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 577 records · Page 32Linked to original sources

Effects of alpha-interferon and prednisone on serum-soluble interleukin-2 receptor (sIL-2R) in chronic hepatitis B infection.

The level of serum-soluble interleukin-2 receptor (sIL-2R) was measured in 32 patients to investigate the effect of prednisone and alpha-interferon therapy on chronic hepatitis B virus infection. All the patients were seropositive for hepatitis B surface antigen and hepatitis B e antigen, with histological evidence of chronic persistent or chronic active hepatitis. Twenty-six patients received oral prednisone, followed by subcutaneous recombinant alpha-interferon, and six patients received multivitamin tablets and served as controls. After 4 wk of prednisone in reducing dosage, serum sIL-2R fell significantly from 673.6 +/- 52.9 U/ml to 584.8 +/- 39.4 U/ml (mean +/- SE, p less than 0.05). It rose to 733.4 +/- 45.7 U/ml (p less than 0.05) on the 4th wk of interferon, but returned to pretreatment level at completion of interferon. There was a significant correlation between serum sIL-2R and alanine aminotransferase levels (r = 0.36, p less than 0.001). The level of serum sIL-2R before treatment and its response to prednisone and interferon were not useful in predicting seroconversion of hepatitis B e antigen and anti-hepatitis B e.

Adolescent↗

Low dose prednisone does not affect calcium homeostasis or bone density in postmenopausal women with rheumatoid arthritis.

To assess whether low doses of prednisone produce generalized alterations in skeletal homeostasis in rheumatoid arthritis (RA), indices of calcium metabolism and bone mineral density (BMD) were measured in 22 women with RA treated without or with prednisone (6.6 mg daily). Ionized and total calcium concentrations, intact parathyroid hormone (PTH) and osteocalcin levels were comparable in the 2 groups. BMD measurements in the lumbar spine, and proximal femur sites including the femoral neck, Ward's triangle, and trochanteric region were not significantly different in patients with RA treated without or with prednisone. In our experience low dose prednisone did not adversely affect indices of mineral metabolism, or bone density in RA.

Adult↗

Effects of thyroid dysfunction on prednisolone and prednisone interconversion and disposition in the rat.

The effects of thyroid dysfunction on the reversible metabolism and disposition of prednisolone and prednisone were examined in male Wistar rats. Hyperthyroid rats were produced by daily ip injections of 20 micrograms of I-triiodothyronine/100 g body weight for 6 days. Hypothyroid rats were obtained by providing 0.05% 6-propyl-2-thiouracil in drinking water ad libitum for 21 days. Rats were given 10 mg/kg of prednisolone or prednisone iv, blood samples were collected, and the steroids in plasma were assayed by HPLC. A recently developed pharmacokinetic model encompassing interconversion kinetics was applied. Unexpectedly, the hyperthyroid state increased the AUC (by 163%) of prednisolone (unlike in man) via reduced (66%) prednisolone elimination clearance (CL10), but also caused enhanced (101%) prednisone elimination clearance (CL20). The hypothyroid state increased the AUC (by 117%) of prednisolone via a 56% reduction in CL10 and a reduction in CL20. Prednisone formation of prednisolone (CL21) was about 13-fold greater than the reverse process (CL12), and both interconversion clearances were increased 20-40% by thyroid dysfunction. Experimental thyroid disorders thus alter prednisolone/prednisone pharmacokinetics in rats primarily by selective and sometimes unusual changes in elimination clearance rather than affecting the relative rates of steroid interconversion. Reversible metabolism is much less important in rats compared to man.

Animals↗

[Effect of 1 week's administration of prednisone on gastric acid secretion and liberation of gastrin in healthy humans].

In a double-blind, randomized study we examined the effects of an oral administration of prednisone (60 mg/day for 6 days) or placebo on gastric acid output basally (BAO), in response to peptone meals 1%, 2%, 4% and 8%, 500 ml each) and to pentagastrin 6 micrograms/kg s.c. to determine maximal acid output, MAO) and on plasma gastrin levels in 14 healthy volunteers. Gastric acid output was measured by intragastric titration (pH 5.5). For gastrin determination we used a specific radioimmunoassay. Experiments were performed one day (day 0) before giving the drugs and one day (day 7) and one month (day 30) after finishing the treatment. Both groups were comparable in their gastric acid responses on day 0. Six days treatment with prednisone did not significantly alter BAO, MAO and the gastric acid response to peptone and pentagastrin. Also, one month after finishing the treatment there were no significant differences in gastric acid output. Both groups had similar plasma gastrin levels on each day. Prednisone did not significantly alter plasma gastrin levels. We conclude that a six-day treatment with prednisone does not alter BAO, MAO and gastric secretory responses to peptone nor release of gastrin in healthy human volunteers.

