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PubMed1976

A controlled trial of inhaled corticosteroids in patients receiving Prednisone tablets for asthma.

The theraprutic efficacy of inhaled beclomethasone dipropionate and inhaled betamethasone valerate in chronic asthma has been studied in 14 treatment centres in 158 patients who had previously been taking prednisone tablets regularly. Doses of 400 mug daily of beclomethasone dipropionate and a dose of 800 mug daily of betamethasone valerate allowed approximately 80% of patients to discontinue prednisone initially and 60% to remain off daily prednisone for 24 weeks. A mean reduction in daily prednisone dose of 8 mg was achieved by patients inhaling corticosteroids whilst placebo inhaler permitted a 5 mg reduction. The three inhaled corticosteroid preparations were equally effective in facilitating prednisone reduction and provided equally good control of asthma, alone or as an ancillary to prednisone. The higher dose of beclomethasone dipropionate was superior to the lower in permitting more patients to remain off daily prednisone for the period of the trial. Although 82% of patients recovered a normal adrenal response to tetracosactrin 24 weeks after prednisone was discontinued and inhaled corticosteroids subsituted, 18% still showed some suppression of adrenal function. There was no significant difference between the treatment groups in this.

Aerosols↗
PubMed1980

Dose-response studies of the suppression of whole blood histamine and basophil counts by prednisone.

If some clinical problems (e.g., radiographic contrast media reactions) arise from mediator release by circulating basophils, prednisone's capacity to prevent such is likely to be at least partly related to its suppressive effects on whole blood histamine and basophil levels. To establish an optimal dosage schedule, 15 healthy male volunteers entered a two-phased study to determine (1) the single dose of prednisone required to produce maximal suppression of histamine and basophil levels and (2) the effects of repeated prednisone doses. Parameters monitored were whole blood histamine, quantitative basophil counts, white blood cell (WBC) and differential counts, and plasma prednisone, prednisolone, and cortisol levels. Fifty milligrams prednisone suppressed whole blood histamine levels as much as a larger dose and also showed a marked effect on circulating basophils and other leukocytes. Three 50-mg prednisone doses given at 6-hr intervals had a greater effect on whole blood histamine and circulating leukocytes than fewer doses. Thus, the commonly used empirical prednisone dosage regimen is supported. One implication of the results of this study is that greater suppression of blood basophils and histamine levels might be obtained by administering the last prednisone dose about 6 hr before procedures in which a very rapid release of mediators from basophils is anticipated.

Adolescent↗
PubMed2006

Effect of two prednisone exposures on mood and declarative memory.

Corticosteroids are essential for life and an integral part of the stress response. However, in excess, corticosteroids can be associated with a variety of effects on the brain including hippocampal atrophy and even neuronal death, mood changes, and declarative memory impairment. The magnitude of mood change in patients receiving prednisone is reportedly associated with previous lifetime corticosteroid exposure, consistent with a sensitization or kindling process whereby greater effects are observed with repeated exposure. To our knowledge, the effect of multiple corticosteroid exposures on mood and memory has not been previously examined prospectively in animals or humans. In this study, 30 human volunteers, with no history of systemic prescription corticosteroid therapy, were given (in random order using a crossover design) two 3-day exposures of prednisone (60 mg/day) and one of identical placebo, with 11-day washouts between each medication exposure. Before and after each 3-day prednisone/placebo exposure, declarative memory was assessed using different versions of the Rey Auditory Verbal Learning Test (RAVLT) to minimize practice or learning effects, while mood was assessed with the 21-item Hamilton Rating Scale for Depression, Young Mania Rating Scale and Internal State Scale. No significant mood changes were found. However, a significant decrease in aspects of RAVLT performance was observed after the first prednisone exposure consistent with a decline in declarative memory performance. The decline in RAVLT performance was significantly smaller after the second prednisone exposure as compared to the initial prednisone exposure. Thus, a second prednisone exposure was associated with an attenuated prednisone-effect on declarative memory. These data suggest tolerance or habituation, rather than sensitization, to prednisone effects on declarative memory during a second exposure. Implications and possible explanations for the findings are discussed.

Adult↗
PubMed1999

Diltiazem retards the metabolism of oral prednisone with effects on T-cell markers.

