THU0660 Polymyalgia rheumatica treatment serum biomarkers versus rheumatoid arthritis
| Autor: | Grethe Neumann Andersen, Allan Stensballe, Michael Kruse Meyer, KJ Elbæk, Marlene Andersen, TV Stausbo |
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| Rok vydání: | 2017 |
| Předmět: |
musculoskeletal diseases
medicine.medical_specialty biology business.industry education Arthritis medicine.disease Gastroenterology Complement system Polymyalgia rheumatica Internal medicine Rheumatoid arthritis Proteome medicine biology.protein Biomarker (medicine) Serum amyloid A Antibody business |
| Zdroj: | Poster Presentations. |
| DOI: | 10.1136/annrheumdis-2017-eular.5844 |
| Popis: | Background Polymyalgia rheumatica (PMR) is a systemic inflammatory disorder with unknown etiology and overlapping symptoms with giant cell arthritis and late-onset rheumatoid arthritis (RA). To date, no proteomics studies have been performed on PMR patients, and the number of biomarker studies remain limited. Objectives The primary aim of this study was to thoroughly investigate the corticosteroid treatment serum proteome of PMR with a focus on acute-phase reactions, complement system, and cytokines. Methods Filter-aided sample preparation for mass spectrometry, cell free DNA (cfDNA) assay, and 10plex cytokine assay were applied to PMR serum samples from the same patients before and after treatment, DMARD-naive RA patients, and healthy controls. Results The core serum proteomes of the four groups were remarkably similar, and consisted of >200 proteins, which included acute-phase reactants, coagulation and complement proteins (figure), immunoglobulins, and apolipoproteins, and several more. Acute Phase Serum Amyloid A (SAA1) was differentially less abundant after PMR treatment, and CRP (after adjusting for two patients with low baseline CRP). cfDNA were more abundant in both groups of PMR compared to healthy controls. Complement factors were narrowly distributed and not affected by PMR treatment. The individual serum proteome of each PMR patient provided more than 100 differentially abundant proteins, and highlights the heterogeneity of patients. Conclusions We have established the core serum proteome of PMR in response to treatment, and compared it with RA and healthy controls. The results suggest a functional role of SSA1, and increased cfDNA in the pathogenesis of PMR indicates the activation of NETs. Disclosure of Interest None declared |
| Databáze: | OpenAIRE |
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