08.09 Effects of anti-tnf therapy on solubile urokinase plasminogen activator receptor (supar) levels in arthritis

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Abstract

Background

The urokinase plasminogen activator receptor (uPAR) is expressed mainly on immune cells, smooth muscle cells and endothelial cells, favouring extracellular matrix degradation, cell adhesion, cell proliferation and regulates cell migration. The suPAR is the soluble form of the cell membrane-bound protein uPAR, elevated levels may reflect increased activation of immune system which observed in the autoimmun diseases. The aim of this study was to assess the effects of anti-TNF therapy on these levels in RA and AS patients. The suPAR levels also correlated with various autoimmun inflammatory markers.

Patients and methods

Altogether 33 arthritis patients including 22 RA patients treated with either etanercept (ETN) or certolizumab pegol (CZP) and 11 AS patients treated with ETN were included in a 12- month follow-up study. Circulating suPAR levels were assessed by suPARnostic Quick Test Reader. In addition,disease activity (DAS28 or BASDAI), CRP, IgM rheumatoid factor, anti-CCP were also assessed. Assessment were performed at baseline, as well as 6 and 12 months after treatment initation.

Results

Anti-TNF treatment was highly effective in both disease, as the mean DAS28 decreased in RA, mean BASDAI decresead in AS. There were no significant change in the suPAR levels after 12 months of anti-TNF therapy, although resulted non-significant decrease (p<0,18) in RA patients with critical suPAR levels (>9 ng/ml). Baseline suPAR levels positively correlated with anti-CCP (p<0,001) and rheumatoid factor (p=0,024) in RA patients. Circulating suPAR levels did not correlate with DAS28, BASDAI or CRP.

Conclusion

In a mixed cohort of RA and AS patients, anti-TNF therapy did not affect the suPAR levels after 12 months. No correlations were observed between suPAR levels and CRP, DAS28, BASDAI. suPAR levels correlated with rheumatoid factor and anti-CCP. Based on these results suPAR may be a marker of autoimmunity rather than that of disease activity.

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