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PubMed1993

Cortisone-induced osteoporosis: effects on bone adenylate cyclase.

Glucocorticoid excess results in osteoporosis by inhibiting bone formation as well as by increasing bone resorption. The cellular mechanism for the glucocorticoid effect is unknown but has been postulated to be due to enhancement of the cyclic AMP response to PTH. This study examined the effect of in vivo administration of a glucocorticoid on adenylate cyclase activity in plasma membranes isolated from mineralized bone. Glucocorticoid excess was induced by implanting cortisone subcutaneously in adult female guinea pigs. At the end of 3 weeks skeletal plasma membranes were obtained, and adenylate cyclase activity was compared with that of normal age-matched guinea pigs. The specific activity of basal adenylate cyclase activity was significantly greater in the cortisone-treated animals (77.7 +/- 10 vs. 41.9 +/- 4.4 pmol cAMP/mg protein/15 min, p < 0.005), but PTH stimulated both to an equal degree. In contrast to the increased specific activity of intact adenylate cyclase, the specific activity of the catalytic unit was lower in the membranes from cortisone-treated animals. We also examined the effect of cortisone treatment on the modulation of adenylate cyclase by divalent cations. Neither the KaMg or the ability of Ca2+ to inhibit enzyme activity was found to differ between normal and cortisone-treated animals. In addition, PTH caused an increase in Mg2+ affinity in both sets of membranes to a comparable degree. The effect of cortisone could not be attributed to altered amounts of Ni present in these membranes; we were unable to satisfactorily quantitate the amounts of Ns.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMedDate not supplied

Interferon, cortisone, and antivirals in the treatment of chronic viral hepatitis: a review of 30 years of therapy.

Over the last 30 years many approaches have been adopted to treat chronic hepatitis. We conducted a meta-analysis to assess the efficacy of various types of treatments. We selected 4 studies of cortisone in chronic hepatitis B; 21 trials of interferon treatment, 6 in chronic hepatitis B, 10 in chronic hepatitis C, and 5 in chronic hepatitis D; and 5 of combined cortisone and interferon treatment in chronic hepatitis B. The Mantel-Haenszel-Peto method was applied to extrapolated data. We completed the study by analyzing four studies of cortisone treatment of chronic hepatitis C, two of cortisone plus interferon alpha (IFN-alpha) for chronic hepatitis C, and antiviral therapy for hepatitis B, C, and D. Trials administering cortisone for chronic hepatitis B had an overall OR of 0.29 (CI 0.12-0.73). No virologic remissions were observed in patients with hepatitis C receiving prednisone, even if those with features of autoimmunity achieved a biohumoral sustained response. Overall ORs in the trials were were as follows: IFN for chronic hepatitis B, 0.27 (CI 0.17-0.46); IFN for chronic hepatitis C, 0.3 (CI 0.21-0.44); IFN for chronic hepatitis D, 0.16 (CI 0.06-0.47); and cortisone plus interferon for chronic hepatitis B, 0.25 (CI 0.15-0.41). Sustained response rates of chronic hepatitis C ranged from 15-24.2%. The only encouraging results were obtained by antivirals. To date the lack of a specific antiviral drug makes it uncertain as to the preferred agent for this disease.

Anti-Inflammatory Agents↗
PubMed1974

[Experimental Study On The Effect Of Cortisone In Mice Infected With Toxocara Canis: Histopathological Findings Of Granuloma In The Liver]

The present study was carried out to examine the effect of "Cortisone" on the worm burden migrated in the organs, and granulomatous change in the liver of mice infected with Toxocara canis eggs. Daily does of 0.5 mg "Cortisone" was administrated subcutaneously to Toxocara-infected mice with different schedule. The results are summarized as follows: 1. More number of Toxocara larvae migrated into the muscle tissue, especially into the carcass through the wall of the large intestine and higher distribution rate and longer persistence of worms were also recognized in the carcass of the experimental group than in the control. 2. Cortisone administration resulted the inhibition of granuloma formation, as well as the resolution of granuloma in the liver. However, the discontinuation of the administration induced the reccurence of heavier grade of inflammation. In non-cortisone treated group (control), cellular infiltration appeared around the worms in the liver on the 10th day of the infection, and typical granulomatosis was followed on the 20th day. As in above results, it is considered cortisone has remarkable anti-inflammatory and immunosuppressive effects in mice infected with T.canis, but histopathological changes on the granuloma formation might be related closely with the duration of Toxocara infection, dosage, duration and timing of cortisone administration.

