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At least 19 recordsLinked to original sources
PubMed1978

The excretion of free cortisol, cortisone, cortisol sulfate and cortisone sulfate in peripheral vascular disease, diabetes mellitus and hyperthyroidism.

In four groups of persons, 1/healthy individuals, 2/ patients with diabetes mellitus, 3/ patients with peripheral vascular disease, and 4/ patients with hyperthyroidism, the urinary excretion of free cortisol, cortisone, cortisol sulfate and cortisone sulfate was estimated. In groups 2 and 3 the excretion of all four substances was elevated. In hyperthyroidism a preponderance of free cortisone over cortisol was registered. The ratios of the followed substances suggest in patients with peripheral vascular disease a detoriation in the normal excretion of the followed corticoids, based on a preponderance of 11-OH-corticosteroids over their 11-oxo-derivatives. This observation could be implicated in the mild hyperglycemia or decreased glucose tolerance, that is often found in atherosclerotic disease.

Adult↗
PubMed1979

The effect of cortisone acetate on pulmonary lesions in a rabbit model of hypersensitivity pneumonitis (cortisone and hypersensitivity pneumonitis).

Rabbits were sensitized with Micropolyspora faeni by intratracheal inoculations and later challenged with the same antigen either with or without parenteral administration of cortisone acetate prior to challenge. Animals developed anti-M. faeni serum precipitins, M. faeni-induced alveolar macrophage migration inhibition, and positive 48-hr skin reactivity to M. faeni. Sensitized animals also demonstrated an augmented pulmonary histopathological response following respiratory challenge with M. faeni when compared to non-sensitized controls. Cortisone acetate abrogated this augmented pulmonary histopathological response following challenge with M. faeni. Cortisone acetate also abolished the positive alveolar macrophage migration inhibition found in sensitized animals.

Alveolitis, Extrinsic Allergic↗
PubMed1992

[Paths to a rational cortisone therapy via urea supplements--countering cortisone phobia].

Not until corticosteroids came into use did it become possible for modern dermatotherapy to cure numerous skin diseases, and if not cure them, at least rapidly lead to major improvements and the transition to symptom-free intervals. Through indiscriminate use, corticosteroid therapy has become discredited by patient and doctor alike due to the increased incidence of side effects. Due to this intensified rejection--bordering on "cortisone phobia"--corticosteroids today are often not being used when justifiable or even when mandatory. Most side effects can be avoided or reduced if the instructions for use are properly adhered to, thus increasing acceptance. Another way of further improving compliance is the use of low-side effect corticosteroids, such as hydrocortisone, since now the difference in effective strength compared to potent halogenated preparations can be compensated by the addition of 10% urea. With regard to active strength, a hydrocortisone/urea combination preparation should be used like a medium-strength cortisone preparation and is particularly suited for the long-term therapy of chronic dermatosis. Additional properties of urea, such as alleviation of itching and water binding, which are important in the treatment of chronic eczemas, enhance hydrocortisone in combination preparations.

Administration, Topical↗
PubMed1975

In vitro cortisone sensitivity of in vivo cortisone-resistant thymocytes.

Thymus cells from untreated or hydrocortisone-treated mice were cultured for 20 hr in the presence or absence of a water-soluble glucocorticoid, hydrocortisone sodium succinate. By two independent assays of cell viability or function, virtually all thymocytes from untreated hosts were inactivated by hydrocortisone sodium succinate, whereas most, but not all, thymocytes from hydrocortisone-treated hosts were inactivated. Thus, the thymocytes which survive after treatment of the animal with glucocorticoids are only partially resistant to the effects of glucocorticoids in vitro.

Animals↗
PubMed1978

Treatment of lupus nephritis in adult (NZB + NZW)F1 mice by cortisone-facilitated tolerance to nucleic acid antigens.

