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Prednisone Dose (prednisone + dose)
Selected AbstractsHigh HDL-cholesterol in women with rheumatoid arthritis on low-dose glucocorticoid therapyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2008C. García-Gómez ABSTRACT Background, Dyslipidaemia has been described in non-treated rheumatoid arthritis (RA), and improves after therapy with disease modifying anti-rheumatic drugs or glucocorticoids; however, it has generally been perceived that glucocorticoids adversely affect lipid metabolism. The association of low dose glucocorticoid therapy with plasma lipid levels was evaluated in female RA patients. Materials and methods, A cross-sectional study was conducted in 78 female RA patients [mean age: 60 (12) years; mean disease duration: 13 (9) years]. Sixty-five (83%) were on glucocorticoid therapy [total equivalent mean prednisone dose: 5·1 (1·7) mg d,1]. Each patient was assessed through a self-reported questionnaire, structured interview and physical examination. Blood samples were obtained for routine biochemistry, lipid profile and haematological tests. Lipid profiles of RA patients who were and were not on glucocorticoid therapy were compared. Results, Clinical and laboratory features of the two groups of patients were similar, except for the Health Assessment Questionnaire and body mass index, which were significantly higher in the patients on glucocorticoid therapy. These patients had 14·7% higher serum high-density lipoprotein cholesterol (HDL-c) levels than untreated patients (P = 0·043), mainly at the expense of HDL2 subfraction, which was 24·4% higher (P < 0·039), whereas HDL3-c was only 7·4% higher (P = 0·219). Serum levels of glucose and total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL -c), very low-density lipoprotein cholesterol, apolipoproteins A-I and B were not increased in patients on glucocorticoid therapy. Conclusions, Low dose glucocorticoid therapy in RA patients is associated with an increase in HDL-c, without increasing LDL-c or triglyceride. These lipid changes may overall be considered favourable. [source] Apparent Reactivation of a Fibrohistiocytic Proliferation with Features of Dermatofibroma and Dermatomyofibroma Following Systemic ImmunosuppressionJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005W.A. High A 41 year-old man presented with an atrophic, hyperpigmented plaque on the right lower abdomen present since"birth". He denied any prior activity at the site, and had been told it was a "scar" from a prenatal insult. Six months earlier, he developed idiopathic focal sclerosing glomerulonephritis and was placed on 70 mg prednisone per day. He had not demonstrated evidence of lupus eythematosus. Shortly after beginning this regimen, erythematous and tender papules developed around the quiescent plaque. He had tapered his prednisone dose to 60 mg per day, but additional papules continued to erupt. An ellipse biopsy was performed which included a portion of the atrophic plaque and several surrounding papules. Histological examination revealed a proliferation of fibrohistiocytes between and amongst collagen bundles. In some areas, fibrohistiocytes entrapped collagen in a fashion reminiscent of a dermatofibroma. In other areas, particularly that of the atrophic plaque, the fibrohistiocytes were less numerous and more delicate in appearance. Scattered rudimentary fascicles were demonstrated. Adnexal structures were preserved. Immunohistochemical staining revealed the fibrohistiocytes to be positive for factor XIIIa and actin, but negative for desmin, CD34, S-100, procollagen I, and CD68. This lesion demonstrated unique clinical/histiological aspects not well characterized in the literature. [source] Prospective monitoring of lipid profiles in children receiving pravastatin preemptively after renal transplantationPEDIATRIC TRANSPLANTATION, Issue 6 2005Lavjay Butani Abstract:, Hyperlipidemia is common after renal transplantation (Tx) and contributes to the increased cardiovascular morbidity seen in the post-transplant period. Limited data are available on the utility of the statins in children after renal Tx. This 12-month prospective study was undertaken to determine the efficacy of pravastatin in reducing dyslipidemia after renal Tx in children and to determine predictors of dyslipidemia after Tx. From August 2001 to April 2004, all 17 newly transplanted pediatric renal transplant recipients at our center were preemptively treated with pravastatin from the immediate post-transplant period. Fasting lipid profiles were obtained at 1, 3, 6 and 12 months after Tx. Trends in the lipid profile were analyzed using the repeated measures general linear model (GLM). A historical cohort of pediatric renal-transplant recipients not treated with pravastatin was used as the control population. The mixed effects GLM was used for multivariable logistic regression analyses to determine the independent effect of age, pretransplant cholesterol (Chol), body mass