Journal Article↗
PubMed1951

Results of long-continued cortisone administration in rheumatoid arthritis.

The administration of cortisone acetate to patients with rheumatoid arthritis usually produces prompt and often dramatic suppression of the disease manifestations. The effects of the hormone are not lasting, however, and after withdrawal relapse ensues. For sustained improvement in a chronic disease such as rheumatoid arthritis, it appears that cortisone must be given more or less continuously. This raises the question whether administration may be continued effectively and safely for long periods.Seventy-six patients with rheumatoid arthritis were given cortisone in the hope that treatment could be continued uninterruptedly for extended periods. For various clinical reasons it was necessary to discontinue treatment in 16 of these before six months, but the remaining 60 patients received the hormone uninterruptedly for six to 15 months. By using initial large suppressive amounts, then gradually reducing the dosage, and finally employing smaller maintenance doses, adequate degrees of rheumatic control were maintained in approximately two-thirds of the original 76 patients. The ability to sustain satisfactory improvement varied indirectly, in general, with the severity of the rheumatoid arthritis. The chief detriment to better results in the more severe cases was the intervention of adverse hormonal side effects which developed frequently when large or relatively large maintenance doses were required to support satisfactory improvement. Unwanted signs of hormonal excess developed in 40 per cent of cases at some time during the course of treatment. Most of them were mild or transient and disappeared or lessened when the dose of cortisone was reduced, but when the dose was reduced the degree of improvement often declined also. During prolonged cortisone therapy evidence of functional suppression of the adrenal cortices, as indicated by a decreased response of circulating eosinophils to exogenous ACTH, was present. The depression of cortical function was temporary, however. Whether irreversible damage may result when the drug is employed for longer periods cannot yet be answered.

Arthritis, Rheumatoid↗
PubMed1951

Experiences with cortisone given orally.

The advantages of the oral administration of cortisone, when compared with cortisone given intramuscularly, include the more rapid appearance of therapeutic effects, which is of importance in the therapy of acute disease, and the faster dissipation of effects when the hormone is discontinued, which is of value when dangerous reactions occur. Oral dose schedules depend upon the degree of urgency or chronicity of the treated disease. In acute diseases the therapeutic results, in general, were disappointing. Cortisone may be of greater value in the long-term maintenance treatment of certain chronic diseases. By long-term therapy the authors mean practically continuous treatment until either the disease goes into spontaneous remission or undesirable effects of the drug require cessation of treatment. Critical selection of patients and constant supervision of therapy are vital to the successful administration of cortisone. Even with these precautions, however, the therapeutic use of cortisone must be regarded as experimental until the passage of time permits better appraisal of harmful effects.

Administration, Oral↗
PubMed1950

The effects of cortisone and adrenocorticotropic hormone (ACTH) on certain rheumatic diseases.

The adrenal cortical hormone, cortisone, and the pituitary adrenocorticotropic hormone (ACTH) possess potent antirheumatic properties. Their administration produces strikingly beneficial effects on a number of rheumatic diseases including rheumatoid arthritis, rheumatoid (ankylosing) spondylitis, acute rheumatic fever, disseminated lupus erythematosus, periarteritis nodosa, psoriatic arthritis, dermatomyositis, and gout. In general the effects of these substances are temporary and they cause suppression rather than cure of the disease processes. Improvement is maintained usually only by continuing administration, and on hormonal withdrawal prompt or fairly prompt relapse of the disease manifestations ensues. In addition to their antirheumatic effects cortisone and ACTH influence a wide variety of physiologic functions. Administration of them therefore may produce a number of metabolic and clinical changes, some of which are not advantageous from a therapeutic standpoint. Adverse side-reactions are more liable to occur when large doses of the hormones are given for prolonged periods; such reactions appear to be reversible and disappear when administration of the hormones is stopped. With cortisone, comparatively few untoward signs develop when smaller amounts are administered continuously even for periods of months. Greater clinical experience is needed before optimal doses and schedules of administration are finally determined. It appears that some severe cases, many moderately severe cases, and most moderate and mild cases of rheumatoid arthritis may be adequately controlled with smaller "maintenance" doses of cortisone ranging from 32 to 65 mg. a day, providing larger doses to suppress the disease manifestations are employed initially. Neither cortisone nor ACTH should be considered as a therapeutic agent for general use until more information regarding their physiologic activities and the consequences of prolonged or repeated administration of them are available. Until the potential dangers of these hormones can be determined precisely, the use of them should be considered as an investigative procedure.

