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Innate immunity
Tumour necrosis factor α in rheumatoid arthritis and osteoarthritis patients in blood serum and synovial fluid
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  1. I Bulina1,2,
  2. D Andersone1,2,
  3. A Sochnev4,5,
  4. V Lavrentjevs2,
  5. J Arajs2,
  6. I Astica2,
  7. E Sikora2,
  8. J Zepa2,
  9. I Jaunalksne3,
  10. L Kovalchuk3,5
  1. 1Latvian University
  2. 2Center of Rheumatology, Pauls Stradins Clinical University Hospital, Riga, Latvia
  3. 3Clinic of Clinical Immunology, Pauls Stradins Clinical University Hospital, Riga, Latvia
  4. 4Riga Stradins University, Riga, Latvia
  5. 5Riga Stradins University Institute of Immunology, Riga, Latvia

https://doi.org/10.1136/ard.2010.129627m

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    Objective

    Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown cause which affects the ability of elderly people to work. There is strong evidence to suggest that inflammatory mediators such as tumour necrosis factor α (TNFα) and interleukin 1 (IL1) have a critical role in the pathogenesis of RA. Biological treatment blocks pathological pathways in the actions of these proinflammatory cytokines. The aim of this study was to analyse concentrations of TNFα in blood serum and synovial fluid in patients with RA to identify patient groups most suitable for anti-TNFα treatment.

    Methods

    Blood serum and synovial fluid from patients with RA and osteoarthritis (OA) at Pauls Stradins Clinical University Hospital Center of Rheumatology were selected for detection of TNFα from January 2005 to December 2007 by ELISA. Histiocyte/macrophage counts were detected in synovial fluid in the hospital laboratory. Statistical analyses were performed by the Student t test.

    Results

    29 patients with RA and 11 with OA participated in the study; 17 of the patients with RA had high disease activity (DAS >5.1) and 12 had medium disease activity (DAS ≤1). A statistically significant difference was detected in TNFα levels in the synovial fluid of the RA group and the OA group (p=019), and in serum from the RA group versus the OA group (p=000154); medium activity RA group vs OA group TNFα in blood serum and synovial fluid (p=007 and p=02) and high activity RA group vs OA group TNFα in blood serum and synovial fluid (p<0.001 and p=001). The difference between high and medium RA activity groups in TNFα levels in serum and synovial fluid was p=162 and p=0037. Histiocyte/macrophage count in synovial fluid differed in OA group vs RA medium disease activity group (p=02) and in OA vs RA high disease activity group (p=004), but in medium disease activity RA vs high disease activity RA group (p=58).

    Conclusion

    Further studies are needed to detect cytokines in blood serum and synovial fluid for the use of one as a possible marker when choosing treatment for individual patients with RA.