SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Treatment of Hodgkin's disease in children should be directed at maximizing cures and minimizing the long-term effects of alkylating agents, anthracyclines, and bleomycin. In this study methotrexate and etoposide were used in the VAMP/VEPA regimens to treat 60 clinically staged pediatric patients with Hodgkin's disease. Twenty-nine patients with stages I-IIA received four courses of VAMP plus low-dose radiotherapy. Thirty-one IIA bulky disease and IIB-IVB patients received four or six courses of VEPA plus low-dose radiotherapy. There were 6 partial remissions after the completion of chemotherapy and all of these patients relapsed, but 4 were successfully salvaged with ABMT. Two patients have died. The 3.1-year overall survival rate is 97% (100% VAMP, 94% VEPA) and the event-free survival rate is 88% (97% VAMP, 77% VEPA). These results suggest that VAMP is a reasonable treatment for low stages of Hodgkin's disease, but more advanced disease is not adequately treated by VEPA and low-dose radiotherapy.
BACKGROUND: Tacrolimus (Tac) and mycophenolate mofetil (MMF) are newly approved immunosuppressive agents. However, the safety and efficacy of the combination of MMF and Tac in primary liver transplantation has not been determined. METHODS: An Institutional Review Board-approved, open-label prospective randomized protocol was initiated to study the efficacy and toxicity of Tac and steroids (double-drug therapy) versus Tac, steroids, and MMF (triple-drug therapy) in primary adult liver transplant recipients. Both groups of patients began on the same doses of Tac and steroids. Patients randomized to triple-drug therapy also received 1 g of MMF twice a day. RESULTS: Between August 1995 and January 1997, 200 patients were enrolled, 99 in double-drug therapy and 101 in triple-drug therapy. All patients were followed until May 1997, with a mean follow-up of 12.7 months. During the study period, 28 of 99 patients in double-drug therapy received MMF to control ongoing acute rejection, nephrotoxicity, and/or neurotoxicity. On the other hand, 61 patients in triple-drug therapy discontinued MMF for infection, myelosuppression, and/or gastrointestinal disturbances. By an "intention-to-treat analysis," the actuarial 1-year patient survival rate was 85.1% in double-drug therapy and 83.1% in triple-drug therapy (P=0.77). The actuarial 1-year graft survival rate was 80.2% for double-drug therapy and 79.2% for triple-drug therapy (P=0.77). Forty-one patients (41.4%) in double-drug therapy and 32 (31.7%) in triple-drug therapy had at least one episode of rejection, but this was not statistically significant (P=0.15). The mean maintenance dose of corticosteroids was slightly lower in triple-drug compared with double-drug therapy. CONCLUSION: Patient and graft survival rates were similar in both groups. There was a trend to a lower incidence of rejection, reduced nephrotoxicity, and a lesser amount of maintenance corticosteroids in triple-drug therapy compared with double-drug therapy.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: To evaluate the immunogenicity of the influenza virus vaccine in children receiving short-course (a burst) prednisone therapy for acute asthmatic exacerbations. DESIGN: Prospective cohort study. SETTING: Outpatient pediatric clinic of a military medical center. PATIENTS: Children aged 6 months to 18 years requiring the 1996 influenza virus vaccine were eligible for the study. A total of 58 children were enrolled initially. The control group included 37 asthmatic children requiring less than 900 microg/d of inhaled prednisone and their siblings. The prednisone group included 21 children vaccinated at the beginning of a course of prednisone prescribed to treat an asthma exacerbation. Thirty-one control subjects (84%) and 19 patients in the prednisone group (90%) completed the study. Dropout was due to failure to come in for the postvaccination serum sampling. INTERVENTIONS: All study patients underwent immunization with the 