Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Prednisone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources

Effect of prednisone on protein metabolism in Duchenne dystrophy.

Prednisone improves strength in Duchenne dystrophy and changes the natural history of the disease. We studied the in vivo effects of prednisone (0.75 mg.kg-1.day-1) on muscle and whole body protein metabolism in six patients with Duchenne dystrophy and three patients with Becker dystrophy. Patients were admitted to the Clinical Research Center for study and consumed a constant flesh-free diet. Strength was measured by manual and quantitative muscle testing. Fractional muscle protein breakdown was estimated by the ratio of 3-methylhistidine to creatinine excretion determined in three consecutive 24-h urine collections. Whole body protein kinetics were studied in the postabsorptive state using a primed continuous infusion of L-[1-13C]leucine. Fractional muscle protein synthesis was determined from tracer incorporation into noncollagen muscle protein obtained by needle biopsy. After 6-8 wk of prednisone treatment, average muscle strength increased by 15% (P < 0.04), and 24-h creatinine excretion (an index of muscle mass) increased by 21% (P = 0.002). 3-Methylhistidine excretion decreased by 10%, but the change was not statistically significant. The ratio of 3-methylhistidine to creatinine excretion decreased by 26% (P < 0.04). Fractional muscle protein synthesis and whole body protein synthesis and breakdown did not change significantly. We conclude that the beneficial effect of prednisone on strength in Duchenne dystrophy appears to be associated with an increase in muscle mass, which may be mediated by inhibition of muscle proteolysis rather than stimulation of muscle protein synthesis.

Adult↗

Prednisone blunts airway neutrophilic inflammatory response due to ozone exposure in asthmatic subjects.

BACKGROUND: The effect of corticosteroids on the ozone (O3)-induced airway inflammation is still debated. OBJECTIVE: The aim of the study was to confirm the effect of a short-term treatment with oral glucocorticosteroids on O3-induced airway inflammation, detected by induced sputum analysis, and on functional response in glucocorticosteroid-naive subjects. METHODS: A randomized, placebo-controlled study using oral prednisone (25 mg o.d. for 4 days) was carried out. Nine mild persistent asthmatics were exposed for 2 h, on separatedays, to 0.27 ppm O3 and to air in random order, after 4 days of treatment with prednisone (25 mg o.d.) and after 4 days of placebo.Before and after exposure, pulmonary function test was measured; 6 h afterexposure, sputum induction was done. RESULTS: Oral glucorticosteroids did not prevent pulmonary function decrement due to O3. After placebo, the percentage of neutrophils in induced sputum was significantly higher after O3 than after air [52.1 (15.7-77.3) vs. 17.8 (1.7-58.4), p=0.02, O3 vs. air]. This difference was lost after 4 days of treatment with prednisone [35.2% (10-96.2) vs. 30.9% (6.1-75.6), n.s., O3 vs. air]. Neutrophil elastase in sputum supernatant increased after O3 exposure in the sample obtained after placebo, but not after prednisone treatment. CONCLUSIONS: This study confirms that glucocorticosteroids reduce inflammatory airway response, but do not prevent the airway functional impairment after O3 exposure.

Administration, Inhalation↗

Hormonal and clinical responses to prednisone treatment in adolescents with congenital adrenal hyperplasia.

The effects of prednisone therapy and the withdrawal of prednisone for 3 days on hormonal relationships was investigated in 6 adolescent patients, age 10--19 years with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency. Prednisone continuously suppressed adrenal release of 17 alpha-hydroxyprogesterone (17-OHP) in 4 patients and adequately controlled 17-oxosteroid (17-OS) excretion in 5. Serum dehydroepiandrosterone sulfate (DS) concentrations were not elevated during or 3 days after withdrawal of medication. Growth hormone (GH) secretion was not suppressed by prednisone. Withdrawal of treatment was associated with a decrease in the follicle-stimulating hormone (FSH) to luteinizing hormone (LH) ratio in 5 patients and a rise in serum testosterone in 4. The clinical courses of these patients emphasize the difficulty in achieving optimum control.

17-Ketosteroids↗

The effects of human growth hormone and prednisone on whole body estimates of protein metabolism.

