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Inhibition by prednisone of growth hormone (GH) response to GH-releasing hormone in normal men.

Glucocorticoids increase GHRH-stimulated GH secretion when added in vitro to cultured monkey, rat, and human pituitary cells and when injected in vivo into anesthetized rats. Yet, in man glucocorticoids inhibit linear growth and GH secretion. To clarify this apparent disparity and to determine if glucocorticoid stimulation can augment GH release in man after direct pituitary stimulation with GHRH, we administered 1 microgram/kg GHRH dosage to seven normal men before and after a 4-day course of prednisone (20 mg, orally, three times daily). The second GHRH test was done 12 h after the last dose of prednisone was given. Prednisone significantly inhibited the mean maximal increase in serum GH after GHRH treatment [20.7 +/- 4.5 (+/- SE) vs. 6.3 +/- 2.4 micrograms/L; P less than 0.01] as well as the GH value obtained by summing and averaging the individual means of the 15, 30, 45, 60, 75, and 90 min serum GH concentrations (11.1 +/- 1.2 vs. 4.3 +/- 0.9 micrograms/L; P less than 0.05). The mean serum insulin-like growth factor I and plasma glucose concentrations were not significantly altered by prednisone administration. These results together with previous in vitro findings imply that glucocorticoid-induced inhibition of GH secretion in man does not occur at the level of the pituitary gland, but, rather, at the hypothalamus or above.

Adrenocortical Hyperfunction↗

Elevated 1,25-dihydroxyvitamin D levels in patients with chronic obstructive pulmonary disease treated with prednisone.

Glucocorticoid administration is a well established cause of osteopenia. Mechanisms underlying the deleterious effect of glucocorticoids on bone may include direct inhibition of bone formation as well as indirect effects through changes in intestinal calcium absorption, renal calcium excretion, and/or levels of the calciotropic hormones. To further examine the potential role of the calciotropic hormones we measured serum levels of PTH and 1,25 dihydroxyvitamin D [1,25(OH)2D], as well as serum and urine levels of calcium and vertebral bone density in patients with chronic obstructive pulmonary disease being managed with or without prednisone. Patients treated with prednisone had lower spinal bone density (53 vs. 106 mg/cm3) and higher serum calcium (2.40 vs. 2.33 mmol/l), urine calcium (6.9 vs. 2.7 mmol/24h), and 1,25(OH)2D levels (147 vs. 95 pmol/L). Compared to the patients not treated with glucocorticoids. PTH levels also tended to be higher (33 vs. 26 microliters-eq/ml), but the difference was not significant. Serum and urine calcium levels correlated positively with 1,25(OH)2D levels, but none of these measurements correlated with PTH levels. Our results suggest that prednisone treatment alters the regulation of 1,25(OH)2D production, and this may contribute to the loss of bone mineral induced by prednisone.

Aged↗

Differential effects of prednisone and cyclophosphamide on autoantibodies in human neuromuscular disorders.

We compared the effects of treatment of patients with prednisone or cyclophosphamide on a series of different types of autoantibodies. Levels of antiacetylcholine receptor (anti-AChR) antibodies and of antibodies to GM1 and GD1a gangliosides were measured in patients with a variety of neuromuscular disorders before and after treatment. Most patients had several autoantibodies present. We showed that prednisone treatment resulted in a reduction in titers of anti-AChR but not antiganglioside antibodies. Cyclophosphamide treatment produced a reduction of antiganglioside antibody titers. An intravenous and oral regimen was more effective than a single intravenous course of cyclophosphamide. We conclude that an immunosuppressive medication such as prednisone may reduce levels of some autoantibodies while producing no change in others, even in an individual patient. In addition, cyclophosphamide can suppress autoantibodies that prednisone does not. These differences in immunopharmacologic responses suggest that there are several distinct mechanisms of autoantibody production in humans. The utility of immunosuppressive medications in specific disease processes may be related in part to the mechanism of production of pathogenic antibodies.

Autoantibodies↗

Factors influencing outcome of prednisone dose reduction in myasthenia gravis.

We reviewed retrospectively 114 prednisone dose reduction attempts in 63 myasthenic patients. Dose reduction was considered successful if a patient remained asymptomatic for more than 1 year on no prednisone or a stable low dose of prednisone. Successful dose reduction attempts were more common in patients taking azathioprine, but thymectomy did not influence taper outcome. Slower rate of dose reduction and higher ending dose of prednisone improved the chance of success.