1996-1997 trivalent subvirion influenza virus vaccine (FluShield; Wyeth Laboratories Inc, Marietta, Pa) containing 15-microg hemagglutinin antigens each of A/Texas/36/91 (H1N1) (A/H1), A/Wuhan/359/95 (H3N2)(A/H3), and B/Beijing/184/93 (B). The prednisone cohort received a burst of oral prednisone therapy (2 mg/kg per day for 5 days). MAIN OUTCOME MEASURES: To assess the immunogenicity of the vaccine between both groups, at least a 4-fold rise in titer and end titers of at least 1:40 to each of the 3 antigens were compared. Mean changes in geometric titers to the 3 antigens were also compared. RESULTS: Proportion of patients in each group with at least a 4-fold rise in titer to each of the influenza antigens was as follows: for A/H3N3 antigen, 15 patients (79%) in the prednisone group vs 22 controls (71%) (P = .74); for A/ H1N1 antigen, 16 patients in the prednisone group (84%) vs 20 controls (64%) (P = .20); and for B antigen, 7 patients in the prednisone group (37%) vs 8 controls (26%) (P = .53). Proportion of patients in each group with an end titer of at least 1:40 to each of the antigens was as follows: for A/ H3N2 antigen, 18 patients in the prednisone group (95%) vs 28 controls (90%) (P = .69); for A/H1N1 antigen, 17 patients in the prednisone group (89%) vs 26 controls (84%) (P = .99); and for B antigen, 7 patients in the prednisone group (37%) vs 13 controls (42%) (P = .99). There were also no significant differences between groups in the mean changes in geometric titers to any of the 3 antigens. CONCLUSIONS: Prednisone bursts did not diminish the response of asthmatic children to the 1996 influenza virus vaccine, compared with controls. Children can be effectively vaccinated against influenza virus while they are receiving prednisone therapy bursts for asthmatic exacerbations.
OBJECTIVE: To evaluate the addition of low-dose interferon-alpha 2b to standard melphalan-prednisone therapy in patients with multiple myeloma. DESIGN: Randomized, multicenter, phase III study. SETTING: 15 university hospitals and 92 county hospitals in Sweden, Norway, Denmark, Finland, and Iceland. PATIENTS: 583 patients with symptomatic multiple myeloma. INTERVENTION: All patients received melphalan-prednisone every 6 weeks. Melphalan-prednisone therapy was interrupted after at least 8 courses in responding patients who achieved a plateau phase, and it was reinstituted at time of relapse. Patients randomly assigned to receive melphalan-prednisone and interferon also received interferon, 5 MU three times weekly, from the start of treatment through response, plateau phase, and relapse, until definitive failure of melphalan-prednisone occurred. MEASUREMENTS: Survival was the main outcome measure. Secondary measures were response rate, response and plateau phase duration, and toxicity. All analyses were done according to the principle of intention-to-treat. RESULTS: 45% of patients receiving melphalan-prednisone and 44% of patients receiving melphalan-prednisone and interferon achieved at least a partial response. Response duration and plateau phase duration were longer for patients receiving melphalan-prednisone and interferon than for patients receiving melphalan-prednisone alone (P < 0.05); the difference in median duration was 5 to 6 months. Toxicity was higher with melphalan-prednisone and interferon, and this led to premature discontinuation of interferon therapy in one third of patients and to a reduced overall dose intensity for melphalan. The median survival time was 29 months for patients receiving melphalan-prednisone and 32 months for patients receiving melphalan-prednisone and interferon. The risk ratio for death for patients receiving melphalan-prednisone compared with patients receiving melphalan-prednisone and interferon was 1.02 (95% CI, 0.89 to 1.40). CONCLUSIONS: Adding continuous low-dose interferon to standard melphalan-prednisone therapy does not improve response rate or survival. However, response duration and plateau phase duration are prolonged by maintenance therapy with interferon.