Adrenocorticotropic Hormone↗
PubMed1983

Centennial Paper. November 1951 (Arch Dermatol Syphilol: Cortisone acetate administered orally in dermatologic therapy by Marion B. Sulzberger, Victor H. Witten and Stanley N. Yaffe.

Thirty-two patients with various severe or selected dermatoses were chosen for treatment with cortisone acetate by mouth. The criteria for selection included refractoriness to previous therapy and absence of ascertainable contraindications. The initial dose of cortisone acetate varied between 100 and 200 mg. per day. The dose was reduced as quickly as each patient's response permitted, with the object of reaching the lowest effective dose as quickly as possible. Response of most patients to the hormone was dramatic, with abatement of symptoms within 24 hours and substantial improvement of clinical signs within 24 to 48 hours. Details of the results are tabulated. Adverse effects, possibly attributable to the hormone, were noted in five patients. In two instances, moon facies developed, one with hypertrichosis and a 20-lb. (9.1-kg.) gain in weight. However, both of these patients had received corticotropin (ACTH) prior to the cortisone. A third patient showed hyperpigmentation of the areas of skin usually exposed and not covered by clothing. Two additional patients each complained of hyperexcitability and insomnia. All these undesirable effects diminished or disappeared after the dose was reduced or administration of cortisone was discontinued. The effectiveness of this new therapeutic approach in a wide variety of skin diseases is clearly demonstrated by the excellent response noted in this series of selected cases. No other modality known to us has comparable beneficial effects. It is to be stressed, however, that the benefits generally stop soon after cortisone therapy is discontinued, unless the disease or the attack is one with spontaneous remissions. Disagreeable and sometimes dangerous effects still preclude the use of this treatment except in serious diseases and situations, and unless the patient can be kept under sufficiently close and expert surveillance.

Administration, Oral↗
PubMed1993

Retinoic acid, cortisone, or thyroxine suppresses the mutant phenotype of the eyelid development mutation, lgMl, in mice.

The development of the mammalian eyelid is one of the last major morphogenetic events during prenatal development. The eyelids originate as outgrowths of epithelium and mesenchyme above and below the eye; they grow and flatten across the eyes, and meet and fuse firmly but temporarily until several days after birth in mice. In mouse lidgap mutants, eyelid development fails. Previously, we have shown that normal eyelid development can be induced in lidgap mutants by maternal treatment with cortisone or thyroxine. These hormones have been reported to interact with members of a receptor superfamily, and their response elements have been shown to induce transcription of hormone-regulated genes; retinoic acid also interacts with members of this superfamily. The purposes of our study were to examine the joint effect of thyroxine and cortisone on induced eyelid development in lidgap-Miller mutant fetuses (lgMl/lgMl), to test for synergism, and also to test whether retinoic acid also induces eyelid development in this mutant. We found that the combined effect of thyroxine and cortisone was significantly greater than that of either hormone alone, but that the dose-response slopes (log dose, probit scale) for eyelid development induced by cortisone alone or by cortisone preceded by 0.1 mg thyroxine were parallel, suggesting that their action is additive, not synergistic. We found that retinoic acid administered on day 14 of gestation induced eyelid development in lgMl/lgMl mutant fetuses, with a significant dose response and ED50 of 24 +/- 6 mg/kg. The response was treatment-time dependent, with optimal responses after day 14 or 11 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

The effects of exogenous cortisone acetate on development (especially skeletal development) and on circulating levels of corticosteroids in chick embryos.