Administration, Oral↗

Bone loss in prednisone treated sarcoidosis: a two-year follow-up.

We followed up 35 sarcoid patients treated with prednisone for two years in order to evaluate bone mineral loss over time. Vertebral cancellous mineral content was detected by quantitative computed tomography and calibration phantom before beginning prednisone therapy and monitored two more times at yearly intervals. The percent mineral loss (ML%) averaged -13.9 +/- 2.1 at the end of the first year and -15.3 +/- 2.6 at the end of second year. We conclude first, that the time course of mineral loss in prednisone treated sarcoidosis is similar to that of other diseases such as asthma and rheumatoid arthritis. In a separate group of 10 early postmenopausal females, we observed a greater ML% averaging -21.9 +/- 16.6 and -26.2 +/- 18.5, at the end of the first and second year respectively. Our second conclusion was thus that the synergic effect of postmenopausal status and prednisone therapy results in an ML% far more significant than expected from the two single conditions.

Adult↗

Glucose intolerance after short-term administration of corticosteroids in healthy subjects. Prednisone, deflazacort, and betamethasone.

Glucocorticoid-induced glucose intolerance has been related to the dose, duration of treatment, and steroid compound. However, a clear demonstration of this phenomenon is still lacking for fluorinated corticosteroids. We performed an oral glucose tolerance test in six healthy volunteers after the short-term administration of deflazacort (18 + 18 mg), prednisone (15 + 15 mg), and betamethasone disodium phosphate (1.5 + 1.5 mg) at equivalent anti-inflammatory doses, in random sequence, and in a triple crossover design. Fasting plasma glucose levels were not modified by deflazacort, whereas fasting plasma glucose levels together with insulin and C-peptide values were progressively and significantly increased by prednisone and betamethasone. During oral glucose tolerance testing a significant increase in the plasma glucose and insulin peaks was recorded after betamethasone and, to a lesser extent, after prednisone and deflazacort. These results suggest that betamethasone induces greater glucose intolerance and insulin resistance than prednisone and deflazacort.

Adult↗

[The NBT test in bacterial infections complicating prednisone-treated nephrotic syndrome].

The spontaneous nitroblue tetrazolium reduction test was done in children with nephrotic syndrome treated with prednisone and with secondary bacterial infections and in children with urinary tract infections not treated with prednisone. In healthy children 9.0 +/- 1.3% of polymorphonuclear leucocytes in peripheral blood showed presence of deposits in the NBT test. In children not treated with prednisone the number of NBT (+) leucocytes was increased over fourfold. The value of the NBT test was highest at the beginning of the disease. In children treated with prednisone the value of the NBT test increased slowly. The highest results were obtained in the second week of infection treatment. In relation to controls the proportion of NBT (+) test in peripheral blood was increased threefold.

Bacterial Infections↗

Alternating-day cyclosporine and prednisone for treatment of high-risk chronic graft-v-host disease.

Therapy of chronic graft-v-host disease (GVHD) has been unsatisfactory in patients with platelet counts less than 100,000/microL. Survival at 5 years after marrow transplant is only 26% in such patients treated with trimethoprim-sulfamethoxazole (TMP-SMX) and every other day with prednisone. Since October 1982, 61 patients with high-risk extensive chronic GVHD were treated with a new alternating-day regimen of prednisone (1 mg/kg every other day) and oral cyclosporine (6 mg/kg every 12 hours every other day) with one double-strength TMP-SMX tablet twice daily. Forty patients (group I) received primary treatment of thrombocytopenic chronic GVHD (median platelet count 35 [range 7 to 87] x 10(3)/microL). Twenty-one patients (group II) received salvage treatment after failing initial prednisone +/- azathioprine. Twenty-one patients in group I and 15 in group II survive with a minimum of 2 years and a median of 3.7 years follow-up. At 4 years after transplant, actuarial survival is 51% (group I) and 67% (group II). Causes of death included interstitial pneumonia (six), relapse (five), GVHD without infection (five), infection (four), organ failure (three), and hemorrhage (two). Mortality increased with the progressive type onset of chronic GVHD and treatment failure. Toxicity included hypertension (13), nephrotoxicity (nine), nausea (seven), aseptic necrosis (five), neurologic abnormalities (four), and diabetes (three). Median cyclosporine levels at four and 36 hours were 296 and 64 ng/mL, respectively. Four patients required permanent discontinuation of cyclosporine, but none required renal dialysis. Karnofsky performance scores for 25 survivors are 90% to 100%, scores for six survivors are 70% to 89%, and scores for five survivors are less than 70%. Alternating-day cyclosporine and prednisone has acceptable toxicity and appears to improve survival in patients with high-risk chronic GVHD.

Adolescent↗

Prednisone-induced bone loss in sarcoidosis: a risk especially frequent in postmenopausal women.

