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Endothelial progenitor cells in active rheumatoid arthritis: Effects of TNF and of glucocorticoid therapy
  1. Johannes C Grisar (johannes.grisar{at}meduniwien.ac.at)
  1. Division of Rheumatology, University of Vienna, Austria
    1. Daniel Aletaha
    1. Division of Rheumatology, University of Vienna, Austria
      1. Carl W Steiner
      1. Division of Rheumatology, University of Vienna, Austria
        1. Theresa Kapral
        1. Division of Rheumatology, University of Vienna, Austria
          1. Sabine Steiner
          1. Division of Angiology, Medical University of Vienna, Austria
            1. Marcus Säemann
            1. Division of Nephrology, University of Vienna, Austria
              1. Ilse Schwarzinger
              1. Department of Medical and Chemical Laboratory , Medical University of Vienna, Austria
                1. Barbara Buranyi
                1. Ludwig Boltzmann Institute of Experimental Endocrinology, Austria
                  1. Günter Steiner (guenter.steiner{at}meduniwien.ac.at)
                  1. Ludwig Boltzmann Institute of Experimental Endocrinology, Austria
                    1. Josef S Smolen (josef.smolen{at}wienkav.at)
                    1. University of Vienna, Austria

                      Abstract

                      Objectives: To study the effects of short term intermediate dose glucocorticoid therapy in patients with active rheumatoid arthritis (RA) on circulating endothelial progenitor cells (EPC), which are known to influence cardiovascular risk, and to elucidate mechanisms potentially responsible for the reduction of EPCs in patients with active RA.

                      Methods: EPC were quantified in 29 patients with active RA by flow cytometry, colony forming unit (CFU) and circulating angiogenic cell (CAC) assays before and after 7 days of intermediate dose glucocorticoid therapy. CFU from RA patients and from healthy referents (HR) were cultured in vitro in the absence or presence of dexamethasone (Dex) and/or TNF.

                      Results: After one week of glucocorticoid therapy, EPC increased from 0.026+/-0.003 % to 0.053+/- 0.010 % (p<0.01), and from 12+/-4 to 27+/-7 CFU/well (p<0.02); CAC also increased from 7+/-2 to 29+/-8 cells/high power field (p<0.05). In parallel, disease activity decreased significantly after glucocorticoid treatment. TNF serum levels also decreased from 36+/-10 to 14+/-6 pg/ml (p<0.0001). Addition of Dex to the RA CFU led to a significant increase of mean CFU counts, whereas addition of TNF induced a decrease of CFU.

                      Conclusions: Our data indicate that TNF may be at least partly responsible for the reduction of EPC seen in RA patients. Intermediate doses of glucocorticoids for a short period of time, aside of reducing disease activity, significantly increase circulating EPC.

                      • TNF
                      • anti-TNF
                      • endothelial progenitor cells
                      • glucocorticoids
                      • rheumatoid arthritis

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