Human growth hormone (GH) increases estimates of whole body protein synthesis, but has little effect on the rates of proteolysis either post-absorptively or when absorption occurs during a meal. In contrast to insulin, GH stimulates protein synthesis in skeletal muscle tissue. Prednisone in high doses induces protein catabolism and has been used as a controlled model for catabolic illness. Prednisone increases the rates of proteolysis and amino acid oxidation, but has little effect on estimates of protein synthesis. The administration of high doses of GH together with prednisone prevents the protein catabolic effects of prednisone alone. Thus, GH may provide a new management strategy in patients with significant protein catabolic conditions.

Growth Hormone↗

Prednisone increases low density lipoprotein in cynomolgus monkeys fed saturated fat and cholesterol.

Cynomolgus monkeys were given prednisone to determine its effects on lipoprotein metabolism and other risk factors for atherosclerotic cardiovascular disease. After 1 month of oral prednisone, the mean total plasma cholesterol (TPC) concentration increased from 240 +/- 36 to 476 +/- 78 mg/dl (p less than 0.01) in animals fed a diet containing 36% of calories as fat (polyunsaturated/monounsaturated/saturated, 1.0:3.9:4.1) and cholesterol (0.39 mg/kcal). The increase in TPC was due to higher concentrations of the apolipoprotein B (apo B)-containing lipoproteins, particularly low density lipoprotein (LDL). LDL cholesterol concentrations also increased in animals fed a diet containing saturated fat and 0.25 mg/kcal of cholesterol, as well as in animals fed monkey chow. Kinetic studies of LDL indicated both an increased flux of apo B into LDL and a decrease in the fractional catabolic rate of LDL. Mean high density lipoprotein cholesterol (HDL-C) concentration decreased from 48 +/- 8.2 to 14 +/- 4 mg/dl, p less than 0.001, in animals fed fat and cholesterol, but there was no significant change in HDL-C in animals fed monkey chow. Blood pressure, fasting serum glucose, and anthropometric measures did not change after 7 months of prednisone therapy. Prednisone increases LDL concentration in the cynomolgus monkey. This animal may be a good model for studying corticosteroid dyslipoproteinemia, and possibly atherosclerosis, in an immunosuppressed host.

Animals↗

Controlled trial of oral prednisone in outpatients with acute COPD exacerbation.

Corticosteroids are often used in the outpatient treatment of acute exacerbation of chronic obstructive pulmonary disease (COPD). To date, there are few data documenting the benefit of this practice. The objective of this randomized, double-blind, placebo-controlled trial was to assess the efficacy of corticosteroids in the outpatient treatment of COPD exacerbations. Twenty-seven patients presenting with acute COPD exacerbation were studied. In addition to continuing their previous medications and increasing their use of beta-agonists, patients were randomized to receive a 9-d tapering dose of either oral prednisone or placebo. Treatment with prednisone rather than placebo resulted in a more rapid improvement in arterial PO2 (PaO2) (1.12 mm Hg/d versus -0.03 mm Hg/day; p = 0.002), alveolar-arterial oxygen gradient (A-aDO2) (-1.16 mm Hg/d versus -0.03 mm Hg/day; p = 0.04), FEV1 (0.05 L/d versus 0.00 L/d; p = 0.006), and peak expiratory flow (PEF) (0.15 L/s/d versus 0.04 L/s/d; p = 0.009). Prednisone also resulted in fewer treatment failures (p = 0.002) and in a trend toward more rapid improvement in dyspnea scale scores. Outpatient treatment of acute COPD exacerbation with prednisone accelerates recovery of PaO2, A-aDO2, FEV1, and PEF, reduces the treatment failure rate, and improves subjective dyspnea.

Administration, Oral↗

Idiopathic pulmonary fibrosis: Impact of oxygen and colchicine, prednisone, or no therapy on survival.

