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dc.identifier.citationJOURNAL OF RHEUMATOLOGY, v. 46, NO 5, Page. 492-500en_US
dc.description.abstractObjective. In cross-sectional studies, elevated osteopontin (OPN) levels have been proposed to reflect, and/or precede, progressive organ damage and disease severity in systemic lupus erythematosus (SLE). We aimed, in a cohort of patients with recent-onset SLE, to determine whether raised serum OPN levels precede damage and/or are associated with disease activity or certain disease phenotypes. Methods. We included 344 patients from the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort who had 5 years of followup data available. All patients fulfilled the 1997 American College of Rheumatology (ACR) criteria. Baseline sera from patients and from age-and sex-matched population-based controls were analyzed for OPN using ELISA. Disease activity and damage were assessed at each annual followup visit using the SLE Disease Activity Index 2000 (SLEDAI-2K) and the SLICC/ACR damage index (SDI), respectively. Results. Compared to controls, baseline OPN was raised 4-fold in SLE cases (p ˂ 0.0001). After relevant adjustments in a binary logistic regression model, OPN levels failed to significantly predict global damage accrual defined as SDI ˃= 1 at 5 years. However, baseline OPN correlated with SLEDAI-2K at enrollment into the cohort (r = 0.27, p ˂ 0.0001), and patients with high disease activity (SLEDAI-2K ˃= 5) had raised serum OPN (p ˂ 0.0001). In addition, higher OPN levels were found in patients with persistent disease activity (p = 0.0006), in cases with renal involvement (p ˂ 0.0001) and impaired estimated glomerular filtration rate (p = 0.01). Conclusion. The performance of OPN to predict development of organ damage was not impressive. However, OPN associated significantly with lupus nephritis and with raised disease activity at enrollment, as well as over time.en_US
dc.description.sponsorshipThis work was supported by grants from the Swedish Rheumatism Association, the County Council of Ostergotland, the Swedish Society of Medicine, the King Gustaf V and Queen Victoria's Freemasons foundation, and the King Gustaf V's 80-year anniversary foundation. Dr. Fortin holds a Canada Research Chair on Systemic Autoimmune Rheumatic Diseases. Dr. Bae's work was supported in part by an unrestricted grant (Hanyang University 201600000001387). Dr. Gordon's work was supported by Lupus UK and the NIHR/Wellcome Trust Clinical Research Facility. The Hopkins Lupus Cohort is supported by the US National Institutes of Health (NIH; grant AR43727). The Montreal General Hospital Lupus Clinic is partially supported by the Singer Family Fund for Lupus Research. Dr. Clarke holds The Arthritis Society Chair in Rheumatic Diseases at the University of Calgary. Dr. Bruce is supported by Arthritis Research UK, the NIHR Manchester Biomedical Research Centre and the NIHR/Wellcome Trust Clinical Research Facility at Manchester University National Health Service (NHS) Foundation Trust. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health. Dr. Jacobsen is supported by the Danish Rheumatism Association (A1028). Dr. Dooley's work was supported by NIH grant RR00046.en_US
dc.publisherJ RHEUMATOL PUBL COen_US
dc.subjectORGAN DAMAGEen_US
dc.titleOsteopontin and Disease Activity in Patients with Recent-onset Systemic Lupus Erythematosus: Results from the SLICC Inception Cohorten_US
dc.relation.journalJOURNAL OF RHEUMATOLOGY-
dc.contributor.googleauthorWirestam, Lina-
dc.contributor.googleauthorEnocsson, Helena-
dc.contributor.googleauthorSkogh, Thomas-
dc.contributor.googleauthorPadyukov, Leonid-
dc.contributor.googleauthorJonsen, Andreas-
dc.contributor.googleauthorUrowitz, Murray B.-
dc.contributor.googleauthorGladman, Dafna D.-
dc.contributor.googleauthorRomero-Diaz, Juanita-
dc.contributor.googleauthorBae, Sang-Cheol-
dc.contributor.googleauthorFortin, Paul R.-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
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