Adolescent↗

Gastric tolerance of high-dose pulse oral prednisone in multiple sclerosis.

BACKGROUND: Prednisone and methylprednisolone are well absorbed orally and have lower treatment costs than IV methylprednisolone, but concern that low-dose corticosteroid may cause increased disease activity and that high oral doses may cause gastric ulceration inhibits use of oral therapy for MS attacks. METHODS: Gastric mucosal injury, detected by measurement of gastric permeability, was examined after five alternate day doses of IV methylprednisolone (1 g) or oral prednisone (1,250 mg) in 21 patients with MS. A triple sugar test solution was consumed at bedtime, and urine was collected overnight. Urine sugar concentrations were determined by high-pressure liquid chromatography. Gastric permeability was expressed as total mg of sucrose excreted. RESULTS: Seventeen patients completed the protocol (12 oral, 5 IV). Baseline sucrose excretion was normal in all. Both groups demonstrated an increase in gastric permeability after steroid treatment, but there was no difference between the two groups (95% CI 95 to 91 mg, p = 0.96). After treatment, three (25%) patients in the oral group, and two (40%) patients the IV group, had modestly abnormal gastric permeability (95% CI 34 to 64%, P = 0.6). CONCLUSIONS: Short-term high-dose oral prednisone is not associated with greater gastric damage, as measured with permeability tests, than IV methylprednisolone. High-dose oral prednisone should be considered a first-line treatment option for MS attacks.

Administration, Oral↗

Adverse side effects associated with prednisone in the treatment of patients with oral inflammatory ulcerative diseases.

Systemic glucocorticoids in the form of prednisone have been effective in reducing signs and symptoms in a variety of acute and chronic oral inflammatory diseases. In the 101 patients prospectively studied, the benefits from prednisone treatment far outweighed the adverse side effects, which occurred in 61 patients. However, none of the adverse side effects was severe enough to require cessation of the prednisone. The adverse effects, which could be minimized by reducing the dosage in most instances, were primarily related to treatment that persisted for more than two weeks. Fluid retention or bloating was the most common symptom, and insomnia was the chief side effect in those patients receiving short-term treatment (less than two weeks). Blood sugar, blood pressure, weight, and white blood cell counts were not meaningfully altered. Variables in patients' drug response and side effects precluded formulation of precise prednisone dosages that would allow predictive outcomes.

Adolescent↗

Decreased insulin binding of human erythrocytes after dexamethasone or prednisone ingestion.

We have investigated changes in insulin binding in erythrocytes in response to overnight ingestion of 1 mg dexamethasone or 10 mg of prednisone in two groups of eight lean, healthy subjects. Dexamethasone administration reduced insulin binding from 9.6 to 6.8% (P < 0.001) with concomitant increase in basal plasma insulin from 10.5 to 14.1 microU/ml (P < 0.05). Prednisone ingestion reduced insulin binding from 9.9 to 7.9% (P < 0.01), but the increase in basal insulin from 16.9 to 20.6 microU/ml was not significantly different. The decrease in insulin binding with both dexamethasone and prednisone was associated with decreased affinity of erythrocyte for insulin at low occupancy and the increase in the dose of unlabeled insulin resulted in 50% inhibition of specific binding without changes in the number of receptors. The earliest decrease in insulin binding was noted within 2 h after ingestion of 1 mg of dexamethasone. These data suggest that acute alteration of insulin receptor function could occur in erythrocytes by small amounts of dexamethasone or prednisone through a mechanism consistent with a decrease in receptor affinity rather than a decrease in the number of receptors.

Adult↗

Treatment of relapsed Langerhans cell histiocytosis by cyclosporin A combined with etoposide and prednisone.

Optimal treatment for Langerhans cell histiocytosis (LCH) has not yet been established. High-risk patients with systemic LCH may have a fatal course of the disease despite intensive treatment. New approaches using cyclosporin A (CSA) showed promising results. Here, we report on a 4-year-old boy who presented with systemic LCH of skin, liver, bone, bone marrow, and soft tissue infiltrates. The patient was refractory to conventional therapy including VP16, prednisone, 6-mer-captopurine, methotrexate, and vinblastine. Therefore the patient was treated with CSA as continuous therapy (serum levels were kept between 300 and 400 ng/mL) as well as intensification with VP16 and prednisone every 4 weeks. As early as 4 months after starting this treatment, clinical symptoms completely disappeared except for a slightly enlarged liver. During the next 12 months all clinical symptoms except a limited skin involvement vanished although treatment with VP16 and prednisone was stopped and CSA serum levels were kept between 100 and 150 mg/mL. In conclusion, intensive therapy using high-dose CSA combined with VP16 and prednisone might be a therapeutic option for patients with otherwise refractory LCH.

