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Osteopontin and Disease Activity in Patients with Recent-onset Systemic Lupus Erythematosus: Results from the SLICC
Lina Wirestam1,2, Helena Enocsson3,4, Thomas Skogh3,4
1From the Rheumatology/Division of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping; Department of Medicine, Unit of Rheumatology, Karolinska Institutet and Karolinska University Hospital, Stockholm; Department of Clinical Sciences Lund, Section of Rheumatology, Lund University, Lund; Unit for Clinical Therapy Research (ClinTRID), Karolinska University, Stockholm, Sweden; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital and University of Toronto, Toronto, Ontario; Division of Rheumatology, Centre Hospitalier Universitaire (CHU) de Québec - Université Laval, Quebec City, Quebec; Division of Rheumatology, Cumming School of Medicine - University of Calgary, Calgary, Alberta; Division of Rheumatology, Department of Medicine, McGill University Health Centre, Montreal, Quebec; Division of Rheumatology, Department of Medicine and Department of Pathology, Queen Elizabeth II Health Sciences Centre and Dalhousie University, Halifax, Nova Scotia; Department of Medicine and Community Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada; Instituto Nacional de Ciencias Médicas y Nutrición, Mexico City, Mexico; Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, Korea; Rheumatology Research Group, School of Immunity and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham; Centre for Rheumatology Research, University College, London; Lupus Research Unit, The Rayne Institute, St. Thomas' Hospital, King's College London School of Medicine, London; Lanarkshire Centre for Rheumatology, Hairmyres Hospital, East Kilbride, Scotland; Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Faculty of Biology, Medicine and Health, The University of Manchester and UK National Institute for Health Research (NIHR) Manchester Biomedical Research Centre, Manchester University Foundation Trust, Manchester, UK; Cedars-Sinai/David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California; Department of Clinical Pharmacology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma; Department of Medicine, State University of New York (SUNY) Downstate Medical Center, Brooklyn, New York; Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama; Department of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Feinstein Institute for Medical Research, Manhasset, New York; Division of Rheumatology and Immunology, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina; Autoimmunity Institute, Allegheny Health Network, Pittsburgh, Pennsylvania; Northwestern University and Feinberg School of Medicine, Chicago, Illinois; Division of Rheumatology, Emory University School of Medicine, Atlanta, Georgia; University of California San Diego School of Medicine, La Jolla, California; Division of Rheumatology, Medical University of South Carolina, Charleston, South Carolina; Division of Rheumatology, Columbia University Medical Center, New York, New York, USA; Department of Rheumatology, Center for Rheumatology Research Fossvogur Landspitali University Hospital, Reyjkavik, Iceland; Autoimmune Disease Unit, Department of Internal Medicine, Hospital Universitario Cruces, BioCruces Health Research Institute, University of the Basque Country, Barakaldo; Josep Font Autoimmune Diseases Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Autoimmune Diseases, Hospital Clínic, Barcelona, Spain; Division of Rheumatology, Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey; Copenhagen Lupus and Vasculitis Clinic, Centre for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; Department of Rheumatology, Kantousspital, Schaffhausen, Switzerland. lina.wirestam@gmail.com.
Objective:
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.
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