Adult female (NZB + NZW)F1 mice were treated with cortisone, cortisone with tolerogen (isologous NZB IgG-nucleosides conjugates) or cortisone with isologous IgG free of nucleosides. Other treatments also included tolerogen or isologous IgG alone, and cortisone together with denatured DNA. All untreated mice died by 10 mo of age. Cortisone prolonged the survival rate. This effect was further improved by combined treatment of cortisone and tolerogen. Prolonged survival was accompanied by a decrease in proteinuria. Other treatments failed to influence either survival or proteinuria. Although cortisone did not prevent the appearance of antibody to denatured DNA, cortisone and tolerogen suppressed them in most of the animals. Preexisting antibody to denatured DNA was reduced by cortisone and cortisone and tolerogen, but not by cortisone and IgG. In contrast, antibody to native DNA bore no relationship to therapy. Animals living beyond 1 yr of age, regardless of the treatment, fall into three histopathological categories: (a) severe nephritis, as in untreated animals, (b) moderate nephritis (with absence of severe alteration of the glomerular basement membrane, i.e. the histological counterpart of prolonged survival), (c) minimal nephritis. In a small number of animals treated with cortisone or cortisone and IgG and in 6/20 animals treated with cortisone and tolerogen, minimal lesions as judged by light, fluorescent, and electron microscopy were found. These last mice were in good health at 15-16 mo of age, twice the life-span of untreated mice. In conclusion, these data suggest that tolerance to nucleic acid antigens facilitated by cortisone offers a promising new approach to treat established murine lupus nephritis.

Animals↗
PubMed1978

Cortisone induced alterations of costal cartilage in single and in parabiosed rats.

Cortisone-treated Buffalo rats have been parabiosed with untreated controls of the same age. The optical and electron microscopy, including histochemistry, of costal cartilage of these rats has been compared with that in single cortisone treated rats, single controls, and control parabiosed with control rats, at 14 and 28 days after parabiosis. Single cortisone-treated rats, in comparison to controls, have shown the greatest alteration in cellular morphology and in the extracellular matrix both at 14 and at 28 days. Cortisone-treated parabiosed rats demonstrate a gradation of these alterations. Cellular alterations include enhancement of lipid and glycogen deposition concrurently with the presence of numerous large cytoplasmic vacuoles containing beaded irregularly-shaped filaments, banded or unbanded collagen-like fibrils, and/or electron dense lamellar bodies. In the extracellular matrix, matrix vesicles, amianthoid fibers, randomly oriented unbanded fibrillar materials, and filament-like materials are most prominent in the single cortisone-treated rats and they are progressively less prominent in the cortisone-treated parabiosed rats, and in the parabiosed and single controls. Calcification of the extracellular matrix follows a similar pattern and is observed initially in pericellular halos of the single cortisone and in cortisone-treated rats parabiosed with controls. Histochemical techniques have shown that chondroitin sulfate is less demonstrable in the single cortisone and in the cortisone-treated parabiosed rats than it is in the single or parabiosed controls at 14 days but, at 28 days, all untreated or treated rats, single or parabiosed are basically comparable. Glycoproteins are prominent in the single cortisone-treated rats both at 14 and at 28 days and, at these same times, they are progressively less prominent in the cortisone-treated parabiosed rats and in the single or parabiosed controls. Many of the cortisone induced alterations in costal cartilage are suggestive of enhancement of the aging process.

Animals↗
PubMed1991

Cortisone and thyroxine modulate intestinal lactase and sucrase mRNA levels and activities in the suckling rat.

Glucocorticoids and thyroxine modulate postnatal intestinal sucrase and lactase activities. Whether changes in enzyme activity are accompanied by changes in enzyme mRNA levels were determined in day 6 rats given thyroxine, cortisone, or thyroxine plus cortisone and killed 3 days later. Cortisone induced precocious expression of jejunal sucrase activity which was enhanced when cortisone plus thyroxine was administered; sucrase mRNA changed in parallel. Jejunal lactase activity was unaffected by thyroxine and was increased after cortisone, but not after thyroxine plus cortisone. Jejunal lactase mRNA levels increased equally after cortisone or after cortisone plus thyroxine. Thus, cortisone induces coordinated increases in sucrase and lactase activities and in corresponding mRNA levels. Thyroxine only enhances cortisone induced sucrase expression and antagonizes cortisone by depressing lactase activity post-translationally.