To assess the effect of a glucocorticoid on thyroid and gonadal endocrine function, prednisone was administered on alternate days to dogs. The prednisone injections resulted in adrenocortical suppression, as shown by the response to ACTH. Basal plasma thyroxine and tri-iodothyronine concentrations were considerably reduced in prednisone-treated dogs. However, the thyroid response to injection of thyrotrophin-releasing hormone was not altered, indirectly demonstrating that pituitary release of TSH was not inhibited by prednisone. Similarly, the response of the thyroid to exogenous TSH was not reduced by prednisone treatment. Electron microscopic examination of thyroid tissue revealed accumulation of colloid droplets in the follicular cell cytoplasm of dogs treated with prednisone. It is postulated that prednisone may interfere with basal thyroid hormone secretion by inhibiting lysosomal hydrolysis of colloid in the thyroid follicular cell. Basal plasma concentrations of LH and testosterone, measured in the male dogs, were reduced by prednisone treatment. Responses of prednisone-treated dogs to luteinizing hormone releasing hormone were not significantly reduced. Prednisone administration did not alter testicular responsiveness to injection of human chorionic gonadotrophin. After orchidectomy, plasma LH values were significantly reduced in prednisone-treated dogs. Taken together, these results suggest that LH secretion in dogs is inhibited at the hypothalamic and/or pituitary level by prednisone administration, which consequently results in reduced testosterone concentrations.
OBJECTIVE: In a previous clinical trial of patients with early rheumatoid arthritis (RA), it was determined that patients who received 10 mg of prednisone per day for 2 years had less radiographic joint damage compared with those who received placebo. Our goal was to investigate whether this beneficial effect persisted after the end of the trial. METHODS: A blinded assessment of radiographic joint damage was performed approximately 3 years after the end of the original 2-year study. Twenty-four patients from the original prednisone group (60%) and 28 patients from the original placebo group (68%) participated in this followup study. At the end of the original trial, prednisone dosages were tapered down in the prednisone group and stopped, if possible. Patients from the original prednisone group took prednisone during 35% of the followup period (approximately 1 year) at a mean daily dose of approximately 5 mg. Two patients from the original placebo group started taking prednisone during followup. Radiographs of the hands and feet were scored according to the van der Heijde modification of the Sharp method. RESULTS: During 3 additional years of followup, radiographic scores showed significantly less progression in the original prednisone group than in the original placebo group. Radiographic damage in the original prednisone group did not show an accelerated rate of progression during the followup period. CONCLUSION: The inhibition of radiographic joint damage in patients with early active RA treated with 10 mg of prednisone per day for 2 years seems to persist after the end of prednisone therapy.
Prednisone-induced insulin resistance may depend on either reduced sensitivity (receptor defect) or reduced response to insulin (postreceptor defect). To clarify the mechanism of prednisone-induced insulin resistance, a [3H]glucose infusion (1 microCi/min) was performed for 120 min before and during a euglycemic clamp repeated at approximately 100, approximately 1,000, and approximately 10,000 microU/ml steady state plasma insulin concentration in 10 healthy, normal weight subjects, aged 35 +/- 7 yr. Each test was repeated after 7-d administration of placebo or prednisone (15 plus 15 mg/d per subject), in a randomized sequence with an interval of 1 mo between the two tests. Mean fasting blood glucose (89.5 +/- 2.1 vs. 83.7 +/- 1.9 mg/dl) and