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Soluble urokinase plasminogen activator receptor (suPAR) levels predict damage accrual in patients with recent-onset systemic lupus erythematosus.
Enocsson, Helena; Wirestam, Lina; Dahle, Charlotte; Padyukov, Leonid; Jönsen, Andreas; Urowitz, Murray B; Gladman, Dafna D; Romero-Diaz, Juanita; Bae, Sang-Cheol; Fortin, Paul R; Sanchez-Guerrero, Jorge; Clarke, Ann E; Bernatsky, Sasha; Gordon, Caroline; Hanly, John G; Wallace, Daniel J; Isenberg, David A; Rahman, Anisur; Merrill, Joan T; Ginzler, Ellen; Alarcón, Graciela S; Chatham, W Winn; Petri, Michelle; Khamashta, Munther; Aranow, Cynthia; Mackay, Meggan; Dooley, Mary Anne; Manzi, Susan; Ramsey-Goldman, Rosalind; Nived, Ola; Steinsson, Kristjan; Zoma, Asad A; Ruiz-Irastorza, Guillermo; Lim, S Sam; Kalunian, Kenneth C; Inanc, Murat; van Vollenhoven, Ronald F; Ramos-Casals, Manuel; Kamen, Diane L; Jacobsen, Søren; Peschken, Christine A; Askanase, Anca; Stoll, Thomas; Bruce, Ian N; Wetterö, Jonas; Sjöwall, Christopher.
Afiliação
  • Enocsson H; Rheumatology/Division of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. Electronic address: helena.enocsson@liu.se.
  • Wirestam L; Rheumatology/Division of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
  • Dahle C; Department of Clinical Immunology and Transfusion Medicine and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
  • Padyukov L; Department of Medicine, Division of Rheumatology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
  • Jönsen A; Department of Clinical Sciences Lund, Section of Rheumatology, Lund University, Lund, Sweden.
  • Urowitz MB; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital and University of Toronto, Toronto, Ontario, Canada.
  • Gladman DD; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital and University of Toronto, Toronto, Ontario, Canada.
  • Romero-Diaz J; Instituto Nacional de Ciencias Médicas y Nutrición, Mexico City, Mexico.
  • Bae SC; Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, South Korea.
  • Fortin PR; Division of Rheumatology, CHU de Québec - Université Laval, Quebec City, Canada.
  • Sanchez-Guerrero J; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital and University of Toronto, Toronto, Ontario, Canada.
  • Clarke AE; Division of Rheumatology, Cumming School of Medicine University of Calgary, Calgary, Alberta, Canada.
  • Bernatsky S; Division of Rheumatology, Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada.
  • Gordon C; Rheumatology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
  • Hanly JG; Division of Rheumatology, Department of Medicine and Department of Pathology, Queen Elizabeth II Health Sciences Centre and Dalhousie University, Halifax, Nova Scotia, Canada.
  • Wallace DJ; Cedars-Sinai/David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
  • Isenberg DA; Centre for Rheumatology Research, University College, London, UK.
  • Rahman A; Centre for Rheumatology Research, University College, London, UK.
  • Merrill JT; Department of Clinical Pharmacology, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
  • Ginzler E; Department of Medicine, SUNY Downstate Medical Center, Brooklyn, NY, USA.
  • Alarcón GS; Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL, USA.
  • Chatham WW; Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL, USA.
  • Petri M; Department of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Khamashta M; Lupus Research Unit, The Rayne Institute, St Thomas' Hospital, King's College London School of Medicine, London, UK.
  • Aranow C; Feinstein Institute for Medical Research, Manhasset, NY, USA.
  • Mackay M; Feinstein Institute for Medical Research, Manhasset, NY, USA.
  • Dooley MA; Division of Rheumatology and Immunology, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.
  • Manzi S; Autoimmunity Institute, Allegheny Health Network, Pittsburgh, PA, USA.
  • Ramsey-Goldman R; Northwestern University and Feinberg School of Medicine, Chicago, IL, USA.
  • Nived O; Department of Clinical Sciences Lund, Section of Rheumatology, Lund University, Lund, Sweden.
  • Steinsson K; Department of Rheumatology, Center for Rheumatology Research Fossvogur, Landspitali University Hospital, Reykjavik, Iceland.
  • Zoma AA; Lanarkshire Centre for Rheumatology, Hairmyres Hospital, East Kilbride, Scotland, UK.
  • Ruiz-Irastorza G; Autoimmune Disease Unit, Department of Internal Medicine, Hospital Universitario Cruces, BioCruces Health Research Institute, University of the Basque Country, Barakaldo, Spain.
  • Lim SS; Division of Rheumatology, Emory University School of Medicine, Atlanta, GA, USA.
  • Kalunian KC; UCSD School of Medicine, La Jolla, CA, USA.
  • Inanc M; Division of Rheumatology, Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey.
  • van Vollenhoven RF; Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, Netherlands; Free University (VU) Amsterdam, Amsterdam, Netherlands; Amsterdam Rheumatology and Immunology Center, Amsterdam, Netherlands.
  • Ramos-Casals M; Josep Font Autoimmune Diseases Laboratory, IDIBAPS, Department of Autoimmune Diseases, Hospital Clínic, Barcelona, Spain.
  • Kamen DL; Division of Rheumatology, Medical University of South Carolina, Charleston, SC, USA.
  • Jacobsen S; Copenhagen Lupus and Vasculitis Clinic, Centre for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
  • Peschken CA; Department of Medicine and Community Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
  • Askanase A; Division of Rheumatology, Columbia University Medical Center, New York, USA.
  • Stoll T; Department of Rheumatology, Kantousspital, Schaffhausen, Switzerland.
  • Bruce IN; Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Faculty of Biology, Medicine and Health, The University of Manchester and NIHR Manchester Biomedical Research Centre, Manchester University Hospital NHS Foundation Trust, Manchester Academic Health Science Center, Ma
  • Wetterö J; Rheumatology/Division of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
  • Sjöwall C; Rheumatology/Division of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
J Autoimmun ; 106: 102340, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31629628
ABSTRACT

