Disease relevance of cortisone

• The increases may be explained by dysregulation of 11 beta-hydroxysteroid dehydrogenase causing increased oxidation of cortisol to cortisone, which cannot be accounted for by obesity [1].
• Nine patients with primary adrenal insufficiency collected five 24-hour urine specimens while taking their usual oral dose of cortisone acetate or hydrocortisone [2].
• In vitro macrophage manifestation of cortisone-induced decrease in resistance to mouse hepatitis virus [3].
• In contrast, normal females have 50- to 100-fold higher serum levels and the acute phase reaction consists of a transient decrease in FP (approximately 50%), followed by a return to normal levels even under adverse conditions such as cortisone treatment (which by itself has a depressing effect on FP levels in normal females) [4].
• 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 [5].

Psychiatry related information on cortisone

• In the social phobia study, cortisone (25 mg) administered orally 1 h before a socio-evaluative stressor significantly reduced self-reported fear during the anticipation, exposure, and recovery phase of the stressor [6].
• Alteration of the critical period for induction of persistent oestrus by early postnatal treatment with gonadal steroids in neonatally cortisone-primed mice [7].
• Cortisone cure of the lidgap defect in fetal mice: a dose-response and time-response study [8].
• Both the psychotic disorder and peripheral involvement responded to cortisone [9].
• For some patients with mild, near-to-asymptomatic disease, glucocorticoid replacement therapy may not be required except during stressful events; for symptomatic patients, replacement doses i.e., mean daily dose 20 mg (0.30 mg/kg) hydrocortisone or 25 mg (0.35 mg/kg) cortisone acetate, are usually sufficient [10].

High impact information on cortisone

• A homing receptor-bearing cortical thymocyte subset: implications for thymus cell migration and the nature of cortisone-resistant thymocytes [11].
• To detect abnormalities in the secretion of insulin and growth hormone in monozygotic twin siblings of patients with juvenile-onset diabetes, their responses during oral, cortisone-primed oral, and intravenous, glucose tolerance tests and intravenous tolbutamide tests were compared to those of matched controls [12].
• Sex difference in ontogenesis of circadian adrenocortical rhythm in cortisone-primed rats [13].
• Of all the heparin fragments tested, the most potent inhibition of angiogenesis in the presence of cortisone was provided by a hexasaccharide with a molecular weight of about 1600 [14].
• As T lymphocytes "mature" in immunologic function--from thymocytes to cortisone-resistant thymocytes to splenic T lymphocytes--their response to histamine increases [15].

Chemical compound and disease context of cortisone

• Because an antiangiogenic activity appears independent of metastasis acceleration by cortisone acetate, the use of steroids other than cortisone acetate having no metastasis-promotion effect should be required for an antiangiogenic tumor therapy in the presence of heparin [16].
• Five patients with adrenal insufficiency were placed on a diet of 60 meq potassium and 100-150 meq of sodium while receiving a constant amount of cortisone acetate and Florinef [17].
• The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD), which catalyses the conversion of cortisol to the inactive steroid cortisone in man (and corticosterone to 11-dehydrocorticosterone in rodents), was demonstrated by immunohistochemistry in skin biopsy samples from healthy volunteers and from patients with psoriasis and eczema [18].
• Clostridium paraputrificum, an obligate anaerobe recovered from human feces, reduces the alpha,beta-unsaturated carbonyl of deoxycorticosterone, corticosterone, cortisone, and cortisol [19].
• RESULTS: Treatment of patients with moderately active (CDAI 150-300) Crohn's disease with MMF/cortisone led to a significant reduction in clinical activity scores comparable to treatment with azathioprine/cortisone [20].