The area under the time-plasma concentration curve (AUC) was measured for prednisolone (the major active metabolite of prednisone) after ingestion of 15 mg of prednisone (phase 1) and again after 3 d of oral diltiazem (180 mg/d) followed by the same dose of oral prednisone (phase 2) in eight normal adult patients. Diltiazem increased the prednisolone AUC by 21% (range 3-38%), from 1297 +/- 157 ng/h/mL to 1560 +/- 169 ng/h/mL (p = 0.001). This effect was associated with a greater decrease from baseline in CD3+ lymphocyte number at 4 h after prednisone ingestion (596 +/- 175 vs. 516 +/- 140, p = 0.05), a larger percentage decrease of circulating CD3+ lymphocytes at 8 h (43 +/- 19% vs. 53 +/- 19%, p = 0.04), and a decrease in the number of CD3+ CD8+ T cells at 4 h post-prednisone ingestion (279 +/- 81 vs. 236 +/- 51, p = 0.04). Diltiazem retards prednisolone metabolism and when used chronically with prednisone could conceivably, in some patients, enhance its immunologic and other clinical effects. Potentiation of prednisone side-effects by diltiazem may be of special interest in pediatric patients, and possible diltiazem-prednisone interactions merit study in this population.

Administration, Oral↗
PubMed2005

Oral administration of prednisone to control refractory vertigo in Ménière's disease: a pilot study.

OBJECTIVE: To establish whether the oral administration of moderate doses of prednisone reduces refractory vertigo in Ménière's disease. STUDY DESIGN: Blinded, randomized, controlled trial. SETTING: Tertiary referral center. PATIENTS: Patients with Ménière's disease with limited vertigo control (Class C) and severe disability (Scale 3). INTERVENTIONS: Two groups (n = 8 per group) were treated orally with either diphenidol (25 mg/d) plus acetazolamide (250 mg/48 h) (control group), or the same treatment plus prednisone (0.35 mg/kg) daily for 18 weeks (prednisone group). MAIN OUTCOME MEASURES: The variables evaluated were the frequency and duration of vertigo, tinnitus, aural fullness, and audiographic parameters. The clinical surveillance was performed for 12 months after prednisone withdrawal. RESULTS: The frequency and duration of vertigo episodes were reduced by 50% and 30%, respectively, by prednisone treatment. Prednisone-treated patients manifested a significant reduction in tinnitus. No changes were observed in aural fullness or hearing. No metabolic or infectious disorders were observed. CONCLUSION: Oral prednisone helps to control refractory vertigo in Ménière's disease. These preliminary data suggest that prednisone can be a good noninvasive antivertigo management regimen for these patients.

Administration, Oral↗
PubMed1992

Prednisone-induced osteopenia in beagles: variable effects mediated by differential suppression of bone formation.

To examine the mechanism of glucocorticoid-induced osteopenia and the basis for variable bone loss after glucocorticoid administration, we gave prednisone (1.3 mg.kg-1.day-1) to normal male dogs (n = 15) for 29 wk to attempt induction of osteopenia. Compared with age-matched control dogs (n = 14), prednisone treatment rapidly decreased spinal bone density by 4.3%, as assessed by quantitative digital radiography, and reduced trabecular bone volume by 14.6%, as measured by quantitative histomorphology of iliac crest bone specimens. Bone loss was attenuated in prednisone-treated dogs after prolonged treatment (greater than 12 wk). Prednisone treatment resulted in diminished bone formation rates (15 +/- 3.4 vs. 47 +/- 4.5 microns/yr) and activation frequency (0.4 +/- 0.1 vs. 1.3 +/- 0.2/day). These findings indicate that suppression of osteoblastic function and recruitment is the primary histological abnormality mediating glucocorticoid-induced osteopenia in beagles. In contrast, prednisone administration had no effect on bone resorption or serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D, which suggests that these factors are not essential for prednisone-induced bone loss. Moreover, 33% of beagles were totally resistant to glucocorticoid-induced osteopenia. Such heterogeneity of bone loss was associated with variable suppressive effects of prednisone on osteoblastic function, as evidenced by greater bone formation rates and activation frequency in prednisone-resistant animals. Collectively, these observations suggest that glucocorticoid-induced bone loss results from a dynamic interplay between steroid-mediated suppression of osteoblastic function and recruitment and undefined compensatory factors that ameliorate the effects of glucocorticoids on osteoblastic precursors.

Animals↗
PubMed1988

Short-term effects of prednisone on serum lipids and high density lipoprotein subfractions in normolipidemic healthy men.