Antineoplastic Agents, Hormonal↗

Combined treatment of giant-cell arteritis with methotrexate and prednisone. a randomized, double-blind, placebo-controlled trial.

BACKGROUND: Corticosteroids remain the cornerstone of therapy for giant-cell arteritis, but relapse during dose tapering and corticosteroid-related adverse events often complicate management of this condition. Although several approaches, including combined therapy with cytotoxic agents, have been suggested to overcome these problems, no study has clearly shown benefits of alternate treatments. OBJECTIVE: To analyze the safety and efficacy of combined therapy with corticosteroids and methotrexate in giant-cell arteritis. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: University-based clinic. PATIENTS: 42 patients with new-onset giant-cell arteritis according to biopsy. INTERVENTION: High initial doses of corticosteroid were given; the dose was then tapered quickly until therapy was completely withdrawn. Methotrexate or placebo was given weekly from the start of corticosteroid therapy for 24 months. MEASUREMENTS: Number of relapses, cumulative dose of corticosteroid, and number of adverse events were assessed on completion of follow-up. RESULTS: Compared with combined prednisone and placebo therapy, treatment with prednisone and methotrexate reduced the proportion of patients who experienced at least one relapse (45% vs. 84.2%; P = 0.02) and the proportion of patients who experienced multiple relapses (P = 0.004). The mean cumulative dose of prednisone was 4187 +/- 1529 mg in the methotrexate group and 5489.5 +/- 1396 mg in the placebo group (mean difference, 1302 mg [95% CI, 350 to 2253 mg]; P = 0.009). Overall, the rate and severity of adverse events were similar between groups. Treatment was discontinued in 3 patients in the methotrexate group who experienced definite drug-related adverse events. In sensitivity analysis that included patients lost to follow-up, differences between groups in number of relapses and cumulative dose of prednisone were significant. CONCLUSIONS: Treatment with methotrexate plus corticosteroid is a safe alternative to corticosteroid therapy alone in patients with giant-cell arteritis and is more effective in controlling disease.

Adrenal Cortex Hormones↗

Prevention of prednisone-induced negative nitrogen balance. Effect of dietary modification on urea generation rate in patients on hemodialysis receiving high-dose glucocorticoids.

To assess whether increasing dietary protein and calorie intake can ameliorate the negative nitrogen balance induced by 70 to 120 mg/d prednisone, we studied nitrogen intake and net urea generation rate in patients undergoing hemodialysis for 10 to 14 days after renal transplantation. Seven patients receiving prednisone with moderately restricted protein (0.73 +/- 0.03 g/kg of body weight per day) and calorie (20 +/- 4 kcal/kg of body weight per day) intake had high urea nitrogen generation rates (199 +/- 18 mg/kg.d) and protein catabolic rates (1.45 +/- 0.12 g/kg.d) and were in marked negative protein balance (-0.72 +/- 0.12 g/kg.d). An increase in protein (1.30 +/- 0.06 g/kg.d) and calorie (33 +/- 3 kcal/kg.d) consumption in another eight prednisone-treated patients resulted in protein balance (-0.02 +/- 0.12 g/kg.d) without further increasing urea generation (174 +/- 9 mg/kg.d). Six control patients undergoing hemodialysis after surgery who were not receiving prednisone had lower urea generation rates (109 +/- 15 mg/kg.d) and were in nitrogen balance. Nitrogen wasting is therefore not an inevitable consequence of high-dose glucocorticoid therapy and can be effectively prevented by simple nutritional modification without increasing hemodialytic requirements.

Adult↗

Prostate specific antigen response to mitoxantrone and prednisone in patients with refractory prostate cancer: prognostic factors and generalizability of a multicenter trial to clinical practice.