index (BMI), creatinine clearance (CrCl), and corticosteroid and tacrolimus doses on the development of dyslipidemia. The mean age of the children at Tx was 8.7 yr. The GLM analysis showed that with time, there was a significant decline in the total Chol, serum triglyceride (TG), LDL and also HDL-Chol (p-value <0.05 for each). Compared with the controls, the mean serum Chol was lower at all time points post-transplant in the treated patients. However, despite treatment, the prevalence of hypercholesterolemia increased from 31% pretransplant to 53% at 1-month, but declined thereafter to 6% at 3 and 6 months and 0% at 1 yr. Multivariable regression analyses showed the prednisone dose, pretransplant Chol and age to be the most important risk factors for the development of dyslipidemia. No child developed complications related to therapy. In summary, pravastatin is safe in the post-transplant period in children and reduces serum Chol, LDL-Chol and TG. An unexpected finding in our study was the decline in HDL-Chol after Tx. Whether the preemptive use of the statins will result in lower cardiovascular morbidity, especially considering the concomitant reduction in HDL-Chol remains to be determined. [source] Treatment of polyarteritis nodosa and microscopic polyangiitis without poor-prognosis factors: A prospective randomized study of one hundred twenty-four patientsARTHRITIS & RHEUMATISM, Issue 4 2010Camillo Ribi Objective To assess the efficacy of systemic corticosteroids alone as first-line treatment of polyarteritis nodosa (PAN) and microscopic polyangiitis (MPA) without poor-prognosis factors as defined by the Five-Factors Score (FFS), and to compare the efficacy and safety of azathioprine versus pulse cyclophosphamide as adjunctive immunosuppressive therapy for patients experiencing treatment failure or relapse. Methods This prospective, multicenter, therapeutic trial included 124 patients with newly diagnosed PAN or MPA (FFS of 0) treated with corticosteroids alone. At the time of treatment failure or disease relapse, patients were randomized to receive 6 months of therapy with oral azathioprine or 6 pulses of cyclophosphamide. Analyses was performed according to an intent-to-treat strategy. Results The mean ± SD followup period was 62 ± 33 months. Treatment with corticosteroids alone induced remission in 98 patients; 50 (40%) of these patients had sustained disease remission, 46 (37%) experienced a relapse, and 2 became corticosteroid dependent (daily prednisone dose ,20 mg). In 26 patients (21%), treatment with corticosteroids alone failed, and 49 patients (40%) required additional immunosuppression. Among the 39 patients randomized, 13 of 19 achieved remission with cyclophosphamide pulses, and 14 of 20 achieved remission with azathioprine. Among all patients, the 1-year and 5-year survival rates were 99% and 92%, respectively. Six deaths occurred in the cyclophosphamide-treated group compared with 2 deaths in the azathioprine-treated group. Disease-free survival was significantly lower for patients with MPA than for those with PAN (P = 0.046). Conclusion For patients with PAN or MPA with an FFS of 0, overall 5-year survival was good, but first-line corticosteroid treatment was able to achieve and maintain remission in only about half of the patients, and 40% of the patients required additional immunosuppressive therapy. Azathioprine or pulse cyclophosphamide was fairly effective for treating corticosteroid-resistant disease or major relapses. [source] Dysfunctional proinflammatory high-density lipoproteins confer increased risk of atherosclerosis in women with systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 8 2009Maureen McMahon Objective Women with systemic lupus erythematosus (SLE) have an increased risk of atherosclerosis. Identification of at-risk patients and the etiology underlying atherosclerosis in SLE remain elusive. The antioxidant capacity of normal high-density lipoproteins (HDLs) is lost during inflammation, and these dysfunctional HDLs might predispose individuals to atherosclerosis. The aim of this study was to determine whether dysfunctional proinflammatory HDL (piHDL) is associated with subclinical atherosclerosis in SLE. Methods Carotid artery ultrasound was performed in 276 women with SLE to identify carotid plaques and measure intima-media thickness (IMT). The antioxidant function of HDL was measured as the change in oxidation of low-density lipoprotein after the addition of HDL cholesterol. Two antiinflammatory HDL components, paraoxonase 1 and apolipoprotein A-I, were also measured. Results Among the SLE patients, 48.2% were determined to have piHDL on carotid ultrasound, while 86.7% of patients with plaque had piHDL compared with 40.7% of those without plaque (P < 0.001). Patients with piHDL also had a higher IMT (P < 0.001). After multivariate analysis, the only factors found to be significantly associated with plaque were the presence of piHDL (odds ratio [OR] 16.1, P < 0.001), older age (OR 1.2, P < 