Biological context of cortisone

• The kinetics of their appearance and disappearance in adult thymectomized mice, the rapid chasing of BrdU from labeled cells, and their in vivo cortisone sensitivity all suggest CD8lo cells are slated for deletion [21].
• The surface phenotypes and differentiative history of specific helper-effector (HE) and specific feedback suppression-inducer (FBSI) cell sets were further defined in reference to the Qa-1 and I-J marker systems by culture of selected sets of cortisone-resistant nylon-purified thymocytes with antigen on primed macrophages [22].
• However, DNA replication was induced in cortisone-resistant thymocytes by lymphocytosis-promoting factor (LPF) [23].
• Our data are consistent with MCF virus-induced transformation of cells in the lineage to small peanut agglutinin-positive, cortisone-sensitive thymocytes, a subpopulation that predominates in the thymus and which is thought to be destined for cell death in situ [24].
• 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 [25].

Anatomical context of cortisone

• In an attempt to modulate the recognition processes that occur on lymphocyte membranes in mixed lymphocyte culture, responding cortisone resistant thymocytes or stimulating spleen cells (treated with mitomycin C) were pretreated with native concanavalin A (N-Con A) or succinyl-Con A (S-Con A) [26].
• 5--10% of the thymus cells, 20--30% of cortisone-resistant thymus cells, 60--70% of lymph node cells, and 60--80% of ATC-spleen and T.TDL showed Ia [27].
• The cultured TdT+ cells are antigenically "null" cells that further resemble their normal counterparts in bone marrow with respect to morphology, size, cortisone sensitivity, and pattern of TdT fluorescence [28].
• In addition, spleen cells from mice treated with cortisone made the resistant C3H macrophages 100 times more susceptible in vitro [3].
• Unprimed, cortisone-resistant, nylon wool-purified thymocytes cultured with adherent peritoneal exudate cells can be primed in vitro with soluble carrier protein to generate carrier-reactive helper cells [29].

Associations of cortisone with other chemical compounds

• Since we found that glomerular mesangial cells (GMC) express 11beta-hydroxysteroid dehydrogenase 1 (11beta-OHSD1), which interconverts 11-keto glucocorticosteroids into 11beta-hydroxy glucocorticosteroids (cortisone/cortisol shuttle), we explored whether 11beta-OHSD1 determines the antiinflammatory effect of glucocorticosteroids [30].
• The sensitivity of erythropoietic (BFU-E) and granulopoietic (CFU-C) progenitor cells to dexamethasone and cortisone was studied in cultures of mouse bone marrow [31].
• 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 [5].
• We have also found that agents that block the arachidonic acid cascade at the level of phospholipase A2 (cortisone, phenytoin) or at the level of cyclooxygenase (indomethacin, aspirin) also block masculine differentiation and that such antimasculinization is reversed by arachidonic acid [32].
• Efficacy of antitumor chemotherapy in C3H mice enhanced by the antiangiogenesis steroid, cortisone acetate [33].

Gene context of cortisone

• Two isozymes of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) interconvert cortisol (F) and inactive cortisone (E), and are thus able to modulate GC action at an autocrine level [34].
• Mechanistically, 11 beta-HSD2 converts cortisol to cortisone [35].
• Mean GH levels, peak GH levels, and GH area under the curves (AUCs) were significantly lower after GHRH + cortisone as compared to GHRH alone [36].
• Release of CRH initiates a cascade of events leading to the release of cortisone and the regulation of inflammatory and immune events [37].
• Inbred and congeneic strains of mice have been examined for susceptibility to cortisone-induced cleft palate, and the role of genes linked to H-2 on chromosome 17 has been confirmed [38].

Analytical, diagnostic and therapeutic context of cortisone

• 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 [39].
• Splenectomy or high-dose cortisone treatment had no effect on the shorter survival of PIGA- RBCs [40].
• These studies suggested that, while clearance of inert particulate matter and of antibody-coated RBC from the blood occurred primarily by a cortisone-suppressible, presumably phagocytic process in the spleen, chemically altered RBC were removed primarily by a cortisone-insensitive filtration process in the splenic microvasculature [41].
• However, a 2-week course of immunosuppression with antilymphocyte serum and cortisone acetate results in reactivation and dissemination of the latent virus in all animals [42].
• A greater than 50% reduction in circulating lymphocytes was observed 4 hr after injection of soluble hydrocortisone and 24 hr after daily subcutaneous injections of depot cortisone acetate [43].

References