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Background/Aim: Knowledge of the usefulness of cystatin C measurement in the detection of chronic kidney disease in patients with rheumatoid arthritis (RA) is scant. The purpose of this study was to evaluate the ability of plasma cystatin C- and creatinine-based methods to predict glomerular filtration rate (GFR) and classify chronic kidney disease in RA patients. Methods: The study population consisted of 64 RA patients aged 41–86 years. Comparisons were made between measured plasma creatinine, cystatin C, creatinine clearance and GFR estimated by the Cockcroft-Gault (CG) and the Modification of Diet in Renal Disease (MDRD) formulas. The plasma clearance of 51Cr-EDTA served as a reference. Results: The Pearson correlation coefficients between plasma clearance of 51Cr-EDTA and the markers of GFR were calculated. The correlation coefficients were 0.800 for plasma creatinine, 0.863 for cystatin C, 0.866 and 0.904 for GFR values estimated by MDRD and CG and 0.922 for plasma creatinine clearance. Statistically significant differences were detected between the correlation coefficients of plasma creatinine and GFR estimated by CG (p = 0.0412) and plasma creatinine and creatinine clearance (p = 0.0099). Creatinine clearance and the MDRD and CG formulas proved to be better at identifying GFR Conclusion: We recommend using the CG formula or creatinine clearance for the estimation of the GFR of RA patients instead of solely creatinine or cystatin C in clinical work.

Objective.To evaluate the performance of biological drugs in psoriatic arthritis (PsA) in a routine care setting, using the Finnish national register of biological treatment (ROB-FIN).Methods.Patients with PsA who started therapy with infliximab or etanercept between June 2000 and February 2006 (n = 127) were followed for up to 24 months. Response was evaluated using American College of Rheumatology response criteria including individual measures.Results.Significantly diminished values for swollen and tender joints, patient’s global and pain assessments, doctor’s global assessment of disease activity, erythrocyte sedimentation rate, C-reactive protein, and Health Assessment Questionnaire score were observed within 3 months after commencement of both infliximab and etanercept. Values remained significantly lower throughout the 24 months of followup. ACR20 response at 3 months was 79% (n = 22/28) for infliximab and 76% (n = 34/45) for etanercept. The first biological drug was discontinued in 16% due to lack of effectiveness and in 6% due to adverse events.Conclusion.Anti-tumor necrosis factor-α therapy, often combined with conventional disease-modifying antirheumatic drugs, appeared to have limited toxicity and persistent effectiveness for up to 2 years in a cohort of Finnish patients with severe peripheral PsA.

Knowledge of the usefulness of cystatin C measurement in the detection of chronic kidney disease in patients with rheumatoid arthritis (RA) is scant. The purpose of this study was to evaluate the ability of plasma cystatin C- and creatinine-based methods to predict glomerular filtration rate (GFR) and classify chronic kidney disease in RA patients.The study population consisted of 64 RA patients aged 41-86 years. Comparisons were made between measured plasma creatinine, cystatin C, creatinine clearance and GFR estimated by the Cockcroft-Gault (CG) and the Modification of Diet in Renal Disease (MDRD) formulas. The plasma clearance of (51)Cr-EDTA served as a reference.The Pearson correlation coefficients between plasma clearance of (51)Cr-EDTA and the markers of GFR were calculated. The correlation coefficients were 0.800 for plasma creatinine, 0.863 for cystatin C, 0.866 and 0.904 for GFR values estimated by MDRD and CG and 0.922 for plasma creatinine clearance. Statistically significant differences were detected between the correlation coefficients of plasma creatinine and GFR estimated by CG (p = 0.0412) and plasma creatinine and creatinine clearance (p = 0.0099). Creatinine clearance and the MDRD and CG formulas proved to be better at identifying GFR90 ml/min than plasma creatinine or cystatin C.We recommend using the CG formula or creatinine clearance for the estimation of the GFR of RA patients instead of solely creatinine or cystatin C in clinical work.

To evaluate mortality and causes of death in patients with rheumatoid arthritis (RA) treated with low-dose oral glucocorticoids.Mortality was analyzed in population-based data of 604 patients with RA. In the original study in 1988, state of general health, severity of RA, and treatment including the use of oral glucocorticoids were recorded. In 1999 vital status and causes of death were evaluated. Mortality in patients with RA who had not received glucocorticoids (Group A, n = 209) was compared to that in patients treated with glucocorticoids for less than 10 years (Group B, n = 276) or for more than 10 years (Group C, n = 119).From onset of RA to 1999, 395 (65%) patients had been treated with oral glucocorticoids. In 1999 a total of 160 (26%) patients had died, 23% of patients in Group A, 21% in Group B, and 45% in Group C. In multivariate Cox regression analysis, male sex (hazard ratio 2.50; 95% CI 1.74-3.59), impaired functional capacity by Health Assessment Questionnaire (HR 2.11; 95% CI 1.65-2.96), heart failure (HR 1.96; 95% CI 1.36-2.84), and diabetes (HR 1.87; 95% CI 1.17-3.01) predicted increased mortality. In the same analysis glucocorticoid treatment for 1 year increased the mortality risk by 14% (HR 1.14; 95% CI 0.98-1.27, p = 0.057) and treatment over 10 years by 69% (HR 1.69; 95% CI 1.12-2.56, p = 0.011) compared to RA patients without treatment. The major cause of death was cardiovascular disease in all groups, but infections and intestinal perforations due to amyloidosis were more frequent in patients with long-lasting glucocorticoid therapy. Lymphomas were more frequent in all patients treated with glucocorticoids (Groups B and C) than in those not receiving glucocorticoids.Patients with RA treated with low-dose oral glucocorticoids for more than 10 years had increased mortality compared to those who did not receive glucocorticoids or whose duration of treatment was less than 10 years. The increased mortality was related mainly to infections and complications caused by systemic amyloidosis.