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The baseline interferon signature predicts disease severity over the subsequent 5 years in systemic lupus erythematosus.
Mai, Lloyd; Asaduzzaman, Arundip; Noamani, Babak; Fortin, Paul R; Gladman, Dafna D; Touma, Zahi; Urowitz, Murray B; Wither, Joan.
Afiliação
  • Mai L; Division of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
  • Asaduzzaman A; Division of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
  • Noamani B; Division of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Canada.
  • Fortin PR; Division of Rheumatology, Department of Medicine, Centre de recherche du CHU de Québec - Université Laval, Quebec City, QC, Canada.
  • Gladman DD; Division of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
  • Touma Z; University of Toronto Lupus Clinic, Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital, University Health Network, Toronto, Canada.
  • Urowitz MB; Division of Rheumatology, Schroeder Arthritis Institute, University Health Network, Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Canada.
  • Wither J; University of Toronto Lupus Clinic, Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital, University Health Network, Toronto, Canada.
Arthritis Res Ther ; 23(1): 29, 2021 01 16.
Artigo em Inglês | MEDLINE | ID: mdl-33451338
ABSTRACT

OBJECTIVES:

Type I interferons (IFNs) play an important role in the pathophysiology of systemic lupus erythematosus (SLE). While cross-sectional data suggest an association between IFN-induced gene expression and SLE disease activity, interest in this as a biomarker of flare has been tempered by a lack of fluctuation with disease activity in the majority of patients. This led us to question whether IFN-induced gene expression might instead be a biomarker of overall disease severity, with patients with high levels spending more time in an active disease state.

METHODS:

Levels of five interferon-responsive genes were measured in the whole peripheral blood at baseline visit for 137 SLE patients subsequently followed for 5 years. Log transformed values were summed to yield a composite IFN5 score, and the correlation with various disease outcomes examined. Receiver operator characteristic analyses were performed for outcomes of interest. Kaplan-Meier curves were generated to compare the proportion of flare-free patients with high and low IFN5 scores over time.

RESULTS:

The baseline IFN5 score was positively correlated with the adjusted mean SLE disease activity index-2000, number of flares, adjusted mean prednisone dose, and number of new immunosuppressive medications over the subsequent 5 years. Optimal cut-offs for the IFN5 score were determined using Youden's index and predicted more severe outcomes with 57-67% accuracy. A high baseline IFN5 level was associated with a significantly increased risk of subsequent flare.

CONCLUSIONS:

Measurement of the type I IFN signature is a useful tool for predicting the subsequent disease activity course.
Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Tipo de estudo: Estudo prognóstico / Fatores de risco Idioma: Inglês Revista: Arthritis Res Ther Assunto da revista: Reumatologia Ano de publicação: 2021 Tipo de documento: Artigo País de afiliação: Canadá

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Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Tipo de estudo: Estudo prognóstico / Fatores de risco Idioma: Inglês Revista: Arthritis Res Ther Assunto da revista: Reumatologia Ano de publicação: 2021 Tipo de documento: Artigo País de afiliação: Canadá