Animals↗
PubMed1976

Cartilage sulfation and serum somatomedin in rats during and after cortisone-induced growth arrest.

The uptake of sulfate by rib cartilage in vitro and in vivo and the serum somatomedin activity by bioassay were determined in male rats during and after cortisone-induced growth arrest. Experimental treatment consisted of subcutaneous injections of cortisone acetate in a dose of 2.5 mg/rat/day for 4 days, beginning at 29 to 30 days of age in Buffalo rats, or 5 mg/rat/day for 4 or 5 days, beginning at 39 to 41 days of age in Long-Evans rats. Groups of hypophysectomized rats were studied in parallel in one experiment. The sulfate uptake in the controls declined linearly with increasing age in both the in vitro and the in vivo studies. Hypophysectomy resulted in a constant low level of sulfate uptake in vitro. At the end of cortisone treatment, the in vitro sulfate uptake was approximately midway between that of the hypophysectomized rats and that of controls; at 7 days recovery, it was at the control level; at 14 days it showed an additional rise above the control value; from 14 days to 35 days it declined parallel with but above the sulfate uptake of controls. The in vivo sulfate uptake was depressed by cortisone treatment. During recovery it approximately control values at recovery day 21. In succeeding recovery periods in vivo sulfate uptake remained at control levels. Serum somatomedin activity was significantly reduced during cortisone treatment; it returned to the control level by 21 days of recovery. The incubation of the cartilage of controls and cortisone-treated rats at 14 days of recovery with and without the presence of normal rat serum, cortisone recovery serum, or hypophysectomy serum resulted in significantly higher sulfate uptake in the cortisone-treated rat cartilage in each medium. These sera did not differ significantly in their stimulation of sulfate uptake in either cortisone recovery cartilage or control cartilage. Both treated and control cartilage had greater sulfate uptake with larger doses of serum added to the medium. The dose-response curves were parallel during treatment and early recovery; but the slopes of the dose-response curves of the cartilage of cortisone-treated rats were greater than those of the controls during late recovery. It is concluded that the increased in vitro sulfation after 14 days of recovery in cortisone-treated rats signifies a persistent alteration in cartilage metabolism. Normal in vivo sulfate uptake during that time may be the result of humoral controls. A mechanism other than the impairment of somatomedin production is probably involved in the failure of catch-up growth after glucocorticoid treatment in the rat.

Animals↗
PubMed1979

Biphasic rate of synthesis of glycoconjugates, phospholipids and DNA in concanavalin A-stimulated mouse thymocytes. Involvement of cortisone-sensitive and -resistant subpopulations.

The time course of the rate of labeling of membrane components (phospholipids, glycolipids and glycoproteins) and DNA was followed in concanavalin A-stimulated CBA/J mouse thymocyte cultures. Two peaks of stimulated biosynthetic activity were noted, the first at the beginning of the cultivation and the second about 25 h later. Both early and late peaks of biosynthesis of membrane components were accompanied by blast transformation and were unimpeded by suppression of DNA synthesis by hydroxyurea. Cortisone-sensitive and cortisone-resistant thymocytes were prepared by selective agglutination of the cortisone-sensitive cells with peanut agglutinin (Reisner et al. Cell. Immunol. 1976. 25: 129) or cortisone treatment of the animals. Cortisone-sensitive cells responded early, while the cortisone-resistant population gave only the late response. The autoradiographic patterns from sodium dodecyl sulfate polyacrylamide gels of [3H]fucose or [3H]galactose-labeled glycoproteins from early and late labeling cells, and cortisone-resistant cells, were compared. Late-labeling and cortisone-resistant cells gave indistinguishable patterns, but differed significantly in their patterns from early-labeling cells. It is concluded that the two peaks of biosynthetic activity during the course of concanavalin A stimulation of thymocytes are caused by two different cell populations which require different times for maximal response and react independently of one another.

