中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2015年
1期
21-25
,共5页
脊柱炎,强直性%肿瘤坏死因子-α%核因子-κB受体活化因子配体%Dickkopf-1
脊柱炎,彊直性%腫瘤壞死因子-α%覈因子-κB受體活化因子配體%Dickkopf-1
척주염,강직성%종류배사인자-α%핵인자-κB수체활화인자배체%Dickkopf-1
Spondylitis,ankylosing%Tumor necrosis factor-alpha%Receptor activator of nuclear factor-κB ligand%Dickkopf-1
目的 检测应用TNF-α拮抗剂治疗AS前后患者血清DKK-1和骨保护素、NF-κB受体活化因子配体(RANKL)和TNF-α水平,探讨抗TNF-α治疗对AS患者骨形成信号通路的影响.方法 自身前后对照,留取43例病历资料完整的AS患者接受TNF-α受体-抗体融合蛋白治疗12周前后血清样本.采用ELISA方法检测血清中DKK-1、骨保护素、RANKL和TNF-α水平.采用配对t检验及Person相关分析.结果 抗TNF-α治疗后患者VAS评分、晨僵时间、BASDAI、BASFI、ESR和CRP等疾病活动指标分别为[(2.7±2.0)cm,(7±4) min,1.1±1.1、0.8±1.2、(10±9) mm/1 h和(16±26)mg/L]较治疗前[(7.6±2.0)cm,(46±33) min,6.0±1.3、4.4±2.0、(39±29) mm/1 h和(76±43) mg/L]显著改善,差异均无统计学意义(t值分别为14.043、8.031、20.166、13.521、7.679、9.563、P＞0.05);治疗前后血清DKK-1[(3.3±1.5)μg/L与(3.2±1.3)μg/L]、骨保护素[(144±71) pg/ml与(136±62 pg/ml]及RANKL [(71±37) pg/ml与(68±30) pg/ml]没有变化(P＞0.05);治疗后TNF-α水平(55.0±50.6) pg/ml较治疗前(1.9±1.3) pg/ml明显升高(t=6.951,P＜0.05).DKK-1与TNF-α、RANKL、骨保护素、患者VAS、晨僵时间、BASDAI、BASFI、ESR和CRP均不相关,差异均无统计学意义(P＞0.05).结论 抗TNF-α治疗AS临床指标改善明显,但不宜骤然停药;血清DKK-1水平与AS患者炎症水平不相关,不受短期抗TNF-α治疗影响.
目的 檢測應用TNF-α拮抗劑治療AS前後患者血清DKK-1和骨保護素、NF-κB受體活化因子配體(RANKL)和TNF-α水平,探討抗TNF-α治療對AS患者骨形成信號通路的影響.方法 自身前後對照,留取43例病歷資料完整的AS患者接受TNF-α受體-抗體融閤蛋白治療12週前後血清樣本.採用ELISA方法檢測血清中DKK-1、骨保護素、RANKL和TNF-α水平.採用配對t檢驗及Person相關分析.結果 抗TNF-α治療後患者VAS評分、晨僵時間、BASDAI、BASFI、ESR和CRP等疾病活動指標分彆為[(2.7±2.0)cm,(7±4) min,1.1±1.1、0.8±1.2、(10±9) mm/1 h和(16±26)mg/L]較治療前[(7.6±2.0)cm,(46±33) min,6.0±1.3、4.4±2.0、(39±29) mm/1 h和(76±43) mg/L]顯著改善,差異均無統計學意義(t值分彆為14.043、8.031、20.166、13.521、7.679、9.563、P＞0.05);治療前後血清DKK-1[(3.3±1.5)μg/L與(3.2±1.3)μg/L]、骨保護素[(144±71) pg/ml與(136±62 pg/ml]及RANKL [(71±37) pg/ml與(68±30) pg/ml]沒有變化(P＞0.05);治療後TNF-α水平(55.0±50.6) pg/ml較治療前(1.9±1.3) pg/ml明顯升高(t=6.951,P＜0.05).DKK-1與TNF-α、RANKL、骨保護素、患者VAS、晨僵時間、BASDAI、BASFI、ESR和CRP均不相關,差異均無統計學意義(P＞0.05).結論 抗TNF-α治療AS臨床指標改善明顯,但不宜驟然停藥;血清DKK-1水平與AS患者炎癥水平不相關,不受短期抗TNF-α治療影響.