0.001), hypertension (OR 3.0, P = 0.04), dyslipidemia (OR 3.4, P = 0.04), and mixed racial background (OR 8.3, P = 0.04). Factors associated with IMT measurements in the highest quartile were the presence of piHDL (OR 2.5, P = 0.02), older age (OR 1.1, P < 0.001), a higher body mass index (OR 1.07, P = 0.04), a cumulative lifetime prednisone dose ,20 gm (OR 2.9, P = 0.04), and African American race (OR 8.3, P = 0.001). Conclusion Dysfunctional piHDL greatly increases the risk of developing subclinical atherosclerosis in SLE. The presence of piHDL was associated with an increased prevalence of carotid plaque and with a higher IMT. Therefore, determination of piHDL may help identify patients at risk for atherosclerosis. [source] Premature atherosclerosis in pediatric systemic lupus erythematosus: Risk factors for increased carotid intima-media thickness in the atherosclerosis prevention in pediatric lupus erythematosus cohort,ARTHRITIS & RHEUMATISM, Issue 5 2009Laura E. Schanberg Objective To evaluate risk factors for subclinical atherosclerosis in a population of patients with pediatric systemic lupus erythematosus (SLE). Methods In a prospective multicenter study, a cohort of 221 patients underwent baseline measurements of carotid intima-media thickness (CIMT) as part of the Atherosclerosis Prevention in Pediatric Lupus Erythematosus (APPLE) trial. SLE disease measures, medications, and traditional risk factors for atherosclerosis were assessed. A standardized protocol was used to assess the thickness of the bilateral common carotid arteries and the mean maximal IMT of 12 segments. Univariable analysis identified potential associations with CIMT, which were examined in multivariable linear regression modeling. Results Based on the mean-mean common or the mean-max CIMT as the dependent variable, univariable analysis showed significant associations of the following variables with increased CIMT: increasing age, longer SLE duration, minority status, higher body mass index (BMI), male sex, increased creatinine clearance, higher lipoprotein(a) level, proteinuria, azathioprine treatment, and prednisone dose. In multivariable modeling, both azathioprine use (P = 0.005 for the mean-mean model and P = 0.102 for the mean-max model) and male sex (P < 0.001) were associated with increases in the mean-max CIMT. A moderate dosage of prednisone (0.15,0.4 mg/kg/day) was associated with decreases in the mean-max CIMT (P = 0.024), while high-dose and low-dose prednisone were associated with increases in the mean-mean common CIMT (P = 0.021) and the mean-max CIMT (P = 0.064), respectively. BMI (P < 0.001) and creatinine clearance (P = 0.031) remained associated with increased mean-mean common CIMT, while increasing age (P < 0.001) and increasing lipoprotein(a) level (P = 0.005) were associated with increased mean-max CIMT. Conclusion Traditional as well as nontraditional risk factors were associated with increased CIMT in this cohort of patients in the APPLE trial. Azathioprine treatment was associated with increased CIMT. The relationship between CIMT and prednisone dose may not be linear. [source] Rate and determinants of progression of atherosclerosis in systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 10 2007Mary J. Roman Objective To determine the rate of atherosclerosis progression as well as the relationship of traditional risk factors, systemic lupus erythematosus (SLE),related factors, and treatment to atherosis progression in SLE patients. Methods Outpatients in the Hospital for Special Surgery SLE Registry underwent serial carotid ultrasound and clinical assessment in a longitudinal study. Results Among 158 patients, 77 (49%) had persistent absence of atherosclerosis (carotid plaque), 36 (23%) had unchanged atherosclerosis, and 45 (28%) had progressive atherosclerosis, defined as a higher plaque score (new plaque in 25 patients and more extensive plaque in 20 patients) after a mean ± SD interval of 34 ± 9 months. Multivariate determinants of atherosclerosis progression were age at diagnosis (odds ratio [OR] 2.75, 95% confidence interval [95% CI] 1.67,4.54 per 10 years, P < 0.001), duration of SLE (OR 3.16, 95% CI 1.64,6.07 per 10 years, P < 0.001), and baseline homocysteine concentration (OR 1.24, 95% CI 1.06,1.44 per ,moles/liter, P = 0.006). SLE patients with stable plaque and progressive plaque differed only in baseline homocysteine concentration. Atherosclerosis progression was increased across tertiles of homocysteine concentration (16.2%, 36.4%, and 56.1%; P = 0.001), and homocysteine tertile was independently related to progression of atherosclerosis (OR 3.14, 95% CI 1.65,5.95 per tertile, P < 0.001). Less aggressive immunosuppressive therapy and lower average prednisone dose were associated with progression of atherosclerosis in univariate, but not multivariate, analyses. Inflammatory markers and lipids were not related to atherosclerosis progression. Conclusion Atherosclerosis develops or progresses in a substantial minority of