The incidence of glucocorticoid-induced osteoporosis is reported in about 40 to 50% of treated patients, but it has never been extensively studied in sarcoidosis. We have studied Vertebral Cancellous Mineral Content (VCMC) of the lumbar spine by Quantitative Computed Tomography (QCT) in 190 normal subjects, 7 patients with sarcoid on no treatment and 64 patients with sarcoid on treatment with prednisone. As compared to the 190 normal subjects and the 7 untreated patients, VCMC was reduced in 46 of 64 patients with sarcoid on treatment with prednisone. Loss of VCMC in the patients varied directly with dose and duration of prednisone treatment. It is concluded that - in sarcoid patients and especially in postmenopausal females - long-term prednisone therapy results in bone mineral loss more frequently than elsewhere reported for other groups of patients. It is not clear if this difference is due to the sarcoidosis itself or to the better sensitivity of Computed Tomography compared to former techniques.

Adult↗

Phase II study of oral methyl-CCNU and prednisone in previously treated alkylating agent-resistant multiple myeloma.

Thirteen patients with multiple myeloma (MM) who either failed to respond to or who were relapsing from standard agents and who received four or more courses of methyl-CCNU + prednisone (adequate drug trial) are reported in this paper. Methyl-CCNU was given orally before breakfast at 6-week intervals at a starting dose of 50 mg/m2 with the intention of increasing the dose to 100, 150, and 200 mg/m2 with each subsequent course. The dose of prednisone was 75 mg/day x 7 with each course. The response rate was 46% (six of 13 patients). No patient had better than a fair response. Drug toxicity, severe enough to prevent further dose escalation, was observed in every case. Prior BCNU therapy or the lack of response to previous alkylating agents did not prevent a response to methyl-CCNU + prednisone. The response rate of methyl-CCNU + prednisone in MM is comparable to the results achieved with other agents in similar groups of patients.

Administration, Oral↗

Acute pancreatitis in two dogs given azathioprine and prednisone.

Acute pancreatitis was diagnosed in 2 dogs given azathioprine and prednisone. Prednisone and azathioprine had been given as immunosuppressive therapy for pemphigus foliaceus in dog 1 and for polymyositis in dog 2. Azathioprine was discontinued in both dogs. In dog 1, prednisone was reinstituted on day 6 of hospitalization. Prednisone was continued throughout the period of hospitalization in dog 2. Both dogs recovered without complication. Glucocorticoid therapy has been associated with the development of pancreatitis. In human beings, a common side effect of azathioprine is the development of drug-induced pancreatitis. Definitive identification of azathioprine as the cause of pancreatitis in these dogs was not possible; the owners refused to permit retreatment with the drug. Therefore, the synergistic action between these 2 drugs could not be ruled out as the cause of pancreatitis.

Acute Disease↗

Anti-thymocyte globulin and prednisone immunotherapy of recent onset type 1 diabetes mellitus.

Increasing evidence that Type 1 (insulin dependent) diabetes mellitus is an autoimmune disease, together with successful cure/prevention in animal models of this disease (e.g. BB/W rat) has led to several trials of immunotherapy in recent onset Type 1 diabetes of man. In this communication we report our experience with short courses of prednisone and antithymocyte globulin (ATGAM) plus prednisone. Prednisone characteristically suppressed Ia positive T lymphocytes into the normal range, but had no long-lasting effect on T-cell phenotype. ATGAM plus prednisone markedly decreased the ratio of T4/T8 ("helper"/"suppressor-cytotoxic") positive T lymphocytes, and this remained suppressed for months. ATGAM treated patients had lower HbA1c on a lower dose of insulin 100 or more days following immune therapy (with 4 out of 5 patients requiring less than 0.2 U/Kg insulin/day). Two patients in the ATGAM treated group did not require insulin for more than 8 months; during remission they had normal fasting blood glucose values, but with abnormal glucose tolerance on oral glucose tolerance testing. Severe, though transient, thrombocytopenia was observed in 2 patients on ATGAM therapy which outweighed its clinical effects.

Adolescent↗

[Pharmacokinetics of prednisone after oral administration in children with renal grafts. Changes induced by phenobarbital and renal insufficiency].

A study of blood and urinary clearance of prednisone after ingestion of a 25 mg/m2 body surface test-dose, at 8 AM, was undertaken in 20 children treated for 18 months with prednisone after renal transplant. Results show important variability between patients: the elimination half life was 2.70 +/- 0.78 hr.; Tmax time to reach Cmax was 2.10 +/- 1.08 hr.; Maximal concentration (Cmax) was 474 +/- 153 ng/ml. With respect to the dose of steroid administered, the urinary excretion of corticosteroids: 17-hydroxycorticosteroids was 12.9 +/- 7.4% and that of unchanged prednisolone 2.8 +/- 3.1%. This level was essentially achieved in the 6 first hours: 55.4 +/- 16.2% for 17-OH steroids and 87.2 +/- 14.3% for prednisolone. Two points emerge from this study: (a) Renal failure slows urinary excretion of prednisone and its metabolites, making a reduction in the doses of corticosteroids necessary at certain doses. (b) The association prednisone-phenobarbital changes the blood kinetics (excretion is faster) without a clear change in 17-OH steroid and prednisolone urinary excretion. It is associated with a decrease in graft tolerance. The kinetic changes do not seem to be the only factors implicated in the decreased therapeutic response.