Animals↗
PubMed1992

The cortisone era: aspects of its impact. Some contributions of the Merck Laboratories.

The announcement in 1949, by Hench at the Mayo Clinic, that cortisone had a dramatic beneficial effect on bed-ridden patients suffering from rheumatoid arthritis ushered in the cortisone era. This medical landmark was made possible by the prior steroid research of distinguished chemists and biologists in several countries. The first partial synthesis of cortisone by Sarett was the culmination of a worldwide chemical effort. This work ultimately enabled the process research department at Merck, under the direction of Max Tishler, to perform the 37-step conversion of deoxycholic acid to cortisone on a scale that made the initial clinical trials possible. In spite of the enormity of the project, and the fact that neither of two closely related analogs of cortisone had shown any interesting biological activity. Merck elected to embark on this synthetically challenging project. The clinical results reported in 1949, combined with the complexity of the partial synthesis, stimulated highly innovative research to discover new routes to cortisone and to cortisol, the active hormone. This research, particularly in the pharmaceutical industry in the United States, Mexico, and Europe, demonstrated, among other things, the value of microbial transformations in synthetic sequences. The recognition that the chronic administration of cortisol produces several unexpected side effects stimulated an intensive effort in many countries to discover an analog with an improved therapeutic index. This led to more novel chemistry and many analogs were discovered that proved to be more potent than cortisol. Prednisolone, discovered at the Schering Corporation, was the first compound that combined a high level of anti-inflammatory activity with reduced salt retention. Derek Barton contributed greatly to steroid research during the 1950s by applying creative structural thinking to systematize a host of seemingly unrelated chemical and biological observations. The cortisone era had a profound impact on drug discovery also, since it led to the logical application of steric and electronic concepts to medicinal chemistry. Last, but not least, the cortisone era taught medicinal chemists many important lessons about drug-receptor interactions.

Anti-Inflammatory Agents↗
PubMed1979

Effect of cortisone and X-irradiation on cellular depletion and regeneration in the thymus of mice: experimental discrimination between thymus lymphocyte precursors in the bone marrow and in the thymus.

The effect of cortisone treatment on the ability of bone marrow cells to repopulate X-irradiated thymus was investigated. In one experimental series, groups of mice were treated first with cortisone and then irradiated with or without bone marrow protection. Mice treated with either cortisone or radiation alone served as controls. During an initial, bone marrow independent phase of thymus regeneration, cortisone had a stronger inhibitory effect on the cellular regeneration of the organ than irradiation. On the other hand, during a subsequent bone marrow dependent phase, thymus regeneration was impaired by radiation exposure but not by cortisone treatment. In another experimental series, irradiated mice were transplanted with bone marrow cells in different numbers from syngeneic donors which had either been treated with cortisone or were left untreated. Twenty days later the cell number was consistently larger in the thymus of animals which has been transplanted with cortisone treated bone marrow than in the animals transplanted with untreated bone marrow. It is concluded that the thymus lymphocyte precursors in the bone marrow and the early precursors of thymocytes in the thymus differ with regard to their sensitivity to cortisone and radiation and, therefore, may represent two distinct cell types.

Animals↗
PubMed1992

[Negative cortisone attitude in patients with bronchial asthma].