Chick embryos were treated with cortisone acetate on day 8 of incubation and the subsequent growth of the whole embryo and the development of the tibia studied to day 18 of incubation. Cortisone, at 10 ng to 2 mg/embryo decreased general body growth; above 0.5 mg/embryo it also retarded morphogenesis by as much as 3 Hamilton-Hamburger stages; and above 1 mg/embryo gross abnormalities were produced. The growth and differentiation of the tibia were affected to a greater extent than was the whole body. The reductions in tibial and total body weight were not linearly related to dose of cortisone injected. The exogenous cortisone acetate resulted in drastic alterations in the circulating levels of cortisone, cortisol, corticosterone, and progesterone, but plasma progesterone level was most readily correlated with the growth retardation. This study emphasizes that avian embryos can readily compensate for exogenous corticosteroids and that caution must be exercised when attributing causality to the substance administered.

Adrenal Cortex Hormones↗
PubMed1978

Palate development after fetal tongue removal in cortisone-treated mice.

Morphological studies of cortisone-induced cleft palate have shown retardation in the rotation of palatine shelves from a sagittal to a transverse plane. Cortisone also reduces fetal muscular movements, which may explain why displacement of the tongue from between the palatine shelves is delayed. Previous work with extrauterine development of control fetuses demonstrated that fetal membranes and tongue were major obstacles to shelf rotation. Thus, removal of these obstacles might permit rotation and fusion of palatine shelves in cortisone-treated fetuses. In the present experiment, fetuses from cortisone-treated strain CD-1 mice were released from uterus and membranes and allowed to develop for eight hours in a fluid medium with the umbilical cord left intact. Compared to 4% fusion in utero, there was palatal fusion in 20% of fetuses released from membranes. When the fetal tongue was removed during extrauterine development, the frequency of fusions increased to 61%. Fusion appeared normal by the criteria applicable through light microscopy. Thus, cortisone induces cleft palate primarily through interference with shelf rotation. The palatine shelves of treated fetuses retain their ability to fuse when they can come in contact during the normal time for palate closure.

Abnormalities, Drug-Induced↗
PubMed1994

Simultaneous quantitation of endogenous levels of cortisone and cortisol in human nasal and bronchoalveolar lavage fluids and plasma via gas chromatography-negative ion chemical ionization mass spectrometry.

Investigation of the influence of pulmonary disease upon local catabolism of cortisol in vivo is limited by the lack of availability of a selective and sensitive assay for simultaneous quantitation of cortisol and cortisone in lung and nasal lavage fluids as well as in plasma. Synthesis of bispentafluorobenzylcarboxymethoxime derivatives of cortisone and cortisol followed by trimethylsilylation yields compounds with almost ideal gas chromatographic properties. The derivatized steroids generate intense M(-.)-181 fragment ions in negative ion chemical ionization mass spectrometry. Monitoring of ions at m/z 829 and m/z 903, respectively, for cortisone and cortisol and corresponding fragment ions generated from multideuterated internal standards provides the analytical basis for assessment of local in vivo conversion of cortisol to cortisone in the respiratory system of human subjects. The assay method displays excellent reproducibility with variations < or = 10%. Detection limits are < or = 1 pg of steroid analyte per injection (S/N > 3). Endogenous levels of cortisone and cortisol, respectively, measured in human samples were as follows: nasal lavage fluid, 47 and 25 pg/ml; bronchoalveolar lavage fluid, 380 and 153 pg/ml; plasma 12.8 and 61.6 ng/ml.

Bronchoalveolar Lavage Fluid↗
PubMed1977

Modification of streptozotocin-induced diabetes in rats by pretreatment with cortisone.

Cortisone pretreatment considerably enhances the mortality of young, male, streptozotocin-injected Holtzman rats. In those that survive, cortisone pretreatment decreases the ensuing hyperglycaemia, extends the period during which streptozotocin-induced B cell damage can be observed from less than two to as much as four to seven days and permits the persistence of poorly granulated B cells in such animals. These effects are at least partially attributable to a cortisone-induced augmentation of the total B cell mass. Compared with the high degree of protection against alloxan-induced damage afforded the pancreatic B cells of cortisone-pretreated rabbits, the protective effect of cortisone against B cell destruction in streptozotocin-injected rats is thus much more limited in scope. Species differences as well as differing pathogenetic mechanisms may account for these results.

