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AB0272 Anti-Rheumatic Treatment Is Not Associated with Reduction of Pentraxin 3 (PTX3) in Rheumatoid Arthritis (RA), Psoriatic Arthritis (PSA) and Ankylosing Spondylitis (AS)
  1. G. Deyab1,
  2. I. Hokstad2,
  3. S. Agewall3,
  4. T. Lyberg4,
  5. J.E. Whist1,
  6. M.C. Smastuen5,
  7. B.B. Bottazzi6,
  8. G.G. Hjeltnes7,
  9. P.L. Meroni8,
  10. I. Hollan2,9,10
  1. 1Department of medical biochemistry, Lillehammer Hospital Trust
  2. 2Lillehammer Hospital for Rheumatic Diseases, Lillehammer
  3. 3Oslo University Hospital Ullevål and Institute of Clinical Sciences
  4. 4Medical biochemistry, Oslo University Hospital, Ullevål
  5. 5Health science, Oslo and Akershus University College, Oslo, Norway
  6. 6Humanitas Research Hospital, Milan, Italy
  7. 7Department of Medicine, Lillehammer Hospital Trust, Lillehammer, Norway
  8. 8Department of Clinical science and Community Health, University of Milan, Milan, Italy
  9. 9Harvard Medical School
  10. 10Brigham and Women's Hospital, Boston, United States

Abstract

Background PTX3, an important component of the innate immune system,has been proposed as a useful biomarker of inflammation and cardiovascular (CV) risk, but its role in inflammatory rheumatic diseases (IRDs) is still uncertain [1,2].

Objectives The aim of this study was to examine if methotrexate (MTX) and/or anti-tumor necrosis factor treatment (anti-TNF) treatment reduced serum PTX3 (s-PTX3) levels in IRDs (RA, PsA and AS), and if s-PTX3 levels were related to other markers of inflammation and to endothelial function (EF).

Methods From the biobank of PSARA, an observational study, we examined samples from 114 IRD patients starting with either MTX or anti-TNF with or without MTX (anti-TNF±MTX) due to active disease, who completed a 6 months follow up. s-PTX3 (enzyme-linked immunosorbent assay), EF (finger plethysmography) and established inflammatory biomarkers were evaluated at baseline and after 6 weeks and 6 months of therapy.

Results The s-PTX3 levels in IRD and all the diagnostic subgroups were above the upper limit of the reference range. In contrast to established inflammatory markers, in particular C- reactive protein (CRP) and erythrocyte sedimentation rate (ESR) (all p-values <0.05), s-PTX3 levels did not change significantly after 6 weeks and 6 months of anti-rheumatic therapy (all p>0.2). The effect of MTX monotherapy and anti-TNF±MTX on s-PTX3 levels was similar. Changes in CRP, ESR and EF were not related to changes in s-PTX3 levels neither in univariate analyses nor in analyses adjusted for potential confounders.

Conclusions IRD patients have increased s-PTX3 levels, which, in contrast to other inflammatory markers, do not seem to improve within 6 months of therapy with MTX and/or anti-TNF. Thus, in theory, s-PTX3 might reflect a persisting immune process, even a causal factor of the inflammation, not inhibited by the standard anti-rheumatic treatment. Furthermore, even though PTX3 is thought to be a strong predictor of CV prognosis, it was not related to EF.

  1. Bottazzi, B., et al., An integrated view of humoral innate immunity: pentraxins as a paradigm. Annu.Rev.Immunol., 2010. 28: p. 157–183.

  2. Jylhävä, J., et al., Pentraxin 3 (PTX3) is associated with cardiovascular risk factors: the Health 2000 Survey. Clinical and Experimental Immunology, 2011. 164(2): p. 211–217.

Disclosure of Interest None declared

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