SLE patients during short-term followup (10% per year on average). Older age at diagnosis, longer duration of SLE, and higher homocysteine concentration are independently related to progression of atherosclerosis. These findings show that aggressive control of SLE and lowering of homocysteine concentrations are potential means to retard the development and progression of atherosclerosis in SLE. [source] Experience with adalimumab for the treatment of non-infectious uveitisACTA OPHTHALMOLOGICA, Issue 2009B DOBNER Purpose Objective: The aim of this study has been to assess the efficacy of adalimumab (ADA) in patients with uveitis in 3 centers. Methods In a retrospective study we identified patients from all instituitions´databases, who were treated with ADA in an average period of 20.16 months (range 1.3-45 months). The 5 criteria that the efficacy of ADA had been judged on are: reduction of macular edema by OCT, visual acuity, anterior chamber cells, reduction of flares and a reduction of prednisone dose during the treatment. At least one of the criteria had to be improved and none of the others worsened to declare treatment as effective. Results Of the 61 patients who were treated with ADA, 38 were treated for uveitis and systemic disease, 3 primarily for active systemic disease and 20 primarily for active uveitis. 15 patients had been treated before with etanercept and 11 with infliximab, with insufficient response. We saw an improvement in 49 out of these 61 patients (80,3%) in 1 or more criteria and worsening in none, 5 patients did not meet improvement criteria and were given additional or alternative treatment, three of them mainly due to activity of systemic disease. 14 out of 49 (28,6%)Patients showed an Improvement in every criteria, the other patients showed increasing in at least one criteria, the other criterias remained stable. At the last follow-up there were 50 (81,9%) patients still on ADA treatment. 11 patients stopped ADA treatment for different reasons (inefficacy, active systemic disease, pregnancy etc.). Conclusion In this retrospective study we judged that the treatment with ADA in patients with uveitis with or without systemic disease was effective in 80,3%. Clinical trials are warrented Commercial interest [source] Effects of Low-Dose Prednisone on Bone Metabolism,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2005Francine N Ton MD Abstract Prednisone 5 mg/day suppresses multiple indices of bone formation in a randomized placebo-controlled trial in healthy postmenopausal females. This suggests that even low doses of prednisone may reduce bone repair or renewal and may have adverse effects on bone mass and/or bone strength. Introduction: High doses of chronic glucocorticoids are known to have adverse effects on bone, and measures to prevent bone loss are well established for doses >7.5 mg daily, because these doses can cause premature or exaggerated osteoporosis. However, it is unclear if chronic prednisone doses of 5 mg daily have the same effects on bone. There are no established recommendations for preventing glucocorticoid-induced osteoporosis in people taking prednisone 5 mg daily, a dose used frequently in medical practice to treat diseases of the lungs, joints, skin, muscles, eyes, nerves, etc. Our primary objective was to test whether prednisone 5 mg daily affects serum and urine indices of bone metabolism in healthy postmenopausal women. Our secondary objectives were to determine if prednisone 5 mg affected systolic or diastolic blood pressure or causes side effects. Materials and Methods: A double-blinded randomized placebo-controlled 8-week trial in 50 healthy postmenopausal women was conducted at the Massachusetts General Hospital Outpatient General Clinical Research Center. Patients were randomly assigned to prednisone 5 mg daily or matching placebo for 6 weeks, followed by a 2-week recovery phase. Markers of bone formation and resorption were determined at weeks 0, 2, 4, 6, and 8. Indices of osteoblast activity included serum propeptide of type I N-terminal procollagen (PINP), propeptide of type I C-terminal procollagen (PICP), osteocalcin, and bone-specific alkaline phosphatase (BSALP). Indices of osteoclast activity included urine and serum type I collagen N-telopeptide (NTX) and free urinary deoxypyridinoline (DPD). Results and Conclusions: Prednisone rapidly and significantly decreased serum PINP (p < 0.01), PICP (p < 0.01), and osteocalcin (p < 0.01) and free urinary deoxypyridinoline (p = 0.017). These changes were largely reversed during the recovery period. Side effects were indistinguishable in the two groups. Neither systolic nor diastolic blood pressure changed significantly throughout the study between the two groups. In conclusion, low-dose prednisone significantly decreases indices of bone formation and may decrease indices of bone resorption in postmenopausal women. Further studies are needed to assess the effects of low-dose prednisone on BMD and fracture risk. [source] | ||||||||||