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Pentraxin 3 in serum and synovial fluid of patients with rheumatoid arthritis with and without autoantibodies

Weitoft, Tomas (författare)
Uppsala University,Uppsala universitet,Centrum för klinisk forskning, Gävleborg
Larsson, Anders (författare)
Uppsala University,Uppsala universitet,Klinisk kemi
Saxne, T. (författare)
Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine
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Manivel, Vivek Anand (författare)
Uppsala University,Uppsala universitet,Klinisk immunologi
Lysholm, J (författare)
Falun Hospital, Clinic of Rheumatology,Falun Central Hospital
Knight, Ann (författare)
Uppsala universitet,Reumatologi,Uppsala University Hospital
Rönnelid, Johan (författare)
Uppsala University,Uppsala universitet,Klinisk immunologi
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 (creator_code:org_t)
2016-12-15
2017
Engelska.
Ingår i: Scandinavian Journal of Rheumatology. - : Informa UK Limited. - 0300-9742 .- 1502-7732. ; 46:5, s. 346-352
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • OBJECTIVES:Pentraxin 3 (PTX3) is a locally produced multifunctional protein involved in inflammation, matrix deposition, and immunity. As patients with seropositive rheumatoid arthritis (RA) have a more severe disease course and higher risk of joint destruction than seronegative patients, the aim of the present study was to examine differences in PTX3 in synovial fluid (SF) (and serum) in seropositive compared to seronegative RA, and other local markers of inflammation and destruction.METHOD:Ninety-seven RA patients with knee effusion were included. Serum and SF levels of PTX3, as well as serum levels of anti-citrullinated protein antibody and rheumatoid factor of immunoglobulin A and M subclasses, and markers of inflammation and potential destruction in SF: white blood cell counts, tumour necrosis factor, interleukin-6, vascular endothelial growth factor, metalloproteinase 3, and cartilage oligomeric matrix protein, were analysed. In addition, a radiographic knee examination was performed.RESULTS:Seropositive patients had significantly higher PTX3 levels in SF than seronegative patients, whereas there was no difference for serum levels. SF-PTX3 levels correlated with disease activity and with local inflammatory markers, especially polymorphonuclear cells, and with autoantibody levels. There was no correlation between PTX3 levels in serum and SF.CONCLUSION:The correlation of disease activity and autoantibody levels with SF-PTX3 levels in antibody-positive patients suggests a role for PTX3 in the inflammatory process specifically in seropositive RA joints, and supports the hypothesis that seropositive and seronegative RA are different disease entities. Polymorphonuclear granulocytes may be an important source of PTX3 in RA SF.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Reumatologi och inflammation (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Rheumatology and Autoimmunity (hsv//eng)

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