To study the effects of short term low dose prednisone administration on serum lipids and lipoproteins we measured the concentration and composition of serum lipoproteins; serum apoproteins (apo) A-I, A-II, and B; and plasma lipolytic enzymes before and during prednisone administration (30 mg/day for 7 days) in eight normal men. We also measured insulin binding to adipocytes. Serum high density lipoprotein (HDL) cholesterol increased significantly after 2 days of prednisone administration; the maximal increase was 27% (P less than 0.01 after 5 days). The rise of HDL cholesterol was accounted for by that of HDL2 cholesterol. There were marked changes in the distribution of HDL particles; HDL2 increased, whereas HDL3 decreased. These changes were also apparent after 2 days of prednisone administration and were maximal at 5 days [mean, 1.58 +/- 0.12 (+/- SE) vs. 2.00 +/- 0.14 g/L (P less than 0.001) for HDL2; 1.82 +/- 0.11 vs. 1.61 +/- 0.06 g/L (P less than 0.05) for HDL3], and they were due to opposing changes in cholesterol, phospholipids, and proteins in the HDL subfractions. The change in HDL2 protein correlated inversely with that in HDL3 protein (r = -0.73; P less than 0.05). Notably, prednisone did not change the apo A-I concentration, but that of apo A-II decreased (0.32 +/- 0.02 vs. 0.27 +/- 0.01 g/L; P less than 0.05). Consequently, the lipid to protein ratio of HDL increased. Prednisone induced no significant changes in very low density or low density (LDL) lipoproteins. Adipose tissue LPL activity did not increase until after 7 days of prednisone intake (1.10 +/- 0.28 vs. 3.43 +/- 1.02 mumol FFA/g.h; P less than 0.05), and the same was true for muscle LPL (0.49 +/- 0.14 vs. 0.82 +/- 0.11 mumol FFA/g.h; n = 4; P = 0.06). Specific insulin binding was normal, but both basal and maximal insulin-stimulated glucose transport decreased significantly. In summary, prednisone induces changes in serum HDL which are characterized by redistribution of particles within HDL density toward less dense particles and a quantitative rise of lipids in the HDL2 fraction.

Adipose Tissue↗
PubMed2001

A controlled study of intravenous immunoglobulin combined with prednisone in the treatment of IBM.

OBJECTIVE: To investigate whether the combination of intravenous immunoglobulin (IVIg) with prednisone improves muscle strength and alters endomysial inflammation in patients with sporadic inclusion body myositis (s-IBM). BACKGROUND: In a previous controlled trial in s-IBM, IVIg did not significantly improve strength in spite of modest benefits in some muscle groups. The possibility that prednisone may have a synergistic effect with IVIg prompted another controlled trial. METHODS: Thirty-six patients with biopsy-proven IBM were randomized to receive IVIg or placebo monthly for 3 months. Before infusions, all patients were started on high-dose prednisone for 3 months. Primary outcome measures were differences in the 1) Quantitative Muscle Strength (QMT) testing; and 2) modified Medical Research Council (MRC) scores, between the patients randomized to IVIg + prednisone compared with those randomized to placebo + prednisone. Repeated open muscle biopsies were performed at random in 24 patients to determine changes in the number of autoinvasive T cells and necrotic muscle fibers. RESULTS: Nineteen patients were randomized to IVIg + prednisone and 17 to placebo + prednisone. No significant change was noted in muscle strength, assessed by QMT and MRC, from baseline to the 2nd, 3rd, or 4th month after treatment between the two groups. The number of necrotic fibers was reduced in the IVIg randomized group (p < 0.01), and the mean number of CD2+ cells was significantly decreased in both groups (p < 0.0001), denoting a steroid effect. CONCLUSION: IVIg combined with prednisone for a 3-month period was not effective in IBM. Endomysial inflammation was significantly reduced after treatment, but the reduction was not of clinical significance.

Aged↗
PubMed1993

Idiopathic facial nerve paralysis: a randomized double blind controlled study of placebo versus prednisone.