mean fasting plasma insulin values (17.8 +/- 1.2 vs. 14.3 +/- 0.8 microU/ml) were significantly higher (P less than 0.01) after prednisone. The insulin sensitivity index (glucose metabolic clearance rate in ml/kg per min) was significantly lower (P less than 0.001) after prednisone at all three steady state plasma insulin levels: 2.8 +/- 0.3 vs. 7.4 +/- 1.1 at approximately 100 microU/ml; 6.0 +/- 0.5 vs. 12.2 +/- 1.1 at approximately 1,000 microU/ml; 7.4 +/- 0.6 vs. 14.4 +/- 0.5 at approximately 10,000 microU/ml. Fasting glucose production (in mg/kg per min) was significantly higher after prednisone: 3.7 +/- 0.2 vs. 2.9 +/- 0.2, P less than 0.001. Suppression of glucose production at steady state plasma insulin level of approximately 100 microU/ml was less after prednisone (1.01 +/- 0.35 vs. 0.14 +/- 0.13, NS), and total at approximately 1,000 and approximately 10,000 microU/ml after both prednisone and placebo. The metabolic kinetic parameters of insulin after prednisone were not significantly different from those after placebo. In addition, insulin binding and 3-ortho-methyl-glucose transport were studied in vitro on fat cells from 16 normal-weight surgical candidates aged 40 +/- 8 yr (10 treated with placebo and 6 with prednisone as above). No significant difference was observed with regard to specific insulin binding (tested with 1 ng/ml hormone only), whereas significant transport differences were noted at the basal level (0.40 +/- 0.10 vs. 0.54 +/- 0.12 pmol/10(5) cells, P less than 0.05), and at increasing concentrations up to the maximum stimulation values (5 ng/ml): 0.59 +/- 0.04 vs. 0.92 +/- 0.12 pmol/10(5) cells, P less than 0.005. These results suggest that (a) administration of an anti-inflammatory dose of prednisone for 7 d induces insulin resistance in man; (b) this is more dependent on depressed peripheral glucose utilization than on increased endogenous production; (c) total insulin binding on isolated adipocytes is not significantly affected; (d) insulin resistance is primarily the outcome of postreceptor defect (impaired glucose transport).
PURPOSE: Time to progression (TTP), overall survival, and quality of life (QL) were compared in patients with hormone-resistant prostate cancer (HRPC) treated with prednisone (5 mg orally, four times a day) or flutamide (250 mg orally, three times a day). PATIENTS AND METHODS: Symptomatic patients were randomized to receive either prednisone (101 patients) or flutamide (100 patients). Subjective response was assessed based on performance status, the use of analgesics, and the need to apply alternative palliative treatment. Prostate-specific antigen (PSA)-based biochemical response (>or= 50% reduction of baseline PSA) was recorded. At baseline and at 6-week intervals during follow-up, patients completed the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire C-30. RESULTS: There was no difference between the groups in median TTP (prednisone, 3.4 months; flutamide, 2.3 months) or overall survival (prednisone, 10.6 months; flutamide, 11.2 months). In the prednisone group, 56% of the patients experienced a subjective response, compared with 45% in the flutamide group (P: = .18). The median response duration was 4.8 months for prednisone and 4.2 months for flutamide. A biochemical response was observed in 21% and 23% of the prednisone and flutamide groups, respectively. Gastrointestinal toxicity was the reason for trial discontinuation in seven patients receiving flutamide and two patients receiving prednisone. The QL assessment parameters favored the use of prednisone with statistically significant differences in pain, fatigue, role functioning, appetite loss, gastrointestinal distress, and overall QL. CONCLUSION: In symptomatic HRPC, treatment with prednisone or flutamide leads to similar rates of TTP and overall survival and no difference in subjective or biochemical response. The QL results favor the use of low-cost prednisone in patients with HRPC.
