International multi-center evaluation of a novel chemiluminescence assay for the detection of anti-dsDNA antibodies.

OBJECTIVE: Anti-double stranded desoxyribonucleic acid (anti-dsDNA) antibodies are considered fairly specific for systemic lupus erythematosus (SLE) and their quantification is useful for the clinical management of SLE patients. We assessed the diagnostic performance of the QUANTA Flash dsDNA chemiluminescent immunoassay (CIA) in comparison to an ELISA, using patients from five participating countries. The main focus was to evaluate the correlation between anti-dsDNA antibody results from the CIA and global SLE disease activity, as measured by the SLE Disease Activity Index 2000 (SLEDAI-2K). PATIENTS AND METHODS: A total of 1431 samples (SLE, n = 843; disease controls, n = 588) from five countries (Canada, USA, Portugal, Sweden and Spain) were tested with QUANTA Flash dsDNA (Inova Diagnostics, San Diego, CA, USA). Data obtained with the QUANTA Lite dsDNA SC ELISA (Inova Diagnostics) were available for samples from three sites (Canada, USA and Sweden, n = 566). The SLEDAI-2K scores were available for 805 SLE patients and a cut-off of > 4 was used to define active disease. RESULTS: QUANTA Flash dsDNA had a sensitivity of 54.3% for the diagnosis of SLE, combined with 89.8% specificity. Anti-dsDNA antibody levels were significantly higher (p < 0.0001) in active SLE (SLEDAI-2K > 4; n = 232; median value 83.0 IU/mL) versus the inactive patients (n = 573; median value 22.3 IU/mL), and the SLEDAI-2K scoring correlated with their dsDNA antibody levels (Spearman's rho = 0.44, p < 0.0001). Similar but less pronounced findings were also found for the ELISA, in relation to disease activity. CONCLUSIONS: The QUANTA Flash dsDNA assay showed good clinical performance in a large international multi-center study. Additionally, the strong correlation between anti-dsDNA antibody results and SLEDAI-2K scores supported the potential utility of QUANTA Flash dsDNA for monitoring disease activity.

Incidence and predictors of cardiovascular events in a cohort of patients with rheumatoid arthritis.

INTRODUCTION: An excess in cardiovascular (CV) morbidity and mortality has been recognized in Rheumatoid Arthritis (RA) patients when compared to the general population. Given the paucity of prospective data, our aim was to estimate the incidence of CV events and the contribution of traditional CVD risk factors and RA-related parameters to future events. METHODS: Incident fatal and non-fatal CV events (hospitalizations due to unstable angina, myocardial infarction, coronary artery revascularization procedures, stroke, or CV death) were assessed in a prospective cohort of RA women followed since 2007 and without CV events at cohort entry. The presence of traditional CV risk factors, disease characteristics, medication, carotid ultrasound, and biomarkers of inflammation and endothelial activation were evaluated at baseline. Univariate Cox proportional hazard models were used to identify risk factors for CV events. RESULTS: Among 106 women followed over 565 patient-years we identified 4 CV events (1 fatal stroke, 2 myocardial infarction and 1 unstable angina), which contributed to an incidence rate of 7 per 1000 person-years (95%CI 2.0- 13.9). Patients who developed CV events were older, but the distribution of other traditional CV risk factors was otherwise similar in both groups. Also, corticosteroid dosage and proportion of patients with carotid atherosclerotic plaques was higher in those with CV events. Erythrocyte sedimentation rate (ESR) (HR 1.036; 95%CI 1.005-1.067) and soluble intercellular adhesion molecule-1 (sICAM-1) serum levels (HR 1.002; 95%CI 1.000-1.003) significantly contributed to CV events. These results remained significant after adjusting for patients' age. CONCLUSION: We found an incidence of cardiovascular events in women with RA of 7 per 1000 patent-years. This value is similar to that found in other Portuguese cohort of RA patients1 and much higher than the incidence reported for the general Portuguese population. Markers of inflammation and endothelial activation contributed significantly to CV events, but the limited number of events prevents further analysis.