The clinical records of 487 patients seen at Mayo Clinic Rochester (MCR) during 1994 through 1996 who were diagnosed as having idiopathic pulmonary fibrosis of the usual interstitial pneumonia type (IPF/UIP) were reviewed. Computed tomography (CT) had been done in 94.7% of patients and surgical open lung biopsy (OLB) in 20.3%. Median survival was 3.2 yr. We compared survival as a function of treatment program, based on intent to treat at the time of the initial contact within the study window. Treatment advised included colchicine alone in 167, no therapy in 157, prednisone at maintenance dosages alone in 54, colchicine plus prednisone in 71, and other programs in 38. Oxygen therapy was advised in 133 patients. By univariate analysis, worse survival was associated with prednisone therapy compared with no therapy, and with oxygen therapy compared with no oxygen therapy. However, on multivariate analysis, worse survival was associated with older age, male gender, lower diffusing capacity for carbon monoxide (DL(CO)), lower alveolar volume (VA), and a history of worsening pulmonary function. When adjustment was made for these factors, there was no significant difference in survival between those patients treated with colchicine or prednisone and those on no therapy, and no difference between those on oxygen therapy and those without oxygen.

Aged↗

Growth hormone: metabolic clearance rates, integrated concentrations, and production rates in normal adults and the effect of prednisone.

A constant withdrawal pump was used to determine the integrated concentration of growth hormone (ICGH) which was used in conjunction with the metabolic clearance rate (MCR) of growth hormone (GH) to calculate the GH production rates (GHPR) in normal adults, acromegalics, and normal controls receiving prednisone. The mean ICGH for 22 premenopausal females on no medication was 3.0+/-1.6 ng/ml (sd) which is significantly lower (P < 0.005) than the mean of 6.6+/-2.9 for 10 women receiving oral contraceptives and significantly higher than the means of 1.5+/-0.75 for 5 postmenopausal females (P < 0.05) and 1.8+/-1.0 for 16 adult males (P < 0.01) which are comparable. The mean GHPR's in mg/24 hr per m(2) for the four groups are: normal females = 0.52+/-0.24 (sd), females receiving contraceptive pills = 1.65+/-0.58 (P < 0.005), postmenopausal females = 0.26+/-0.12 (P < 0.025), and adult males 0.35+/-0.23 (P < 0.025).Three untreated acromegalic patients had ICGH's of 59, 82, and 93 ng/ml and GHPR's ranging from 14.5 to 17.9 mg/24 hr. Prednisone in a dose of 20 mg t.i.d. for 8 days significantly decreased both the ICGH and GHPR. Alternate day prednisone (60 mg in a single q.o.d. dose) resulted in less consistent inhibition of GH release which may play a role in the more normal growth seen in children receiving q.o.d. prednisone.

Acromegaly↗

Long-term, small dose prednisone therapy in frequently relapsing nephrotic syndrome of childhood. Effect on remission, statural growth, obesity, and infection rate.

A prospective study was performed to evaluate the effect of long-term small-dose prednisone therapy in frequently relapsing nephrotic syndrome (NS); 37 patients were included, with a relapse rate 4.6/patient/year (range, 3-8) (mean age, 6.7 years; range, 2-15 years). Prednisone was started 2 mg/kg/day once remission was induced. Prednisone was progressively reduced over weeks until 10 mg/day was reached, and then the daily dose was changed to 10 mg on alternate days. On follow-up (mean, 25.4 months; range, 10-58 months), only five had subsequent relapses and their relapse rate decreased significantly to 1.2/patient/year (p less than 0.05). Forty-six episodes of infection were associated with exacerbation of NS; 41 of these excerbations remitted spontaneously without an increase in the dose of prednisone. Serial height and weight measurements revealed evidence of improved height velocity and obesity persisted in only two of 13 initially obese children.

Adolescent↗

Pharmacokinetic and adrenal interactions of IL-10 and prednisone in healthy volunteers.