Based on its efficacy for the treatment of human asthma, the corticosteroid prednisone is commonly used in horses for treatment of recurrent airway obstruction. However, recent studies have failed to show any benefit of prednisone tablets for the treatment of this condition. The purpose of this study was to determine why oral prednisone has poor efficacy for the treatment of heaves in horses. In a crossover study, 5 horses were given the following treatments: prednisone tablets, prednisone liquid, prednisolone tablets, prednisolone liquid and i.v. prednisolone sodium succinate (positive control). Blood samples were taken before drug administration and at selected time points during a 24 h period. Serum concentrations of prednisone and prednisolone were determined in order to evaluate gastrointestinal absorption and hepatic metabolism. Serum concentrations of the endogenous glucocorticoid hydrocortisone were also determined as an indicator of the biological activity of the drugs. Both prednisolone tablets and liquid were absorbed rapidly, with prednisolone detectable in serum within 15 min of administration and with peak concentrations occurring within 45 min. Small amounts of prednisone were detected in the serum samples after administration of both prednisone tablets and liquid. Prednisolone was not detected in serum samples after administration of prednisone liquid and was detected in serum samples from only one horse after administration of prednisone tablets. Endogenous hydrocortisone production was suppressed when horses received prednisolone. The results of these studies indicate that prednisone has poor efficacy for the treatment of heaves because it is poorly absorbed and the active metabolite prednisolone is rarely produced. In contrast, prednisolone tablets have excellent bioavailability and should be useful as a therapeutic agent in horses.
OBJECTIVE: To evaluate the efficacy of two therapies, high-dose prednisone and COP in the treatment of patients with active thyroid-associated ophthalmopathy (TAO). METHODS: According to severity and compliance, the patients admitted in Peking Union Medical College Hospital from August 2000 to July 2003 were divided into two groups. Thirteen patients with active TAO were treated with high-dose prednisone. The initial dosage was 1.5-2.0 mg.kg(-1).d(-1) (maximal dosage 200 mg), tapering gradually, and shifting to alternate-day treatment. Fourteen patients in the COP group were treated with cyclophosphamide (CTX), oncovin (VCR) and prednisone. This therapy was modified from CHOP in the treatment of patients with non-Hodgkin's lymphoma: CTX 600 mg/m(2), VCR 1.1 mg/m(2) were administrated by intravenous infusion every 2-4 weeks, prednisone was given orally at 1 mg.kg(-1).d(-1) for seven days after each infusion. The duration of treatment for both groups was approximately 10 months. The parameters including clinical activity score (CAS), thickness of extra-ocular muscle as well as 24 h urinary GAG were used to evaluate the efficacy of treatment in both groups. RESULTS: There was no significant difference in age and sex between two groups. However the patients in the COP group were more severe than that in prednisone group (P < 0.05). CAS in the patients treated with prednisone before and after treatment were 4.4 +/- 1.8, 1.6 +/- 1.1 respectively, that in patients treated with COP were 6.5 +/- 1.6, 1.9 +/- 1.3 respectively. All these changes were highly significant (P < 0.01). The thickness of extra-ocular muscles in the patients treated with prednisone decreased from (6.5 +/- 1.5) mm to (5.8 +/- 1.1) mm, that in patients treated with COP decreased from (6.8 +/- 1.7) mm to (5.3 +/- 1.1) mm. Both changes were highly significant (P < 0.01). Comparative study of the changes in the thickness of extra-ocular muscle by percentage between two groups demonstrated that the muscle thickness in patients treated with COP was decreased by (23.7 +/- 4.3)%, that in patients treated with prednisone was by (13.3 +/- 4.6)%. The difference between the two groups was highly significant (P < 0.01). The 24 h urinary GAG level in patients treated by prednisone decreased from (33.6 +/- 6.6) mg/24 h before treatment to (16.7 +/- 2.5) mg/24 h after treatment. Those in COP group were (40.6 +/- 10.1) mg/24 h and (15.7 +/- 5.1) mg/24 h respectively. The difference was significant (P < 0.01) in each group. There were no serious complications during treatment. CONCLUSIONS: Both the prednisone and COP therapy are effective in the treatment of patients with active TAO. The preliminary results indicate that COP is more effective than prednisone, it suggests that COP might be feasible for treating patients with progressive and severe TAO.