OBJECTIVE:

The soluble urokinase plasminogen activator receptor (suPAR) has potential as a prognosis and severity biomarker in several inflammatory and infectious diseases. In a previous cross-sectional study, suPAR levels were shown to reflect damage accrual in cases of systemic lupus erythematosus (SLE). Herein, we evaluated suPAR as a predictor of future organ damage in recent-onset SLE.

METHODS:

Included were 344 patients from the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort who met the 1997 American College of Rheumatology classification criteria with 5-years of follow-up data available. Baseline sera from patients and age- and sex-matched controls were assayed for suPAR. Organ damage was assessed annually using the SLICC/ACR damage index (SDI).

RESULTS:

The levels of suPAR were higher in patients who accrued damage, particularly those with SDI≥2 at 5 years (N = 32, 46.8% increase, p = 0.004), as compared to patients without damage. Logistic regression analysis revealed a significant impact of suPAR on SDI outcome (SDI≥2; OR = 1.14; 95% CI 1.03-1.26), also after adjustment for confounding factors. In an optimized logistic regression to predict damage, suPAR persisted as a predictor, together with baseline disease activity (SLEDAI-2K), age, and non-Caucasian ethnicity (model AUC = 0.77). Dissecting SDI into organ systems revealed higher suPAR levels in patients who developed musculoskeletal damage (SDI≥1; p = 0.007).

CONCLUSION:

Prognostic biomarkers identify patients who are at risk of acquiring early damage and therefore need careful observation and targeted treatment strategies. Overall, suPAR constitutes an interesting biomarker for patient stratification and for identifying SLE patients who are at risk of acquiring organ damage during the first 5 years of disease.
Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Idioma: Inglês Revista: J Autoimmun Assunto da revista: Alergia e Imunologia Ano de publicação: 2020 Tipo de documento: Artigo

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Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Idioma: Inglês Revista: J Autoimmun Assunto da revista: Alergia e Imunologia Ano de publicação: 2020 Tipo de documento: Artigo