PURPOSE: We determine prostate specific antigen (PSA) response and durability, and prognostic factors associated with response and survival in patients with symptomatic hormone refractory prostate cancer treated with mitoxantrone and prednisone at a single institution. We then compare the results with those of a randomized phase III clinical trial. MATERIALS AND METHODS: A retrospective review of all 133 patients treated with mitoxantrone and prednisone at Princess Margaret Hospital since 1994 was performed. PSA response and duration, and overall survival were determined as well as the influence of baseline factors on these outcome parameters. Results were compared to those for patients randomized to receive mitoxantrone and prednisone in the Canadian clinical trial which demonstrated palliative benefit of this regimen. RESULTS: Patients treated after trial closure had shorter survival (p = 0.003) but represented a poorer prognosis cohort. PSA response of the trial and post-trial cases was 34% and 28%, respectively (p = 0.36), and median duration of response was 118 and 175 days or greater, respectively. Factors predictive of PSA response in the non-trial cohort were longer time from diagnosis of prostate cancer (p = 0. 027) and higher baseline PSA (p = 0.013). Factors predictive of increased survival in both groups were younger age (p <0.04), better baseline Eastern Cooperative Oncology Group performance status (p <0. 02), and higher hemoglobin (p </=0.05) and PSA response (p <0.0001). Gleason score was not predictive of response or survival. CONCLUSIONS: Although patients treated outside of the trial had poorer prognostic features, rates of PSA response to mitoxantrone and prednisone were comparable. Factors predictive of survival were similar in the 2 cohorts. Results of the randomized trial are generalizable to clinical practice.

Adenocarcinoma↗

Influence of prednisone and cytostatics on human blood B-, T- and O-lymphocytes in diseases.

B-, T- and O-lymphocytes detected as EAC-, E- and non-rosette forming lymphocytes were investigated in venous blood in 49 patients with connective tissue diseases, psoriasis and chronic lymphogenous leukaemia (CLL) during treatment with either prednisone alone, prednisone and cytostatic agents or cytostatic agents alone. Prednisone alone did not change the B-, T- and O-lymphocyte counts. Cytostatics alone or in combination with prednisone reduced the B- and T-lymphocyte counts concomitant with a significant increase in the O-lymphocyte count. The findings could be explained by assuming that cytostatics disturb the immunological functions of the lymphocytes and finally deprive the cells of their B- and T-markers. The optimal immunosuppressive treatment with cytostatic agents may be associated with a certain reduction of B- and T-lymphocytes which may be used as a guideline for dosage.

Adolescent↗

Effects of prednisone on gastric secretion and development of stomach lesions in swine.

In pigs treated with various doses of prednisone, pathologic changes appeared in the glandular region of the stomach, mainly in the fundic area and rarely and less severely in the cardiac and pyloric mucosae. The characteristic lesion was hemorrhagic gastritis; this was associated with massive gastric hemorrhages in pigs given the larger doses of prednisone. Epithelial changes were found in the esophageal area, but there were no ulcers. In pigs with gastric fistulas, prednisone administered at dose levels of 10 mg/kg of body weight for 8 days produced a significant increase in the volume and the acidity of gastric secretion. Hexosamine output, but not concentration, increased significantly during the treatment period. Change in pepsin secretion was sit significant. Prednisone did not produce an immediate change in gastric secretion--there being a latent period lasting 1 to 2 days before marked changes were observed. After peak changes occurred (3rd or 4th day of treatment), acidity gradually decreased to pretreatment level toward the end of the treatment period. This indicates that although increased acidity may be involved in the development of lesions in the glandular region, other factors probably have a role also in the pathogenesis of steroid-induced stomach lesions in swine.

Animals↗

The effect of prolonged prednisone treatment on human costal cartilage.

Costal cartilage (biopsy) from a 13-year-old boy receiving prolonged prednisone treatment (discontinuously from 2 6/12 to 13 11/12 years) for hepatosplenomegaly and lymphadenopathy has been studied and compared with costal cartilage from untreated individuals. Optical and electron microscopic studies including histochemistry have been employed. Chondrocyte degeneration characterized by lipidic material and glycogen in cells is enhanced following prednisone treatment. Acid proteoglycans are reduced in comparison to those in the untreated controls. Amianthoid (asbestoid) collagen fibers, derived from electron-dense bodies which represent remnants of degenerating chondrocytes, occur in all cartilages. A type of collagen similar to fibrous long-spacing collagen has been observed and is prominent in cartilage from the prednisone-treated individual. Evidence suggests that this type of collagen is cellular in origin and represents a transitional form of native collagen. Morphologic changes suggestive of aging are present following prolonged prednisone treatment.