A chromatographic procedure that allows measurement of [3H]prednisone and [3H]prednisolone in biologic fluids and tissues was developed and used to determine some of the biochemical properties of prednisone and its distribution and metabolism in mice, dogs, and monkeys. When prednisone was added to mouse serum in vitro at a concentration of 50 microgram/ml, approximately half of the drug became bound to serum proteins. Homogenates of mouse liver metabolized prednisone to prednisolone. Following ip or oral doses of prednisone to mice, serum levels of prednisone, prednisolone, and other metabolites were maximum at 15 minutes. 20-Dihydroprednisolone was identified as a metabolite in several biologic samples. For dogs and monkeys given in iv dose of prednisone, disappearance from the serum was biphasic with apparent half-lives of 15 and 82 minutes and 33 and 78 minutes respectively. The serum levels of prednisone and prednisolone in mice, dogs, and monkeys were not increased beyond expected levels by simultaneous administration of iv doses of vincristine. The prednisone content of the kidneys, liver, intestine, and bile of a monkey killed 30 minutes after an iv dose was higher than that in serum. Oral doses of prednisone were absorbed erratically by dogs and monkeys. Only small amounts of prednisone and prednisolone were excreted in the urine of dogs and monkeys given an iv or oral dose.
The effect of plasma exchange on the pharmacokinetics of prednisone and prednisolone was studied. Two patients undergoing plasma exchange while receiving oral prednisone therapy were studied. Patient 1 received prednisone 50 mg daily; patient 2 received 60 mg daily. On a day when the patients were to undergo plasma exchange, blood samples for determination of prednisone and prednisolone concentrations were obtained just before the daily prednisone dose and at various times before, during, and after plasma exchange. The amount of both drugs in plasma removed by plasma exchange was also determined. On a day when the patients were not receiving plasma exchange therapy, additional blood samples were obtained just before the daily prednisone dose and at 0.5, 1, 2, 4, 6, and 8 hours after the dose. Values for elimination rate constant, half-life, area under the curve, clearance, and volume of distribution on and off plasma exchange were calculated from serum concentration-time curves for prednisone and prednisolone. Only prednisolone data proved adequate for pharmacokinetic calculations. Values of pharmacokinetic variables for prednisolone on and off plasma exchange did not differ substantially in either patient. The amount of combined prednisone and prednisolone removed by plasma exchange in each patient was less than 1% of the administered prednisone dose. In the two patients studied, changes in pharmacokinetic values for prednisolone attributable to plasma exchange and the amount of combined prednisone and prednisolone removed by plasma exchange were minimal. Supplemental dosing of prednisone following plasma exchange appears unnecessary.
OBJECTIVE: To determine the longterm outcome including disease activity, mortality, and adverse events in patients with rheumatoid arthritis (RA) treated with prednisone. METHODS: A case-control study was performed, based on our cohort of 893 mostly Caucasian patients with adult onset RA, followed since 1966. Data collection was based on protocols and included single physician global assessment. Prednisone was started in 122 patients (85 women, 37 men) after 1966. All were matched for age, sex, disease duration, and global assessment to 122 controls from the same cohort who have never received prednisone. RESULTS: Mean disease duration before prednisone was 14.1 years. Mean duration of use was 6.9 years with a mean dose of 8.0 mg/day. Prednisone was eventually stopped in 34% of patients. Life expectancy and causes of death were similar in both groups. No differences in hemoglobin, erythrocyte sedimentation rate, global assessment, Lansbury index, functional class or Health Assessment Questionnaire (HAQ) disability index were seen between the 2 groups before or 5 years after starting prednisone. Ten years after starting prednisone, HAQ scores were similar but Lansbury and global assessment were worse in the prednisone treated group. As expected, adverse events, notably cataracts and fractures, were observed more often in the prednisone group. CONCLUSION: Case-control matching can only reduce, not eliminate, potential selection bias. Nonetheless, the lack of demonstrable longterm benefit with prednisone use in this and other studies is disconcerting. Caution and further studies are required before the more aggressive use of longterm prednisone therapy in RA is embraced.