The pharmacokinetic and adrenal interactions of recombinant human interleukin-10 and prednisolone were examined in this open-label, randomized, four-way crossover study in 12 healthy adult male volunteers. Single doses of IL-10 (8 micrograms/kg s.c.), IL-10 with prednisone (15 mg p.o.), placebo with prednisone, or placebo were administered on four separate occasions with at least 3-week interceding washout periods. Measurements included plasma prednisone, prednisolone and cortisol, unbound prednisolone, and serum IL-10 concentrations. Pharmacokinetic parameters were determined using noncompartmental and model-fitting analysis, while area analysis and an indirect response model were used to assess cortisol dynamics. IL-10 exhibited prolonged serum concentrations owing to dual-absorption processes that were largely unaffected by prednisone. The Cmax values were about 3 ng/mL, while the tmax occurred at 7 to 9 hours. Prednisolone exhibited rapid systemic kinetics with a Cmax of 235 ng/mL, tmax at 1.11 hours, and t1/2 of 2.54 hours with no significant alterations owing to IL-10. Both prednisolone and prednisolone/IL-10 caused marked suppression of cortisol concentrations with similar magnitude and IC50 values; however, IL-10 alone significantly increased the 24-hour AUC of cortisol by 20%. Thus, IL-10 and prednisolone do not interact in disposition or adrenal suppression to a clinically significant degree.

Adrenal Glands↗

Prednisone-induced morphologic and chemical changes in the liver of dogs.

Glucocorticoid treatment in dogs is known to cause hepatocellular swelling due to accumulation of cytoplasmic compounds which variably have been identified histochemically as fat, glycogen, or water. In the present study changes in dog liver, after treatment for 15 days with two different doses of oral or intramuscular prednisone, were examined using histological, histochemical, and ultrastructural techniques as well as quantitative chemical analysis. Thirty mongrel dogs were divided into two control groups and three treatment groups of six dogs each. Dogs which received prednisone orally at 1.2 mg/kg body weight/day, or 4 mg/kg body weight/day, respectively, or received intramuscular prednisone injections of 4 mg/kg body weight/day had hepatomegaly due primarily to hepatocellular accumulation of glycogen. Compared to controls, no changes in the hepatic water concentration were observed, whereas the relative amounts of liver fat were decreased slightly and those of protein were decreased markedly. Hepatocellular glycogen could be demonstrated histochemically in tissues fixed in absolute alcohol, but not in tissues treated with aqueous fixative, such as 10% buffered formalin or Bouin's solution. Glycogen deposition occurred predominantly in the midzone of hepatic acini. Affected hepatocytes varied in size and shape. The most severely affected cells were enlarged five to ten fold with glycogen occupying most of the cytoplasmic space restricting the mitochondria, endoplasmic reticulum, and other organelles to a narrow zone around the cell periphery and the nucleus. It was concluded that treatment with prednisone causes hepatomegaly due to glycogenosis in the dog.

Administration, Oral↗

Reversal of erythema multiforme major with cyclophosphamide and prednisone.

OBJECTIVE: To report a case of erythema multiforme (EM) major treated with cyclophosphamide and prednisone. SETTING: General medicine and dermatology consult services, Department of Veterans Affairs Medical Center. CASE SUMMARY: A 44-year-old man with C4-C5 quadriplegia developed a skin reaction characterized by a painful, generalized maculopapular rash, bullae, ulceronecrotic lesions, and mucosal and epidermal sloughing after taking trimethoprim/sulfamethoxazole. The patient was treated with intravenous cyclophosphamide 150 mg infused over 1 hour every 24 hours and oral prednisone 15 mg every 6 hours. After two doses of cyclophosphamide, formation of bullae and epidermal sloughing had ceased, and the erythema was markedly diminished. Cyclophosphamide was discontinued before the third dose because of evolving leukopenia. Prednisone therapy was continued until the patient was discharged on hospital day 5, at which time the dosage was tapered. DISCUSSION: Cyclophosphamide has been used extensively for other dermatologic reactions. Relief of pain and regression of the lesions in our patient occurred more quickly than anticipated. CONCLUSIONS: Treatment of EM major with cyclophosphamide combined with prednisone appeared to be highly successful in this patient. Cyclophosphamide may be an effective, empiric initial treatment in reversing EM major.

Adult↗

Thromboembolic events in children with acute lymphoblastic leukemia (BFM protocols): prednisone versus dexamethasone administration.

