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Systemic Lupus Erythematosus in a Multiethnic
Cohort (LUMINA): XXIX. Elevation of Erythrocyte Sedimentation Rate Is Associated with Disease Activity and Damage Accrual
LUIS M. VILÁ, GRACIELA S. ALARCÓN, GERALD MCGWIN JR, HOLLY M. BASTIAN, BARRI J. FESSLER, and JOHN D. REVEILLE, for the LUMINA Study Group
ABSTRACT.
Objective. To determine if different categories of erythrocyte sedimentation rate (ESR) elevation are associated with disease activity and/or damage in systemic lupus erythematosus (SLE). Methods. We studied 2317 study visits in 553 SLE patients (≥ 4 American College of Rheumatology criteria, ≤ 5 years' disease duration at enrollment) from a multiethnic (Hispanic, African American, and Caucasian) longitudinal study of outcome. A study visit was done every 6 months for the first year and annually thereafter. Erythrocyte sedimentation rate (ESR) was measured using the Westergren method; results were expressed in 4 categories: < 25 (normal), 25–50 (mild elevation), 51–75 (moderate elevation), and > 75 (marked elevation) mm/h. Anti-dsDNA antibodies were measured at enrollment with the Crithidia luciliae assay. Disease activity was assessed with the Systemic Lupus Activity Measure (SLAM) and the Physician's Global Assessment (PGA). Because ESR is one of the measures evaluated in the SLAM, it was excluded from the total SLAM score. Disease damage was assessed with the Systemic Lupus International Collaborating Clinics damage index (SDI). The relationship between the SLAM (total and PGA) and SDI scores (at baseline and for all visits) and anti-dsDNA antibodies (at enrollment) with ESR was examined by univariable and generalized estimating equation (GEE) regression analyses. Ethnicity, age, and sex were entered in all regression models. Results. The cohort consisted of 89.7% women with mean age 36.8 (SD 12.6) years and disease duration 4.6 (SD 3.2) years. GEE analyses showed that increasing levels of ESR and anti-dsDNA antibody positivity were independently associated with SLAM and PGA scores, at enrollment and for all visits. Overall, the associations of ESR with SLAM and PGA scores were stronger than for the presence of anti-dsDNA antibodies. At baseline, there was no relationship of ESR elevation or anti-dsDNA positivity with SDI scores. However, when all visits were studied, moderate and marked elevations of ESR were independently associated with SDI scores. Conclusion. Mild, moderate, and marked ESR elevations are strongly associated with disease activity in SLE. Moderate and marked ESR elevations are also associated with damage accrual. These associations are stronger than those for the presence of anti-dsDNA antibodies. Our data suggest that ESR could be used to assess disease activity and predict organ/system damage in a relatively rapid and inexpensive manner in SLE. (J Rheumatol 2005;32:2150-5) Key Indexing Terms:
SYSTEMIC LUPUS ERYTHEMATOSUS
From the Division of Rheumatology, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico; Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham; Departments of Surgery (Section of Trauma, Burns, and Critical Care) and Epidemiology, Schools of Medicine and Public Health, University of Alabama at Birmingham, Birmingham, Alabama; and Division of Rheumatology and Clinical Immunogenetics, University of Texas Health Science Center at Houston, Houston, Texas, USA. Supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AR42503, General Clinical Research Centers M01-RR02558 (UTH-HSC) and M01-RR00032 (UAB), and from the National Center for Research Resources (NCRR/NIH) RCMI Clinical Research Infrastructure Initiative (RCRII) award 1P20 RR11126 (UPR-MSC). L.M. Vilá, MD, Associate Professor of Medicine, Chief, Division of Rheumatology, University of Puerto Rico Medical Sciences Campus; G.S. Alarcón, MD, MPH, Jane Knight Lowe Chair of Medicine in Rheumatology, Department of Medicine, Division of Clinical Immunology and Rheumatology; G. McGwin Jr, PhD, Associate Professor, Departments of Surgery (Section of Trauma, Burns, and Critical Care) and Epidemiology, Schools of Medicine and Public Health; H.M. Bastian, MD, MSPH, Assistant Professor of Medicine; B.J. Fessler, MD, Assistant Professor of Medicine, Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham; J.D. Reveille, MD, George S. Bruce Professor in Arthritis and Other Rheumatic Disorders, Director, Division of Rheumatology and Clinical Immunogenetics, University of Texas Health Science Center at Houston. Address reprint requests to Dr. L.M. Vilá, Division of Rheumatology, University of Puerto Rico Medical Sciences Campus, PO Box 365067, San Juan, PR 00936-5067, USA. E-mail: lvila@rcm.upr.edu Accepted for publication June 17, 2005. |