OBJECTIVE: To determine whether men with rheumatoid arthritis (RA) have abnormal hypothalamic-pituitary-gonadal axis function and to measure the effects of low dose prednisone therapy in these patients. METHODS: We measured testosterone, follicle stimulating hormone (FSH), and luteinizing hormone (LH) in 36 men aged 38-75 (mean age +/- 1 sd = 62 +/- 10 years) who had longstanding active RA (mean disease duration = 17 +/- 12 years) and in 70 healthy elderly male controls, aged 53-83 (mean age 68 = +/- 6 years). We divided the group with RA into those taking no prednisone (n = 12) and those taking 5 to 10 mg/day of prednisone (n = 24) and analyzed these groups separately to determine whether low doses of prednisone affected testosterone levels. RESULTS: Compared to the healthy controls, patients with RA not taking prednisone had normal testosterone levels but significantly elevated levels of FSH and LH (p < 0.01 for both comparisons). In contrast, patients with RA taking prednisone had significantly lower testosterone levels (p < 0.05), but levels of FSH and LH were only slightly elevated compared to controls. Compared to patients not taking prednisone, patients taking prednisone had lower levels of testosterone, FSH, and LH. CONCLUSION: Male patients with RA who are not taking prednisone have significantly elevated levels of FSH and LH with normal testosterone levels, suggesting a state of compensated partial gonadal failure. Male patients with RA taking low doses of prednisone have lower testosterone and gonadotropin levels, suggesting that prednisone may suppress the hypothalmic-pituitary-testicular axis. Since testosterone affects immune function as well as bone and muscle metabolism, androgen deficiency in some men with RA may predispose these patients to more severe disease and to increased complications of steroid therapy such as myopathy and osteoporosis.
Corticosteroid withdrawal after orthotopic liver transplantation (OLT) represents an attractive therapeutic option for ameliorating post-OLT metabolic complications, although several reports suggest patients who undergo transplantation for autoimmune hepatitis (AIH) may have a greater incidence of acute and chronic rejection when withdrawn from corticosteroid therapy. The aim of this study is to evaluate the success of corticosteroid withdrawal in patients with AIH after OLT. Twenty-six patients underwent successful OLT for AIH. In 21 of these patients, stable maintenance immunosuppression consisted of cyclosporine (CSA) and prednisone (n = 20) or tacrolimus (TAC) and prednisone (n = 1). In this group, a trial of prednisone withdrawal was initiated when patients were 6 months or more post-OLT, with normal liver function, and receiving an average prednisone dosage of 10 mg/d. Five additional patients treated with either TAC (n = 4) or CSA (n = 1) plus mycophenolate mofetil underwent a 14-day taper of prednisone. Overall, 17 of 25 patients (68%) were successfully withdrawn from corticosteroids, with a mean follow-up of 22 months (range, 1 to 34 months). Of the remaining 8 patients, 5 patients received a lower dosage of prednisone or required prednisone to control inflammatory bowel disease. Only 3 patients remained dependent on prednisone to maintain stable liver allograft function. Withdrawal from 10 to 5 mg of prednisone (n = 21) resulted in four episodes of steroid-responsive and two episodes of steroid-resistant rejection in 3 patients, and 18 of 21 patients (86%) were rejection free. Withdrawal from 5 to 0 mg prednisone (n = 17) resulted in eight episodes of steroid-responsive and no episodes of steroid-resistant rejection in 4 patients; 13 of 17 patients (76%) were rejection free. Of the 5 patients in the 14-day prednisone-taper group, 3 patients had steroid-responsive rejection and 1 patient required OKT3. Seventeen of 21 patients (81%) with AIH were successfully withdrawn from corticosteroids. It is notable that corticosteroid withdrawal was associated with a reduction in serum cholesterol levels, decreased use of antihypertensive agents, and reduced need for insulin or oral hypoglycemic agents. We propose corticosteroid withdrawal should be attempted in patients with underlying AIH who undergo OLT because most will benefit without significantly jeopardizing the liver allograft.