Animals↗
PubMed1990

Growth inhibition of the 9L glioma using polymers to release heparin and cortisone acetate.

Malignant gliomas are difficult to treat systemically because of exclusion of many chemotherapeutic agents by the blood brain barrier. Furthermore, as opposed to other neoplasms, malignant gliomas recur locally, at the site of original presentation. These tumors are remarkably vascular and hence may be more dependent on angiogenesis for continued growth than other tumors. The inhibition of tumor angiogenesis can control tumor growth by preventing the exponential vascular growth phase. We report the inhibition of the growth of the 9L glioma by the localized, controlled release of known angiogenesis inhibitors administered in a biodegradable polyanhydride polymer matrix. In the presence of heparin and cortisone and of cortisone alone there was a 4.5- and 2.3-fold reduction, respectively, in the growth of the 9L glioma. We compared these results to the inhibition of tumor neovascularization in the rabbit cornea by the localized delivery of the same agents. In the rabbit cornea model, the local release of heparin and cortisone and of cortisone alone resulted in a 2.5- and 2.0-fold reduction, respectively, in the angiogenesis response evoked by the VX2 carcinoma. This study introduces two new potential therapeutic modalities for the treatment of malignant gliomas: the use of the combination of heparin and cortisone as antineoplastic agents and the use of polymeric carriers for the local delivery of such agents in the central nervous system.

Animals↗
PubMed1983

Immune suppression and histophysiology of the immune response. I. Cortisone acetate and lymphoid cell migration.

Seven daily intramuscular (im) injections of cortisone acetate (25 mg/Kg b.w.) given to rats or rabbits produced, (i) a pronounced reduction in the numbers of small lymphocytes in thymus-independent areas, (ii) atrophy of the thymic cortex, (iii) atrophy of germinal centres and (iv) a consequent depressed production of germinal centre-derived cells. Lymphocyte depletion was not caused by cell lysis. Moreover cell traffic between peripheral lymphoid organs did not seem to be altered. A revival of the depressed germinal centres in cortisone-treated (inbred) rats could be achieved by a transfer of bone-marrow cell suspensions from normal, cortisone-treated or T-cell-deprived animals. It was concluded that cortisone acetate arrests the migration of B-lymphocytes from the bone marrow to germinal centres in peripheral lymphoid organs, and that the accumulations of lymphoid cells in the bone marrow of cortison-treated animals might be composed of immature or mature T- and B-lymphocytes.

Animals↗
PubMed2003

Improvement of treatment of primary adrenal insufficiency by administration of cortisone acetate in three daily doses.

In the present study, we compared the effects of 3 daily administrations of cortisone acetate vs a classical regimen with 2 daily administrations, in patients with primary adrenal insufficiency (PAI). We enrolled 34 patients with PAI treated with 2 daily doses of cortisone acetate (2/3 of the total daily dose early in the morning, 1/3 in the afternoon) who were subdivided into two groups: group A (no. = 18; 4 males, 14 females; age: median 55 yr, range 24-88) continued with the standard 2 daily administrations, group B (no. = 16; 8 males, 8 females; age: median 44 yr, range 27-70) switched to 3 daily administrations (3/6 of the daily dose early in the morning, 2/6 after lunch, 1/6 after dinner), but without any change of the total daily dose. After 6 months of therapy, basal and 90-min post-cortisone acetate ACTH levels in group B (219 pg/ml, range 19.9-1197, and 84 pg/ml, range 14.4-480, respectively) were significantly lower than those observed at the beginning of the study (482 pg/ml, range 58-1900 and 215 pg/ml, range 52-1832, respectively; p = 0.001 and p = 0.027, respectively). No statistically significant differences were observed in group A. Similarly, 24-h urinary cortisol (UFC) excretion increased significantly after 6 months of a 3-dose therapy in group B (from 74.6 microg/24 h, range 24-148, to 98.8 microg/24 h, range 48-214; p = 0.006), but not in group A (p = ns). Moreover, UFC excretion after 6 months of a 3-dose therapy was significantly higher than after 6 months of a 2-dose therapy (98.8 microg/24 h, range 48-214 vs 49.8 microg/24 h, range 11-183, p = 0.032). No significant variations of basal and 90-min post-cortisone levels of cortisol were observed in either group. Our study demonstrates that the subdivision of the total daily dose of cortisone acetate in 3 administrations increases total UFC excretion and reduces plasma ACTH levels, thus improving the substitutive therapy.

