Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose
The interleukin-20 (IL-20) is a pro-inflammatory cytokine of the IL-10 family and sequence amino acid is very similar. It has been reported to be involved in the pathogenesis of several autoimmune diseases, but pathophysiological importance is poorly understood. TNF alpha plays an important role in AS patients with axial and peripheral joint involvement. It has been reported that TNF alpha induce IL-20 in macrophage and synovial cells. For this reason, we investigated serum IL-20 levels in AS patients with axial and peripheral joint involvement who had not received anti- TNF treatment.
Methods
63 patients with AS (11 female, 52 male) and 17 healthy controls (2 female, 15 male; mean age 26.5 ± 6.9 years) were enrolled in this study. Thirty-eight of the AS patients were axial involvement (mean age; 25,9 ± 7.2 years, median disease duration 7 years) and the other 24 patients were peripheral joint involvement (mean age; 27.3 ± 6.9 years, median disease duration; 9 years). Serum IL-20 levels were determined by ELISA.
Results
The median serum IL-20 levels were 55,2 pg/ml in healthy controls, 308.5 pg/ml in the patients with peripheral joint involvement and 109.3 pg/ml in the patients with axial involvement. Serum IL-20 levels in patients with AS were significantly higher than in healthy controls (p<0.001). Serum IL-20 levels were significantly high in the patients with peripheral joint involvement compared with in the patients with axial involvement (p<0.001). in the patients with peripheral joint involvement, there are statistically significant correlation between serum IL-20 and serum CRP and ESR (r=0.645, p <0.001, and r=0.588, p<0.001 respectively). In the patients with axial involvement, it was not correlated with CRP and ESR (r=0.262, p=0.298 and r=0.292, p=0.355 respectively).
Conclusion
Serum IL-20 levels are high in the AS patients with peripheral joint involvement and, correlated with CRP and ESR. So, it may be involved in pathogenesis of the disease.
Disclosure:
G. Keskin,
None;
B. Mavi,
None;
L. Ozisik,
None;
R. Ilikci,
None;
M. Yildiz,
None.
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