Idiopathic facial nerve paralysis (IFNP) is a common malady. Because its etiology is unclear, there are a variety of treatment options. Studies to date have not clearly established the benefits of treatment with oral steroids (prednisone). The authors performed a randomized double-blind controlled study comparing the use of placebo versus prednisone which shows that prednisone-treated patients benefit from early treatment. Seventy-six patients met inclusion criteria and completed follow-up until recovery; 35 patients received prednisone and 41 received placebo. Their mean age was 36.8 years. Facial nerve function was assessed using the House-Brackmann facial nerve grading scale, as well as a variety of other measures. Patients were evaluated pretreatment, regularly post-treatment until judged recovered (return of facial function to a grade III or better), and at 6 months after recovery. Difference in mean time to resolution for the prednisone (51.4 days) and placebo (69.3 days) groups was not statistically significant. There was a significant difference in grade at recovery, with the placebo group having a higher proportion of grade III results (P < .03). Eight of 10 patients with electroneurography (ENOG) evidence of denervation were in the placebo group and accounted for 6 of the 7 grade III results. However, the difference in proportion of patients with evidence of denervation for the prednisone (5.7%) and placebo (19.5%) groups did not achieve statistical significance. This study shows that patients treated with prednisone have less denervation than placebo-treated patients. They also have a significant improvement in facial grade at recovery compared to placebo-treated patients. Therefore, the authors recommend that all patients at risk for developing denervation receive prednisone treatment.

Adolescent↗
PubMed1995

Empiric prednisone therapy for pulmonary toxic reaction after high-dose chemotherapy containing carmustine (BCNU).

STUDY OBJECTIVE: To determine pretreatment factors that predict for pulmonary toxic reactions after high-dose chemotherapy containing carmustine (BCNU) and to determine the utility of prednisone in preventing pulmonary toxic reactions. DESIGN: Retrospective review. SETTING: Tertiary care referral center. PATIENTS: Forty-five patients with relapsed or refractory lymphoma and 27 patients with breast cancer with normal cardiopulmonary function were treated with one of two high-dose combination chemotherapeutic regimens containing the same dose of BCNU. MEASUREMENTS: Recorded pretreatment patient characteristics included previous chemotherapy or radiation therapy, history of pulmonary metastases, history of chronic obstructive pulmonary disease, and history of smoking. Spirometry and single-breath carbon monoxide diffusing capacity (DCO) were obtained before and after high-dose chemotherapy. INTERVENTIONS: Patients were treated with prednisone for a 5% or more drop in postchemotherapy DCO whether or not symptoms were present. RESULTS: Fifty-nine patients were evaluable. No pretreatment characteristic predicted for declines in pulmonary function postchemotherapy. The FEV1/FVC ratio did not change significantly after high-dose chemotherapy, but the DCO decreased 12.1% (p < 0.001). Of the 59 evaluable patients, 30 were treated with prednisone for declines in postchemotherapy DCO. Sixteen (53%) of these 30 patients were asymptomatic. The DCO increased 10.3% in patients treated with prednisone compared with a decrease of 2.3% in patients not treated (p = 0.017). There was no statistically significant difference in FEV1/FVC in patients treated with prednisone compared with those not treated. Regression analysis of pretreatment characteristics, type of high-dose chemotherapy received, and treatment with prednisone identified only treatment with prednisone as a significant variable in predicting an increase in DCO (p = 0.03; regression coefficient = +11.5%, SE = +/- 5.2%) after high-dose chemotherapy containing BCNU. CONCLUSIONS: High-dose BCNU-containing chemotherapeutic regimens cause decreases in DCO that are often asymptomatic and likely represent subclinical pulmonary toxic reactions. Pretreatment clinical parameters cannot predict which patients will manifest pulmonary toxic reactions after high-dose chemotherapy. Empiric treatment with prednisone will reverse chemotherapy-induced decreases in DCO. Earlier institution of glucocorticoids for evidence of pulmonary dysfunction is recommended.

Adult↗
PubMed1995

Pharmacokinetic interactions between zileuton and prednisone.

A randomized double-blind placebo-controlled crossover study evaluated the effects of zileuton 600mg 4 time daily on the pharmacokinetics of prednisolone after a single 400mg oral dose of prednisone. the effects of the single prednisone dose on the steady-state pharmacokinetics of zileuton were also evaluated. Multiple doses of zileuton had no significant effects on mean peak plasma concentration (Cmax), time to Cmax(tmax), or area under the plasma concentration-time curve from 0 to infinity (AUC0-infinity) values for prednisolone after oral administration of prednisone 40mg. A slight but statistically significant increase in the mean half-life (t1/2) of prednisolone was detected with zileuton + prednisone administration compared with prednisone + placebo (from 2.8 to 2.9 hours); however, this change was of no clinical relevance. Mean Cmax values of zileuton after coadministration with prednisone were similar to those of zileuton alone. While the single 40mg dose of prednisone resulted in a slight but statistically significant decrease in the mean zileuton AUC value from 0 to 6 hours (AUC0-6) [from 23 to 20 mg/L/h] and a reduction in tMAX (from 2.3 to 1.7 hours), these results were not considered to be clinically significant. Therefore, it is considered that zileuton and prednisone may be coadministered with minimal risk of a clinically significant pharmacokinetic interaction.