Adrenal Insufficiency↗
PubMed1990

Prevention of necrotizing enterocolitis in the rat with prenatal cortisone.

Cortisone acetate is known to accelerate maturation of the immature intestine. The effect of prenatal administration of cortisone acetate on the morbidity and mortality of necrotizing enterocolitis was examined in a rat pup model. Pregnant rats were administered cortisone acetate, 20 mg/100 g of body weight, or normal saline by daily IP injection from day 18-21 of gestation. Rat pups were taken from the mothers before suckling was initiated, fed a simulated rat milk formula, and subjected to daily ischemic insults to produce an animal model of necrotizing enterocolitis. Both morbidity and the mortality rates were significantly improved with prenatal cortisone treatment. Maturation of the intestinal mucosal barrier was accelerated with the cortisone treatment as measured by decreased serum concentrations of a fed antigen, ovalbumin. Aerobic bacterial colonization of the small intestine and translocation of bacteria to the liver were decreased in the pups pretreated with steroids. These changes observed in a rat model of necrotizing enterocolitis may explain the decreased incidence of necrotizing enterocolitis in human infants born to mothers who received corticosteroids late in gestation.

Animals↗
PubMed1992

Effects of prenatal administration of testosterone and cortisone on the reproductive system of the female rat.

Testosterone propionate, cortisone, or sesame oil vehicle were given to rats during the last week of pregnancy so that effects of the hormones on anogenital distance, breeding capacity and vaginal opening of the female progeny could be contrasted. Testosterone significantly increased anogenital distance and delayed vaginal opening of progeny. When females that had been exposed to testosterone in utero were tested for breeding capacity, a significantly smaller number mated than in the control group. Female rats that had been exposed to cortisone in utero exhibited premature vaginal opening but did not differ from controls in anogenital distance, and, unlike the testosterone-exposed rats, mated. Cortisone-exposed rats carried litters to term and the litters did not differ from those of controls in numbers of pups or numbers of living pups at birth. The pups born to cortisone-exposed rats had greater birth weights and a higher survival rate to 20 days of age than pups of controls. Results indicate that testosterone administration to rats during pregnancy is far more detrimental to the development and subsequent function of the reproductive system of female progeny than cortisone and suggest that similar changes which occur in response to maternal stress or to administration of ACTH during pregnancy are more likely to result from increases in testosterone than from increases in glucocorticoid secretion.

Analysis of Variance↗
PubMed1975

The metabolism of 3-H-cortisone and 3-H-cortisol by the isolated perfused rat and guinea pig lungs.

Isolated perfused rat lungs removed more than 35% of 3-H-cortisone (1 times 10-9M) from the perfusate during one passage through the pulmonary circulation. The cortisone in the lungs was then rapidly converted to cortisol, which was returned to the perfusate. The tritiated steroid taken up was so rapidly washed from the lung, that only 10% remained after a 12 minute perfusion with steroid-free medium. In recirculating experiments, nearly 60% conversion to cortisol occurred over 32 cycles; in addition, there was a slow increase in the percentage of polar compounds in the medium. Similarly, the perfused hindlimbs preparation from the rat converted cortisone to cortisol and returned the cortisol to the perfusate. In contrast, guinea pig isolated perfused lungs had neglible effect on cortisone. Rat lungs demonstrated only a limited ability to convert 3-H-cortisol to cortisone. The results suggest that the lungs may play an important role in maintaining cortisone/cortisol levels in the plasma.

Animals↗