Anti-rheumatic treatment is not associated with reduction of pentraxin 3 in rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.
Anti-rheumatic treatment is not associated with reduction of pentraxin 3 in rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.
复制标题
DOI：
10.1371/journal.pone.0169830
复制
发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Hollan I
中科院分区：
文献类型：
--
作者：
Deyab G;Hokstad I;Whist JE;Småstuen MC;Agewall S;Lyberg T;Bottazzi B;Meroni PL;Leone R;Hjeltnes G;Hollan I
Pentraxin 3 被认为是炎症和心血管风险的标志物，但其在炎症性风湿性疾病 (IRD) 中的作用仍不确定。因此，我们想要检查抗风湿治疗是否降低 IRD 中的血清 PTX3 (s-PTX3) 水平，以及 s-PTX3 水平是否与其他炎症标志物和内皮功能 (EF) 相关。我们对来自 PSARA 研究的 114 名 IRD 患者在接受甲氨蝶呤 (MTX) 或抗肿瘤坏死因子 α（抗 TNF）治疗（联合或不联合 MTX 联合用药）治疗 6 周和 6 个月之前和之后检查了 s-PTX3、EF 和确定的炎症生物标志物。所有 IRD 诊断中的 s-PTX3 水平均高于参考范围的上限。与已建立的炎症标志物，特别是 CRP 和 ESR 相比，s-PTX3 水平在抗风湿治疗 6 周和 6 个月后没有显着变化。 MTX 单药治疗和抗 TNF 治疗方案之间，s-PTX3 水平从基线到 6 周和 6 个月的变化没有差异。在粗略分析和调整分析中，CRP、ESR 和 EF 均与 s-PTX3 的变化无关。 IRD 患者的 s-PTX3 水平升高，与其他炎症标志物相比，该水平在 MTX 和/或抗 TNF 治疗后 6 个月内似乎没有改善。因此，s-PTX3可能反映了持续的免疫过程，甚至是炎症的致病因素，不受标准抗风湿治疗的抑制。此外，尽管 s-PTX3 被认为是心血管预后的有力预测因子，但它与 EF 无关。
Pentraxin 3 is proposed to be a marker of inflammation and cardiovascular risk, but its role in inflammatory rheumatic diseases (IRDs) is still uncertain. Therefore, we wanted to examine if anti-rheumatic treatment reduced serum PTX3 (s-PTX3) levels in IRDs, and if s-PTX3 levels were related to other markers of inflammation and to endothelial function (EF). We examined s-PTX3, EF and established inflammatory biomarkers in 114 IRD patients from the PSARA study before and after 6 weeks and 6 months of treatment with methotrexate (MTX) or anti-tumor necrosis factor alpha (anti-TNF) therapy with or without MTX co-medication. s-PTX3 levels in all IRD diagnoses were above the upper limit of the reference range. In contrast to established inflammatory markers, in particular CRP and ESR, s-PTX3 levels did not change significantly after 6 weeks and 6 months of anti-rheumatic therapy. There was no difference in change in s-PTX3 levels from baseline to 6 weeks and 6 months between MTX monotherapy and anti-TNF regimens. CRP, ESR and EF were not related to changes in s-PTX3 neither in crude nor adjusted analyses. IRD patients have increased s-PTX3 levels, which, in contrast to other inflammatory markers, do not seem to improve within 6 months of therapy with MTX and/or anti-TNF. Thus, s-PTX3 might reflect a persisting immune process, even a causal factor of inflammation, not inhibited by the standard anti-rheumatic treatment. Furthermore, even though s-PTX3 is thought to be a strong predictor of cardiovascular prognosis, it was not related to EF.