Patients with bronchial asthma often exhibit irrational fears of cortisone medication beyond justified worries about side-effects. A negative cortisone image, which means overemphasizing the damaging and threatening aspects of cortisone, often underlies non-compliant illness behaviour. In the present study, cortisone image was investigated in 54 patients with bronchial asthma before and after participation in the Düsseldorf Asthma treatment and teaching programme (ATTP) and one year later. By participating in ATTP, a significant reduction of the negative cortisone image and thus a more realistic view of cortisone could be achieved in most patients. This effect was also evident at the follow-up examination one year later. On the other hand, persistence of a negative cortisone image in a subgroup of patients turned out to be a potent predictor of later non-compliant illness behaviour. Psychological implications of a persistent negative cortisone image are discussed.

Adult↗
PubMed1977

Suppression of the hypothalamic-pituitary-adrenal axis after subcutaneous cortisone acetate administration in rats.

Groups of female rats were injected daily for 14 days with 10 mg of cortisone acetate subcutaneously, to study the mechanisms of glucocorticoid suppression on the hypothalamic-pituitary-adrenal axis. Pituitary adrenocorticotropic hormone (ACTH) content, plasma ACTH, adrenal venous corticosterone, adrenal weights, and the catabolic effects on body weight were studied simultaneously (under stressful and non-stressful conditions) before, during, and up to six weeks after cortisone. This study confirmed the results of other investigators that cortisone acetate caused catabolic weight loss and adrenal atrophy, but it was noted to persist up to six weeks after the injections. Glucocorticoid acetate was more effective in causing ACTH-axis suppression than succinate or phosphate preparations, and the effects were dose and time related. Significant depletion of pituitary ACTH content, suppression of plasma ACTH, and corticosterone secretion occurred five to seven days after beginning cortisone acetate (p=<0.001); it was continuous throughout the injection schedule (p=<0.001); it remained for two to four weeks after the cortisone was discontinued (p=<0.001). The animals showed minimum plasma ACTH responsiveness to severe acute stress during this two to four-week suppression phase, but rapid recovery occurred thereafter. Plasma ACTH was undetectable up to six weeks post-cortisone when the animals were not under stress. This may be related to residual cortisone acetate found at the injection sites, or to an altered or different ACTH-axis control mechanism. The sequence of events during recovery from cortisone suppression appeared to be (1) repletion of corticotrophin-releasing hormone (by inference), (2) repletion of pituitary ACTH content, (3) secretion of plasma ACTH, (4) reversal of adrenal atrophy, and (5) subsequent secretion of corticosterone.

Adrenal Glands↗
PubMed1976

Inducing effect of cortisone and insulin on the activity of beta-galactosidase in the E. coli strains K12.

Individual and combined effects of cortisone and insulin on the synthesis of beta-galactosidase in the strains E. coli K 12 200 PS/Flac and M-308 and the possiblity of cortisone uptake by the bacterial cell under different temperature conditions were investigated in their dynamics. When insulin and cortisone are applied simultaneously in doses showing individually the greatest stimulative effect on the synthesis of beat-galactosidase, no summation of the effect of the hormones occurs in the strain E. coli 200 PS/Flac in the presence of IPTG while in the strain E. coli ML-308 simultaneous application of insulin and cortisone induces a negligible increase in the activity of beta-galactosidase. Tests for the incorporation of [3H] cortisone into the strains E. coli 200 PS/Flac and ML-308 have shown that the hormone is taken up by the bacterial cell immediately after its addition to the incubation medium, reaching its maximum after 5 min of incubation and maintaining the same level in the subsequent 30 min. The incorporation of [3H] cortisone at a temperature of 37degrees C is markedly higher than at 4degrees C. Preliminary incubation of the cultures with unlabelled cortisone and insulin resulted in a decrease in the uptake of [3H] cortisone by the bacterial cell.

Cortisone↗
PubMed1976

The role of growth hormone and cortisone on glucose and gluconeogenic substrate regulation in fasted hypopituitary children.