Alterations in hemostasis leading to symptomatic thromboembolism have been observed in patients with acute lymphoblastic leukemia (ALL) receiving Escherichia coli asparaginase (CASP) combined with steroids. Moreover, hereditary prothrombotic risk factors are associated with an increased risk for venous thromboembolism in pediatric ALL patients treated according to the BFM 90/95 protocols (including CASP combined with prednisone during induction therapy). To assess whether the thromboembolic risk associated with established prothrombotic risk factors is modified by treatment modalities (prednisone or dexamethasone), the present analysis was performed. Three hundred thirty-six consecutively recruited leukemic children treated according to different BFM protocols (PRED group, n = 280, 60 mg/m(2) prednisone; DEXA group, n = 56, 10 mg/m(2) dexamethasone during induction therapy) were studied. Study end point was the onset of symptomatic vascular accidents during induction therapy. Cumulative thromboembolism-free survival was significantly reduced in children in the PRED group (thrombosis frequency, 10.4%) compared with children in the DEXA group (thrombosis frequency, 1.8%; P =.028). Although no significant difference was found in the overall prevalence of prothrombotic risk factors, 46.5% of patients in the PRED group who experienced thromboembolic events were carriers of a prothrombotic risk factor, whereas no carrier in the DEXA group had a thromboembolism. At the time of maximum CASP activity, fibrinogen and activities of antithrombin, plasminogen, and protein S were significantly reduced in the PRED group. No significant correlation could be found between CASP activity and levels of coagulation factors. In conclusion, the use of dexamethasone instead of prednisone, administered with CASP, significantly reduced the onset of venous thromboembolism.

Adolescent↗

Effects of prednisone and genetic polymorphisms on etoposide disposition in children with acute lymphoblastic leukemia.

Etoposide is a substrate for P-glycoprotein, CYP3A4, CYP3A5, and UGT1A1. Glucocorticoids modulate CYP3A and P-glycoprotein in preclinical models, but their effect on clinical etoposide disposition is unknown. We studied the pharmacokinetics of etoposide and its catechol metabolite in children with acute lymphoblastic leukemia, along with polymorphisms in CYP3A4, CYP3A5, MDR1, GSTP1, UGT1A1, and VDR. Plasma pharmacokinetics were assessed at day 29, after 1 month of prednisone (n = 102), and at week 54, without prednisone (n = 44). On day 29, etoposide clearance was higher (47.4 versus 29.2 mL/min/m2, P <.0001) than at week 54. The day 29 etoposide or catechol area under the curve (AUC) was correlated with neutropenia (P =.027 and P =.0008, respectively). The relationship between genotype and etoposide disposition differed by race and by prednisone use. The MDR1 exon 26 CC genotype predicted higher day 29 etoposide clearance (P =.002) for all patients, and the CYP3A5 AA and GSTP1 AA genotypes predicted lower clearance in blacks (P =.02 and.03, respectively). The UGT1A1 6/6, VDR intron 8 GG, and VDR Fok 1 CC genotypes predicted higher week 54 clearance in blacks (P =.039,.036, and.052, respectively). The UGT1A1 6/6 genotype predicted lower catechol AUC. Prednisone strongly induces etoposide clearance, genetic polymorphisms may predict the constitutive and induced clearance of etoposide, and the relationship between genotype and phenotype differs by race.

Base Sequence↗

Dexamethasone-based regimens versus melphalan-prednisone for elderly multiple myeloma patients ineligible for high-dose therapy.

Dexamethasone alone increases life expectancy in patients with relapsed multiple myeloma (MM); however, no large randomized study has compared dexamethasone and dexamethasone-based regimens with standard melphalan-prednisone in newly diagnosed MM patients ineligible for high-dose therapy. In the Intergroupe Francophone du Myélome (IFM) 95-01 trial, 488 patients aged 65 to 75 years were randomized between 4 regimens of treatment: melphalan-prednisone, dexamethasone alone, melphalan-dexamethasone, and dexamethasone-interferon alpha. Response rates at 6 months (except for complete response) were significantly higher among patients receiving melphalan-dexamethasone, and progression-free survival was significantly better among patients receiving melphalan (P < .001, for both comparisons), but there was no difference in overall survival between the 4 treatment groups. Moreover, the morbidity associated with dexamethasone-based regimens was significantly higher than with melphalan-prednisone, especially for severe pyogenic infections in the melphalan-dexamethasone arm and hemorrhage, severe diabetes, and gastrointestinal and psychiatric complications in the dexamethasone arms. Overall, these results indicated that dexamethasone should not be routinely recommended as first-line treatment in elderly patients with MM. In the context of the IFM 95-01 trial, the standard melphalan-prednisone remained the best treatment choice when efficacy and patient comfort were both considered. These results might be useful in the context of future combinations with innovative drugs.