Administration, Oral↗
PubMed1991

Differential effects of prednisone and growth hormone on fuel metabolism and insulin antagonism in humans.

Human growth hormone (hGH) and prednisone cause insulin resistance and glucose intolerance. However, it is unknown whether hGH and prednisone antagonize insulin action on protein, fat, and carbohydrate metabolism by a common or independent mechanism. Therefore, protein, fat, and carbohydrate metabolism was assessed simultaneously in four groups of eight subjects each after 7 days of placebo, recombinant DNA hGH (rhGH; 0.1 mg.kg-1.day-1), prednisone (0.8 mg.kg-1.day-1), or rhGH and prednisone administration after an 18-h fast and during gut infusion of glucose and amino acids (fed state). Fasting plasma glucose concentrations were similar during placebo and rhGH but elevated (P less than 0.001) during combined treatment, whereas plasma insulin concentrations were higher (237 +/- 57 pmol/ml, P less than 0.001) during combined than during placebo, rhGH, or prednisone treatment (34, 52, and 91 pM, respectively). In the fed state, plasma glucose concentrations were elevated only during combined treatment (11.3 +/- 2.1 mM, P less than 0.001). Plasma insulin concentrations were elevated during therapy with prednisone alone and rhGH alone (667 +/- 72 and 564 +/- 65 pmol/ml, respectively, P less than 0.001) compared with placebo (226 +/- 44 pmol/ml) but lower than with the combined rhGH and prednisone treatment (1249 +/- 54 pmol/ml, P less than 0.01). Protein oxidation [( 14C]leucine) increased (P less than 0.001) with prednisone therapy, decreased (P less than 0.001) with rhGH treatment, and was normal during the combined treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2007

A systematic review and economic model of the clinical effectiveness and cost-effectiveness of docetaxel in combination with prednisone or prednisolone for the treatment of hormone-refractory metastatic prostate cancer.

OBJECTIVES: A systematic review was undertaken and an economic model constructed to evaluate the clinical effectiveness and cost-effectiveness of docetaxel (Taxotere, Sanofi-Aventis) in combination with prednisone/prednisolone for the treatment of metastatic hormone-refractory prostate cancer (mHRPC). The main comparators considered were other established chemotherapy regimens and best supportive care. DATA SOURCES: Twenty-one resources (including MEDLINE, EMBASE and the Cochrane Library) were searched to April 2005. REVIEW METHODS: Two reviewers independently assessed studies for inclusion. Data from included studies were extracted and quality assessed. Where appropriate, outcomes were synthesised using formal analytic approaches. A new economic model was developed in order to establish the cost-effectiveness of docetaxel compared with a range of potential comparators. A separate review was undertaken to identify sources of utility data required to estimate quality-adjusted life-years (QALYs). Sensitivity analyses were also undertaken to explore the robustness of the main analysis to alternative assumptions related to quality of life. Monte Carlo simulation was used to propagate uncertainty in input parameters through the model in such a way that the results of the analysis could be presented with their uncertainty. The impact of uncertainty surrounding the decision was established using value of information and implementation approaches. RESULTS: Seven randomised controlled trials were identified that met the inclusion criteria. A direct comparison of docetaxel plus prednisone versus mitoxantrone plus prednisone in an open-label randomised trial showed improved outcomes for docetaxel plus prednisone in terms of overall survival, quality of life, pain and prostate-specific antigen decline. Two other chemotherapy regimens that included docetaxel: docetaxel plus estramustine and docetaxel plus prednisone plus estramustine, also showed improved outcomes in comparison with mitoxantrone plus prednisone. Indirect comparison suggested that docetaxel plus prednisone seems to be superior to corticosteroids alone in terms of overall survival. Conclusions on cost-effectiveness were primarily informed by the results of the in-house model. This indicated that mitoxantrone plus a corticosteroid is probably cheaper and more effective than corticosteroid alone. Compared with mitoxantrone plus prednisone/prednisolone, the use of docetaxel plus prednisone/prednisolone (3-weekly) appears cost-effective only if the NHS is prepared to pay 33,000 pounds per QALY. The incremental cost-effectiveness ratio associated with docetaxel plus prednisone (3-weekly) remained fairly robust to these variations with estimates ranging from 28,000 pounds to 33,000 pounds per QALY. Value of information analysis revealed that further research is potentially valuable. Given a maximum acceptable ratio of 30,000 pounds per QALY, the expected value of information was estimated to be approximately 13 million pounds. CONCLUSIONS: This systematic review of the research suggests that docetaxel plus prednisone seems to be the most effective treatment for men with mHRPC. The economic model suggests that treatment with docetaxel plus prednisone/prednisolone is cost-effective in patients with mHRPC provided the NHS is prepared to pay 33,000 pounds per additional QALY. Future research should include the direct assessment of quality of life and utility gain associated with different treatments, including the effect of adverse events of treatment, using generic instruments, which are suitable for the purposes of cost-effectiveness analyses.