Panhypopituitarism may be associated with spontaneous hypoglycemia and marked insulin sensitivity. Five children with both growth hormone (GH) and adrenocorticotrophin (ACTH) insufficiency were studied in three periods: a) on no therapy; b) during cortisone acetate; and c) during GH and cortisone acetate replacement. With total caloric restriction prior to therapy, all patients became hypoglycemic (109 +/- 18 leads to 37 +/- 3.5 mg/dl, mean +/- SEM) and ketonemic (beta-hydroxybutyrate 0.10 +/- 0.02 leads to 3.04 +/- 0.63 mM and acetoacetate 0.05 +/- .01 leads to 0.80 +/- 0.15 mM) within 30 hours. Glutamine and alanine concentrations fell with fasting (511 +/- 13 leads to 293 +/- 26 muM and 394 +/- 58 leads to 137 +/- 12 muM, respectively) but to levels lower than in normal children. However, only alanine was significantly lower (P less than 0.05). With cortisone plus GH therapy, fasting glycemia was improved (73 +/- 6 mg/dl) at 30 hours fasting and was associated with increased alanine and glutamine concentrations (206 +/- 28 muM and 448 +/- 40 muM, respectively) and less ketonemia (beta-hydroxybutyrate 1.13 +/- 0.39 mM). Cortisone therapy alone resulted in intermediate improvement of these values. Only combined therapy resulted in increased lactate and pyruvate concentrations, which fell to normal with fasting. Fasting urinary ammonia excretion was unchanged whereas urea nitrogen excretion decreased significantly with therapy. The responses to alanine infusions following each study period in one patient were normal. The glycemic response to iv glucose was similar during each study period; however, post-prandial and glucose-stimulated insulin responses were increased with cortisone and cortisone plus GH therapy. We suggest that the hypoglycemia observed in hypopituitary patients is a substrate-mediated phenomenon, and that cortisone and growth hormone replacement therapy improve fasting glucose homeostasis, increase circulating alanine and glutamine concentrations, and decrease hepatic gluconeogenesis. These effects may be mediated through an increase in fat catabolism.

Adolescent↗
PubMed1975

Effect of cortisone and an anabolic steroid upon plasma hydroxyproline during fracture healing in rabbits.

The effect of cortisone and an anabolic steroid on plasma hydroxyproline (HOP) was investigated in young male rabbits, following operative fracture of the radius. The action of these hormones was studied in three groups of animals, a cortisone (hydrocortisone sodium succinate 5mg/kg every day), an anabolic (norandronolone-19-phenylpropionate 5 mg/kg every other day) and a cortisone plus anabolic treated group. A fourth group of animals served as controls. Plasma HOP was found to increase during the fracture healing in control animals, particularly in the first week and during callus remodelling. Cortisone produced elevation of HOP level during the first two weeks followed by a decrease to low normal values. Animals treated with the anabolic did not present the initial rise but a sustained increase during callus remodelling. When both the anabolic and cortisone were administered, a curve similar to that of cortisone-treated animals was obtained. The initial increase of HOP is attributed to bone destruction and to a lesser degree to synchronous bone formation at the site of the fracture. This catabolic process seems to be enhanced by cortisone and inhibited by the anabolic. When, however, the two hormones are given together the protective anticatabolic effect of the anabolic is almost abolished.

Anabolic Agents↗
PubMed1992

Simultaneous determination of cortisol and cortisone in human plasma by stable-isotope dilution mass spectrometry.

A method for the simultaneous determination of cortisol and cortisone in human plasma was developed using capillary gas chromatography-mass spectrometry-selected ion monitoring. [2H5]Cortisol and [2H5]cortisone were used as internal standards. Cortisol and cortisone in plasma were determined from the peak-height ratios of the [M-31] fragment ions of the methoxime-trimethylsilyl derivatives of cortisol and [2H5]cortisol (m/z 605 and 610) and of cortisone and [2H5]cortisone (m/z 531 and 536). Sensitivity, specificity, precision, accuracy and reproducibility of the method were demonstrated to be satisfactory for measuring the circulating concentrations of cortisol and cortisone.

Cortisone↗