天津医药

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强直性脊柱炎患者血清Dkk-1的检测及其临床意义

隋立1,张凯1,王毅2   

  1. 1. 天津市天津医院
    2. 天津医院
  • 收稿日期:2010-12-03 修回日期:2011-03-04 出版日期:2011-10-15 发布日期:2011-10-15
  • 通讯作者: 隋立

A study on the measurement of DKK-1 in the serum of ankylosing spondylitis patients

凯 张2,   

  • Received:2010-12-03 Revised:2011-03-04 Published:2011-10-15 Online:2011-10-15

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摘要： 目的 本研究检测强直性脊柱炎（ankylosing spondylitis，AS）患者血清中Dkk-l的表达水平，探讨其在AS疾病中的应用价值。方法 应用酶联免疫吸附法(ELISA)检测两组疾病活跃期AS患者血清中Dkk-1的表达水平，一组是14例未用任何抗肿瘤坏死因子（TNF）-α生物制剂治疗的AS患者，另一组是15例应用TNF-α生物制剂治疗3个月以上的AS患者。同时对比检测了8例未用TNF-α生物制剂治疗的疾病活跃期类风湿性关节炎（rheumatoid arthritis，RA）患者和20名正常对照个体血清Dkk-1的水平。AS患者的病情活动度采用（Bath AS Disease Activity Index, BASDAI）进行评估，RA患者的病情活动指数采用Disease Activity Score in 28 joints (DAS28)进行评估。所有研究对象均测定炎性指标ESR和CRP水平。结果 未用药AS患者血清中Dkk-l水平显著低于RA患者组（p=0.037）和正常对照组（p=0.012）。AS患者血清Dkk-l水平与BASDAI、ESR和CRP均无显著相关性。使用TNF-α生物制剂治疗的AS患者血清Dkk-l水平显著高于未用药治疗的AS患者（p=0.000）。结论 我们的研究发现，AS作为典型的骨形成性疾病其患者血循环中骨形成抑制因子Dkk-1的水平降低，血清Dkk-1的水平与炎症活跃程度无关。此外，TNF-α生物制剂可诱导AS患者血清Dkk-1的表达。

关键词: 脊柱炎, 强直性, Dkk-1

Abstract: Objective This study was undertaken to explore the expression of Dkk-1 and its potential role in patients with ankylosing spondylitis (AS). Methods Serum Dkk-1 levels were measured by sandwich enzyme linked immunosorbent assay (ELISA). Two groups of AS subjects were tested. The first group consisted of patients who have not been treated with biological agents. In the second group, patients had been receiving anti- TNFα treatment more than 12 weeks. These were compared to serum samples from 8 patients with rheumatoid arthritis (RA) and 20 healthy subjects. Disease activity assessment was performed using the Bath AS Disease Activity Index (BASDAI) in patients with AS, the Disease Activity Score in 28 joints (DAS28) in patients with RA. All patients with AS and RA had active disease. Markers of inflammation (erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP] levels) were measured in all patients. Results Serum Dkk-1 levels were significantly decreased in AS patients who have not been treated with biological agents as compared with patients with RA (p=0.037), and normal subjects (p=0.012). The BASDAI，ESR and CRP in patients with AS did not correlate with serum Dkk-1 levels. Patients with AS receiving anti-TNFα treatment had significantly higher serum Dkk-1 levels compared with patients with AS not receiving this treatment (p=0.000). Conclusion Our results indicate that the levels of serum Dkk-1 in patients with AS, a prototype bone-forming disease, is decrease. No association between circulating Dkk-1 levels and disease activity or markers of inflammation (ESR and CRP) in any AS patient group. Furthermore, TNFα could induce the expression of Dkk-1 in patients with AS.

Key words: Spondylitis, ankylosing, Dkk-1