Antineoplastic Agents↗
PubMed1980

Effect of prednisone dose spacing on plasma lipids.

We have previously reported a low prevalence of hyperlipidemia in renal transplant recipients who were treated with alternate-day corticosteroid. To determine whether alternate-day prednisone per se is associated with lower plasma lipids than is daily prednisone, we studied 14 renal transplant recipients with good allograft function (serum creatinine less than 2.5 mg/dl) who were normolipidemic on alternate-day prednisone. All patients were treated with 6 months of daily prednisone (10.9 +/- 0.4 mg, mean +/- S.E.) and then returned to 6 months of alternate-day prednisone (21.6 +/- 1.0 mg). Mean plasma triglyceride, cholesterol, and cholesterol fractions on either regimen were normal and not different. There were no differences in fasting or 2 hr postprandial glucose and insulin levels. Twelve patients gained weight on daily prednisone, and 11 patients lost weight on reversion to alternate-day prednisone. The changes in ideal body weight in both periods correlated (p less than 0.05) with changes in plasma triglycerides. These data suggest that a daily prednisone regimen per se as compared to an alternate-day regimen does not dispose normolipidemic patients to hyperlipidemia. The factors contributing to the low prevalence of hyperlipidemia in our renal transplant recipients remain obscure.

Adult↗
PubMed1981

Decreased bioavailability of prednisone due to antacids in patients with chronic active liver disease and in healthy volunteers.

To investigate the potential action of antacids on prednisone absorption and on prednisolone serum levels, we studied 5 healthy volunteers and 12 patients with chronic active liver disease. Six patients responded to treatment and 6 did not. After administering two 5-mg tablets of prednisone with 60 ml of water, 60 ml of Melox (AlOH 3.75 g/100 ml + MgOH 4.0 g/100 ml), or 60 ml of Aldrox (AlOH 8.0 g/100 ml + MgOH 1.95 g/100 ml), we measured prednisolone by radioimmunoassay. Both peak heights and areas under the serum-concentration curves were significantly reduced when prednisone was administered with antacids. The relative bioavailability of prednisone after prednisone-antacid treatments compared to that after prednisone-water treatment was 74% +/- 13% (p less than 0.05) with Melox and 57% +/- 15% (p less than 0.01) with Aldrox in healthy volunteers. In patients with chronic active liver disease responding to treatment, prednisone bioavailability was 65% +/- 120% (p less than 0.01) and 87% +/- 20%, respectively. Among patients with chronic active liver disease not responding to treatment, this parameter was 76% +/- 12% (p less than 0.05) and 80% +/- 21% (p less than 0.05), respectively. To insure adequate prednisolone levels in patients with chronic active liver disease, prednisone should not be given simultaneously with antacids.

Adult↗
PubMed1995

Alternate-day prednisone in the maintenance immunosuppressive therapy after orthotopic liver transplantation.