목적 검측응용TNF-α길항제치료AS전후환자혈청DKK-1화골보호소、NF-κB수체활화인자배체(RANKL)화TNF-α수평,탐토항TNF-α치료대AS환자골형성신호통로적영향.방법 자신전후대조,류취43례병력자료완정적AS환자접수TNF-α수체-항체융합단백치료12주전후혈청양본.채용ELISA방법검측혈청중DKK-1、골보호소、RANKL화TNF-α수평.채용배대t검험급Person상관분석.결과 항TNF-α치료후환자VAS평분、신강시간、BASDAI、BASFI、ESR화CRP등질병활동지표분별위[(2.7±2.0)cm,(7±4) min,1.1±1.1、0.8±1.2、(10±9) mm/1 h화(16±26)mg/L]교치료전[(7.6±2.0)cm,(46±33) min,6.0±1.3、4.4±2.0、(39±29) mm/1 h화(76±43) mg/L]현저개선,차이균무통계학의의(t치분별위14.043、8.031、20.166、13.521、7.679、9.563、P＞0.05);치료전후혈청DKK-1[(3.3±1.5)μg/L여(3.2±1.3)μg/L]、골보호소[(144±71) pg/ml여(136±62 pg/ml]급RANKL [(71±37) pg/ml여(68±30) pg/ml]몰유변화(P＞0.05);치료후TNF-α수평(55.0±50.6) pg/ml교치료전(1.9±1.3) pg/ml명현승고(t=6.951,P＜0.05).DKK-1여TNF-α、RANKL、골보호소、환자VAS、신강시간、BASDAI、BASFI、ESR화CRP균불상관,차이균무통계학의의(P＞0.05).결론 항TNF-α치료AS림상지표개선명현,단불의취연정약;혈청DKK-1수평여AS환자염증수평불상관,불수단기항TNF-α치료영향.
Objective Dickkopf-1 (DKK-1) is an antagonist of the Wnt signaling pathway of bone formation and it is the target gene of TNF.When DKK-1 is inhibited,osteoprotegerin (OPG) would increase,OPG can antagonize bone erosion caused by receptor activator of NF-κB ligand (RANKL).Detection the levelsof serum DKK-1,OPG,RANKL and TNF-α of patients with AS before and after applying TNF-α antagonist,the effects of anti-TNF-α treatment on signaling pathway of bone formation was explored.Methods Medical records and serum samples of 43 AS patients receiving TNF-α receptor-Ⅱ IgG Fc fusion protein for 12 weeks were collected and the levels of serum DKK-1,OPG,RANKL and TNF-α were detected by enzyme-linked immunosorbent assay.Paired t-test and Person's correlation analysis were used for data analysis.Results Disease activity indexes in AS patients with anti-TNF-α treatment,including VAS score,time of morning stiffness,BASDAI,BASFI,ESR and CRP,which were [(2.7±2.0) cm,(7±4) min,1.1±1.1,0.8±1.2,(10±9) mm/1 h and (16±26) mg/L] respectively,were reduced when compared with those before treatment,[(7.6±1.9) cm,(46±33) min,6.0±1.3,4.4±2.0,(39±29) mm/1 h and (76±43) mg/L] respectively,and the differences were statistically significant (P＜0.05).Serum levels of DKK-1,(3.3±1.5) μg/L vs (3.2±1.3) μg/L,OPG,(144±71) pg/ml vs (136±62) pg/ml,and RANKL,(71±37) pg/ml vs (68±30) pg/ml,were not changed (t=14.043,8.031,20.166,13.521,7.679,9.563,all P＞0.05).The levels of TNF-α increased from (1.9±1.3) pg/ml to (55.0±50.6) pg/ml (t=6.951,P＜0.05).There were no relations between DKK-1 and TNF-α,RANKUOPG,patient VAS,duration of morning stiffness,BASDAI,BASFI,ESR and CRP,allP＞0.05.Conclusion Clinical indicators are improved significantly by anti-TNF-α therapy; however,it should not be withdrawal suddenly.There is no relationship between serum levels of DKK-1 and level of inflammation in AS patients.