Administration, Oral↗

Prednisone and T-cell subpopulations.

Alteration of T-cell subset relationships may cause many of the anti-inflammatory and immunoregulatory effects of glucocorticosteroids. The effect of oral administration of lactose or 60 mg of prednisone on peripheral blood T-lymphocyte subset profile and total eosinophil count (TEC) was examined. A purified T-cell peripheral blood population was obtained and the proportion of T cells with T3, T4, T8, M1, and la surface antigens was determined before and five hours after ingestion of lactose or prednisone. Lactose caused no change of any of the measured values. Prednisone caused a large (72%) decrease of the total lymphocyte number and the TEC (97%) but no change of the proportion of T cells with the previously mentioned antigens. Administration of 60 mg of prednisone does not acutely selectively deplete subclasses of T lymphocytes from peripheral blood.

Adult↗

Adrenocortical suppression in the dog given a single intramuscular dose of prednisone or triamcinolone acetonide.

Adrenocortical function was assessed in dogs given a single intramuscular dose of either prednisone or triamcinolone acetonide (TCA; or saline solution to controls) to determine the duration of adrenocortical suppression caused by 2 commonly used glucocorticoids. The glucocorticoids were administered at recommended therapeutic doses; therefore, dogs given prednisone received a greater amount of glucocorticoid activity than did in dogs given TCA. Basal and ACTH-stimulated plasma cortisol concentrations, as determined by radioimmunoassay, were obtained once a week. Total intravascular eosinophil concentration and skin responses to intradermally injected histamine phosphate were quantitated. Dogs given TCA showed suppressed basal and ACTH-stimulated plasma cortisol concentrations 1 week after injection; the latter change persisted 2 weeks after injection. Adrenocortical function in 1 of 4 dogs given TCA remained suppressed for 4 weeks. In contrast, prednisone did not significantly alter adrenocortical function. Although intravascular eosinophil concentrations did not vary among groups, skin responses to intradermally injected histamine phosphate were reduced 6 days after prednisone and TCA were given.

Adrenal Cortex↗

Effects of a new glucocorticoid, oxazacort, on some variables connected with bone metabolism in man: a comparison with prednisone.

The urinary elimination of calcium, other electrolytes, and hydroxyproline and the oral absorption of 47Ca have been evaluated in three groups of 8 patients before and during a 15-day treatment with prednisone at daily doses of 25 and 50 mg and with oxazacort, a new glucocorticoid, at a daily dose of 50 mg. The results obtained demonstrate that oxazacort in short-term teatment with a high dose has no significant effect on the urinary elimination of calcium and hydroxypyroline in experimental conditions in which prednisone produces statistically significant and clinically relevant increase, both when given at the same dose and when given at half that dose. On the other hand, the oral absorption of 47Ca is decreased by oxazacort, but less than by prednisone at the same dose. As the antirheumatic activity of oxazacort appears to be only slightly lower than that of prednisone (activity ratio of about 0.84: 1), these findings may have interesting therapeutic implications.

Adult↗

High pressure liquid chromatographic assay for prednisone in bulk drug substances and tablets.

A high pressure liquid chromatographic (HPLC) method was developed for the assay of prednisone in bulk drug substances and tablets. The sample was dissolved in water-methanol and an aliquot was analyzed by using HPLC. The average recovery of prednisone added to a prednisone tablet composite was 99.5% with a coefficient of variation of 1.07%. Prednisone was determined in 46 tablets (1-50 mg prednisone/tablet) formulated by 22 manufacturers, using the HPLC method and the USP blue tetrazolium assay. The results show that the HPLC method is more specific and faster than the USP method.

Chromatography, High Pressure Liquid↗

A study on the release of prednisone from new ointment bases containing various additives.

The effect of various additives on the release of prednisone from new ointment bases, was investigated. It was found that the rate of release of prednisone was greater from the oil in water emulsion ointment base that both the water in oil or oleagenous bases. The incorporation of water in the water in oil emulsion base decreased the rate of diffusion of prednisone than any of the other additives used. It was also concluded that the best release of prednisone was obtained from the bases which were of similar nature to the diffusion medium. Other factors such as the characteristics of bases and the additives as well as their effect upon the solubility of the drug in the mixture may play a part.

Emulsions↗