Increased levels of soluble TNF-like cytokine 1A in ankylosing spondylitis

巴斯代人 医学 巴斯菲 强直性脊柱炎 阿达木单抗 依那西普 内科学 英夫利昔单抗 胃肠病学 细胞因子 肿瘤坏死因子α 脊柱炎 免疫学 疾病 银屑病性关节炎
作者
Maria Konsta,Giorgos Bamias,Maria G. Tektonidou,P. Christopoulos,Alexios Iliopoulos,PP Sfikakis
出处
期刊:Rheumatology [Oxford University Press]
卷期号:52 (3): 448-451 被引量:38
标识
DOI:10.1093/rheumatology/kes316
摘要

Objective. To determine the expression of soluble TNF-like cytokine 1A (sTL1A), a new member of the TNF superfamily, in patients with AS. Methods. Seventy-five consecutive patients with AS [61 males, mean (s.d.) age: 47.2 (15.5) years, disease duration: 20.3 (13.9) years] were included in this study. Forty-four patients were anti-TNF treatment naïve, whereas the remaining patients were on infliximab (n = 21), adalimumab (n = 3) or etanercept (n = 7). The patients' perceived disease activity was recorded by BASDAI and AS DAS using serum CRP levels (ASDAS-CRP), whereas functional status was assessed by BASFI and measurements of spinal mobility (AS Metrology). Serum concentrations of TL1A were measured by ELISA. Twenty-five age- and sex-matched healthy individuals served as controls. Results. Anti-TNF treatment-naïve patients demonstrated a 2.6-fold higher sTL1A average value [mean (s.e.m.) 581 (157.5) pg/ml] compared with healthy controls [226.7 (48.24) pg/ml, P = 0.042]. The sTL1A levels of anti-TNF-treated patients [178 (42)] were significantly lower than anti-TNF treatment-naïve patients (3.3-fold decrease, P = 0.0038) and comparable to those of healthy controls. No significant association was found between sTL1A level and functional status (BASFI score, AS Metrology parameters) or CRP measured in the same sera; however, a positive correlation was observed between individual levels of sTL1A and both BASDAI (P = 0.008) and ASDAS-CRP (P = 0.058) scores suggesting that sTL1A levels may reflect disease activity in patients with AS. Conclusion. TL1A is up-regulated in AS, associates with disease activity and is influenced by anti-TNF treatment, suggesting that TL1A may be of pathogenic and potentially of therapeutic importance in AS patients.
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