Glucocorticoids have been an important part of maintenance immunosuppressive therapy following orthotopic liver transplantation (OLT). However, long-term daily glucocorticoid use is associated with a high incidence of unpleasant side effects. In an effort to minimize side effects while maintaining adequate immunosuppression, we have treated 48 adult patients with low dose alternate-day prednisone, 15 mg q.o.d. Pre-OLT diagnoses included primary biliary cirrhosis (16 patients), alcoholic liver disease (8 patients), sclerosing cholangitis (8 patients), cryptogenic cirrhosis and/or non-A, non-B hepatitis (11 patients), acute hepatic failure (3 patients), and hepatocellular carcinoma and bile duct carcinoma (1 patient each). Conversion to alternate-day prednisone was attempted when patients were clinically stable and the daily prednisone dose was 15 mg. The average interval between OLT and beginning of the conversion to alternate-day prednisone was 38 weeks. The mean time for conversion to alternate-day prednisone was 35 weeks, but decreased as more experience was gained. The mean follow-up was 106 weeks. Cushingoid side effects diminished in all. In 47 of the 48 patients, there were no clinical laboratory or histologic changes suggestive of rejection after the initiation of alternate-day prednisone. A single episode of rejection occurred during the taper. This episode responded promptly to increased glucocorticoid therapy, and the patient was easily converted to alternate-day prednisone at a later date. There was no increase in concurrent immunosuppressives dosage after the conversion. Alternate-day prednisone is effective and safe for chronic immunosuppression after OLT in patients receiving cyclosporine and azathioprine.

Adolescent↗
PubMed1993

Prednisone withdrawal in HLA identical and one haplotype-matched live-related donor and cadaver renal transplant recipients.

Prednisone withdrawal was attempted in 121 of 915 renal transplants recipients between 1967 to 1992. There were 57 males, 64 females. Age range was 21 to 62 (mean 39.2 years). Etiology of renal failure was chronic glomerulonephritis (54), diabetic nephropathy (36), interstitial disease (17), hypertensive nephrosclerosis (6), and other (8). Kidney source was from HLA-identical living-related donors (LRD) in 54 (Group I), one haplotype-matched LRD in 23 (Group II), and cadaver in 44 (Group III). Prior to the introduction of cyclosporin A (CsA) in 1984, prednisone withdrawal was attempted only in Group I. After 1984, prednisone withdrawal was also attempted in patients in Groups II and III, selected on the basis of having had no rejection episodes during the six months after transplantation. Forty-five patients in Group I were treated with azathioprine (Aza) and prednisone, and the remaining patients in Groups I to III were treated with Aza, prednisone and CsA. Mean follow-up was 93 months (6 to 207). Prednisone was gradually tapered and withdrawn in 94 of 121 patients after a mean period of 22.5 months (9 to 60). In 27 other patients, the prednisone dosage has been tapered to 5 mg/day or less with the aim of discontinuing the drug. There were seven episodes of acute rejection (3 during taper, and 1 each at 6, 7, 24 and 114 months after prednisone withdrawal); all seven were successfully reversed. Four other patients developed chronic vascular rejection (2 during taper and 2 after withdrawal).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Studies on the interaction of antidepressant drugs with adrenocorticotropic hormone or prednisone in rats.

The influence of adrenocorticotropic hormone (ACTH) and prednisone on the effects of amitriptyline (AMI), imipramine (IMI), mianserin (MIA) or nomifensine (NOM) was investigated in forced swimming and in open field tests. ACTH (50 I.U./kg) or prednisone (1 mg/kg) were given in a single dose or for 7 consecutive days alone or together with AMI (10 mg/kg), IMI (10 mg/kg), MIA (10 mg/kg) or NOM (2 mg/kg). It was found that neither ACTH nor prednisone administered alone in a single dose or for 7 days influenced the behavior of rats. ACTH co-administered with AMI or NOM in a single dose or with AMI, IMI or NOM for 7 days potentiated the antiimmobility effect of antidepressant drugs. Prednisone potentiated only antiimmobility effect of NOM in forced swimming test. ACTH as well as prednisone co-administered with NOM (but not with the other drugs), in a single dose as well as for 7 days, increased also locomotor activity in open field. Neither ACTH nor prednisone influenced the effect of MIA in both tests used. It was concluded that the specific synergism exists only between ACTH and tricyclic antidepressants (AMI, IMI). The observed behavioral interaction between ACTH and AMI or IMI does not seem to be mediated by adrenocorticoids (prednisone was without effect). The potentiation of NOM effects by ACTH as well as by prednisone and lack of any interaction with MIA seems to be related with different mechanism of action of those antidepressant drugs.

Adrenocorticotropic Hormone↗