Aged↗

Octreotide alone or with prednisone in patients with advanced thymoma and thymic carcinoma: an Eastern Cooperative Oncology Group Phase II Trial.

PURPOSE: To determine the objective response rate, duration of remission and toxicity of octreotide alone or with the later addition of prednisone in patients with unresectable, advanced thymic malignancies in whom the pretreatment octreotide scan was positive. PATIENTS AND METHODS: Forty-two patients with advanced thymoma or thymic carcinoma were entered onto the trial, of whom 38 were fully assessable (one patient had inconclusive histology; three patients had negative octreotide scan). Patients received octreotide 0.5 mg subcutaneously tid. At 2 months, patients were evaluated. Responding patients continued to receive octreotide alone; patients with progressive disease were removed from the study. All others received prednisone 0.6 mg/kg orally qid for a maximum of 1 year. RESULTS: Two complete (5.3%) and 10 partial responses (25%) were observed (four partial responses with octreotide alone; the remainder with octreotide plus prednisone). None of the six patients without pure thymoma responded. The 1- and 2-year survival rates were 86.6% and 75.7%, respectively. Patients with an Eastern Cooperative Oncology Group performance status of 0 lived significantly longer than did those with a performance status of 1 (P =.031). CONCLUSION: Octreotide alone has modest activity in patients with octreotide scan-positive thymoma. Prednisone improves the overall response rate but is associated with increased toxicity. Additional studies with the agent are warranted.

Adult↗

Kinetics and interconversion of prednisolone and prednisone studied with new radioimmunogassays.

To determine the kinetics of metabolism and interconversion of prednisolone and prednisone, the plasma levels of these synthetic glucocorticoids were measured by new radioimmunoassays (RIA) after intravenous (iv) or oral administration to normal humans. Following the iv injection of prednisolone phosphate in 8 normal subjects, the mean half-time of prednisolone was 240+/-20 min (mean+/-SE) and the metabolic clearance rate was 82+/-7.2 1/24 h/m2. Of 10 mg of prednisone given orally to 5 normal subjects, 69+/-5% was absorbed and converted to peripheral plasma prednisolone within 8 h. The data indicate that prednisone is extensively metabolized to prednisolone before it clears the splanchnic circulation and the formation prednisone by oxidation of the 11-hydorxyl group of prednisolone appears to occur mainly in peripheral tissues.

Adult↗

Endogenous hydrocortisone, a possible factor contributing to the genesis of cushingoid habitus in patients on prednisone.

To establish if the cushingoid habitus in patients taking prednisone is associated with relatively high total or free prednisolone and low endogenous hydrocortisone concentrations in plasma, 15 stable renal transplant patients and 12 patients treated with prednisone for oral mucocutaneous vesiculo-erosive diseases were investigated. After the patients' usual prednisone doses, the areas under the plasma concentration time curve of total and free prednisolone were not different when the 14 patients without cushingoid appearance were compared to the 13 patients with cushingoid appearance. Patients with cushingoid habitus more frequently exhibited peak hydrocortisone levels within the normal range (6 of 14 vs. 1 of 13) and had higher areas under the plasma concentration time curve of hydrocortisone (median, range), i.e. 2672 ng/ml.min (0-21, 637 ng/ml.min) vs. 308 ng/ml.min (0-12, 495 ng/ml.min) compared to those without cushingoid appearance (P less than 0.05). These results indicate that pharmacokinetic differences of prednisone do not explain the presence or absence of cushingoid habitus and that there is an association between cushingoid habitus and endogenous hydrocortisone levels.

Adult↗