Adolescent↗

[Comparative study of the treatment of autoimmune uveitis with prednisone and with cyclophosphamide and azathioprine].

BACKGROUND: Uveitis is considered an autoimmune disease that compromises any internal structure of eye; its main characteristic is the inflammatory process inside eye. OBJECTIVE: To determine which is the most effective therapy for autoimmune uveitis: cyclophosphamide, azathioprine and prednisone. MATERIAL AND METHODS: Patients between 16 and 65 years old, both sexes, with diagnosis of autoimmune uveitis (anterior, intermediate and posterior). Patients were submitted to clinical history, physical exploration and clinical studies. Their written informed consent was requested and patients were divided into three treatment groups: group 1 (azathioprine) 14 (42.4%) patients; group 2 (prednisone) 15 (45.5%) patients, and group 3 (cyclophosphamide) 4 (12.1%) patients. Blind double observations and assessments at day 0 and at week 1, 2, 4 and 6 of treatment were performed. RESULTS: Out of 33 patients studied, 13 (39.4%) were male and 20 (60.6%) female, the most frequent diagnosis was uveitis due to Toxoplasmosis. With azathioprine 100 mg/day it was observed a better and faster control of inflammation after 6.2 weeks at anterior chamber with p < 0.0001, with prednisone, p = .000, and with cyclophosphamide, p = 135. In the posterior chamber there were no significant inflammatory changes for three groups with p = .353. The most frequent adverse effects occurred in the prednisone group with p < 0.05 in 24.2%, characterized by neutropenia and urinary tract infection. CONCLUSIONS: Azathioprine, 100 mg/day oral during six weeks, is considered the most effective drug, since it demonstrated significant diminishment of inflammatory process in less time, with less side effects and with conservation of visual acuity.

Adolescent↗

Nevirapine, prednisone and rash.

Findings from a recent study show that people taking prednisone with nevirapine (Viramune) were more likely to develop nevirapine-related rash compared to people not taking prednisone. Prednisone is commonly used to treat rash, a potentially harmful side effect of nevirapine. Researchers theorized that pre-treating people with prednisone might minimize rash. This contrary finding is different from reported anecdotes of experiences in the community.

Diphenhydramine↗

The use of low-dose prednisone in the management of rheumatoid arthritis.

Low doses of prednisone are safe and effective in the management of RA. Yet, some clinicians continue to manage their RA patients with glucocorticoid doses that are too high or avoid them altogether. Glucocorticoids in low doses have proven to be very effective in suppressing the inflammation associated with RA. In addition, there is good evidence that low doses of prednisolone retard bony erosions of RA. Potential side effects of low doses of glucocorticoids can be anticipated and avoided with prudent preventative measures and appropriate management. Therefore, prednisone should be initiated as early as possible in the treatment of RA usually with another DMARD. Treatment of the inflammation in RA should not exceed 10 mg/day and often may need to be given in daily divided doses (5 mg BID). Supplemental daily calcium at 800-1,000 mg/day and vitamin D at 400-800 units/day should always be initiated with treatment. Tapering of prednisone should be done slowly using 1 mg decrements every couple weeks to a month. One should not deem it a failure to hold the patient on the lowest effective dose of prednisone.

Arthritis, Rheumatoid↗

[Treatment of chronic refractory idiopathic thrombocytopenic purpura in children with multiglycosidorum Tripterygii and prednisone].

In order to determine the curative effect of multiglycosidorum Tripterygii and prednisone for treatment of children with chronic refractory idiopathic thrombocytopenic purpura (ITP), a total of 28 patients had been treated with multiglycosidorum Tripterygii and prednisone. Multiglycosidorum Tripterygii was given at a dose of 1 mg/kg body weight per day and the prednisone was given at a dose of 0.5 mg/kg body weight per day for two consecutive months. Bone marrow examination and blood platelet associated immunoglobin G (PAIgG) measurement were performed during the treatment. The results showed that in 21 patients acquired effectiveness, of whom, according the common criteria, 9 patients achieved curative effective, 7 achieved significant effectiveness and 5 effective. 7 patients did not achieve effectiveness. There were no serious side effects associated with therapy. The number of proplatelets on bone marrow smears was increased and the titers of IgG to platelet were restored to normal range in patients achieving remission. In conclusion, combination of multiglycosidorum triptergii with prednisone is effective and safe for treatment of chronic refractory idiopathic thrombocytopenic purpura in children.

Adolescent↗