as does progesterone, it was not equivalent to progesterone in efficacy or action.

Animals↗
PubMed1976

Comparative effects of cortisone, dianabol and enovid on isoprenaline-induced myocardial infarction in arteriosclerotic vs nonarteriosclerotic rats.

Male and female nonarteriosclerotic (virgin) and arteriosclerotic (breeder) Sprague-Dawley rats were subjected to acute myocardial infarction with isoprenaline. When myocardial necrosis was most intense, animals were given cortisone (high and low doses), Dianabol, or Enovid. Animals receiving large doses of cortisone manifested the best survival rate during the early stages of myocardial infarction. Although their serum enzyme levels were least elevated and their hearts showed tha least amount of damage, these animals had undergone the most intense body weight loss and began to die suddenly during the later stages of the experiment. These animals also manifested hyperlipidaemia, hyperglycaemia, septicaemia, severe disuse atrophy of their adrenal glands, and reduced Cmpd. B production. Animals treated with low doses of cortisone or with the anabolic and androgenic steroid, Dianabol, manifested none of the myocardial pretective effects of the larger dose of cortisone. These animals displayed a high incidence of left ventricular aneurysm formation concomitant with extensive cartilaginous metaplasia within the aneurysmal sites. Treatment with the contraceptive drug, Enovid, caused body weight loss, hyperlipidaemia, hyperglycaemia, gonadal atrophy and reduction of Cmpd. B production. Although the high dose of cortisone exercised definite salutary effects during early myocardial infarction, chronic treatment led to adrenal disuse atrophy and hypoadrenocorticism associated with sudden death during the later stages of myocardial repair. These findings indicate that proper adjustment of the dose and chronicity of corticosteroids used for treating the crisis of acute myocardial infarction must be made in order to provide effective protection against untoward pathophysiological conditions, acceleration of myocardial repair, but without suppression of adrenal function.

Adrenal Glands↗
PubMed1975

Effect of cortisone on the disappearance kinetics and tissue localization of soluble immune complexes.

The effect of cortisone treatment on the disappearance kinetics, the hepatic uptake, and the glomerular deposition of i.v. administered, soluble immune complexes (HSAantiHSA) was examined in mice. An initial rapid disappearance of complexes from the circulation occurred after the injection of complexes into control mice, which was caused by increased vascular permeability. This phase was absent in the cortisone-treated group. The half life of complexes composed of more than two antigen and two antibody molecules (greater than Ag2Ab2)was prolonged from 1.93 hr in control mice to 4.71 hr in cortisone-treated mice while the half life of Ag2Ab2 complexes was unchanged (11.40 hr vs 12.04 hr). Although the clearance velocity of greater than Ag2Ab2 complexes was suppressed in cortisone-treated mice, the quantity of complexes specifically located in the liver at 1, 2, and 4 hr was not significantly different in the two groups. Persistence of circulating greater than Ag1Ab2 complexes was associated with enhanced and prolonged glomerular depostion of complexes in the cortisone-treated mice.

Animals↗
PubMed2001

[Forgotten episodes of the birth of cortisone].

During World War II, a rumor reached the United States and the United Kingdom that the Germans were successfully using an adrenal hormone product to protect Luftwaffe pilots from the adverse effects of high altitudes. The product was said to be obtained from adrenal glands collected in a huge amount in Argentina and transported by U-boats to Germany. The U. S. and the U. K. exerted their war efforts by setting up urgent research projects to produce similar products. The war ended in 1945, however, before the goal was achieved. The German rumor turned out to be groundless. Cortisone acquired fame in 1949 as "a miracle drug" for the relief of rheumatic pain. Its therapeutic discovery was an outcome of the untenable assumption that rheumatoid arthritis patients must have suffered from adrenal insufficiency and hormone deficiency. The war efforts have led to successful syntheses of cortisone after the war, and its industrial production has reduced its cost drastically from $200.00 per gram in 1949 to $10.00 in 1951. To overcome the cumbersome synthetic routes for cortisone, natural product sources were sought as possible starting materials, but without much success. A microbiological transformation of steroidal compounds was developed in 1952 to introduce an oxygen function into the molecular position 11 by a microorganism found at a window of a laboratory. The fermentation process required progesterone which found its timely supply in Mexico. The cost of progesterone went down from $2.00 per gram to $0.15 and that of cortisone further from $10.00 to $3.50 in 1955. An ample supply of cortisone at an affordable price was admirably achieved by the combination of progesterone derived from diosgenin of the Mexican yam and a microbiological oxidation process developed by a chance discovery of suitable organisms. The former is attributed to R. E. Marker and the latter to D. H. Peterson.

Cortisone↗