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Damage Accumulation in Systemic Lupus Erythematosus and Its Relation to Disease Activity and Mortality
ANDREA BECKER-MEROK and HANS C. NOSSENT ABSTRACT. Objective. To describe damage accrual and the interconnections between disease activity measures, damage accrual, and death in a Nordic lupus cohort. Methods. Longitudinal study in the population-based Tromsø lupus cohort. Disease activity [SLE Disease Activity Index (SLEDAI)] and disease damage [by Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology (ACR) Damage Index (SDI)] were recorded for each visit. Weighted average SLEDAI scores (WAS) were calculated to correct for variable observation times. Development of damage (SDI > 0), severe damage (SDI ≥ 3), and death were used as separate endpoints. Univariate nonparametric analysis identified and hazard ratios (HR) by Cox regression techniques confirmed the independence of predictors for each outcome. Results. Through 11.9 years of followup, 72 patients (46%) remained free of damage, 51 (32%) developed moderate damage, and 35 (22%) developed severe damage. SDI scores were higher in 37 nonsurvivors (23.4%; SDI 2.1) than in survivors (SDI 0.9; p < 0.05). Damage accrual was linear throughout the first decade of disease. The only independent predictor for SDI ≥ 3 was a WAS score > 3 (hazard ratio 2.34; 95% CI 1.1–4.9). Age > 40 years at diagnosis (HR 5.6, 95% CI 2.4–12.7) and WAS > 3 (HR 2.4, 95% CI 1.2–4.9) were significant predictors for death. Conclusion. Damage accrual in SLE occurred in 54% of patients in a linear fashion over the first decade of disease. Global disease activity was the main determinant of damage accrual. Accrued damage was not an independent risk factor for death, which was predicted by age > 40 years and WAS > 3. (First Release July 15 2006; J Rheumatol 2006;33:1570–7) Key Indexing Terms:
DAMAGE From the Department of Rheumatology, Institute of Clinical Medicine, University of Tromsø; and the Department of Rheumatology, University Hospital Northern Norway, Tromsø, Norway. Supported by a grant from Helse Nord (grant SFP-23-04). A. Becker-Merok, MD, Fellow, Department of Rheumatology, Institute of Clinical Medicine, University of Tromsø; H.C. Nossent, MD, PhD, Professor of Medicine, Department of Rheumatology, Institute of Clinical Medicine, University of Tromsø, Department of Rheumatology, University Hospital Northern Norway. Address reprint requests to Dr. A. Becker-Merok, Department of Rheumatology, University Hospital Northern Norway, N-9038 Tromsø, Norway. E-mail: Andrea.Becker-Merok@unn.no Accepted for publication March 2, 2006.
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