中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2011年
8期
531-536
,共6页
岳涛%范晓蕾%肖涟波%邓少华%李善%陈广洁%陈继红%张湛明%何东仪%倪立青
嶽濤%範曉蕾%肖漣波%鄧少華%李善%陳廣潔%陳繼紅%張湛明%何東儀%倪立青
악도%범효뢰%초련파%산소화%리선%진엄길%진계홍%장담명%하동의%예립청
关节炎%类风湿%人鼠嵌合单克隆抗体%RANK%RANKL%骨保护素
關節炎%類風濕%人鼠嵌閤單剋隆抗體%RANK%RANKL%骨保護素
관절염%류풍습%인서감합단극륭항체%RANK%RANKL%골보호소
Arthritis,rheumatoid Infliximab%RANK%RANKL%Osteoprotegerin
目的 探讨重组抗肿瘤坏死因子(TNF)-α人鼠嵌合单克隆抗体(Infliximab)对类风湿关节炎(RA)患者外周血核因子κB受体因子(RANK)/核因子κB受体活化因子(RANKL)/骨保护素系统的影响.方法 50例经严格筛选的类风湿关节炎(RA)患者按随机分配原则分为2组.一组患者接受Infliximab(3 mg/kg)+甲氨蝶呤治疗;一组患者接受甲氨蝶呤单独治疗作为对照,分别于0、2、6、14周给药.观察0周与18周Infliximab治疗组与对照组患者相关临床指标的改变,对比外周血中RANK、RANKL mRNA表达情况以及血清中骨保护素蛋白水平的变化.用t检验和x2检验做统计学分析.结果 经Infliximab治疗后,在RA患者关节放射成像中,可以观察到骨破坏程度有减缓趋势.与对照组比较,Infliximab治疗组(病史＞1年)患者骨丢失情况得到控制;Infliximab治疗组(0周:80.25;18周:63.2)与对照组(0周:83.37;18周:30.87)患者外周血中RANK、RANKL mRNA表达水平均下降(P＞0.05);与对照组比较,Infliximab可使RA患者外周血骨保护素/RANKL比值下降趋势减缓.虽然,经甲氨蝶呤或Infliximab+甲氨蝶呤治疗后,对照组[0周:(238±15)pg/ml;18周:(118±l0)pg/ml]和Infliximab治疗组[0周:(223±6)pg/ml;18周:(162±6)pg/ml)]患者血清中骨保护素水平均下降(P＞0.05),但Infliximab治疗组患者血清骨保护素下降趋势得以减缓.结论 RA患者经Infliximab联合甲氨蝶呤治疗后,骨破坏受到抑制,其作用机制可能是部分通过对RANK/RANKL/骨保护素系统的调节来行使的.
目的 探討重組抗腫瘤壞死因子(TNF)-α人鼠嵌閤單剋隆抗體(Infliximab)對類風濕關節炎(RA)患者外週血覈因子κB受體因子(RANK)/覈因子κB受體活化因子(RANKL)/骨保護素繫統的影響.方法 50例經嚴格篩選的類風濕關節炎(RA)患者按隨機分配原則分為2組.一組患者接受Infliximab(3 mg/kg)+甲氨蝶呤治療;一組患者接受甲氨蝶呤單獨治療作為對照,分彆于0、2、6、14週給藥.觀察0週與18週Infliximab治療組與對照組患者相關臨床指標的改變,對比外週血中RANK、RANKL mRNA錶達情況以及血清中骨保護素蛋白水平的變化.用t檢驗和x2檢驗做統計學分析.結果 經Infliximab治療後,在RA患者關節放射成像中,可以觀察到骨破壞程度有減緩趨勢.與對照組比較,Infliximab治療組(病史＞1年)患者骨丟失情況得到控製;Infliximab治療組(0週:80.25;18週:63.2)與對照組(0週:83.37;18週:30.87)患者外週血中RANK、RANKL mRNA錶達水平均下降(P＞0.05);與對照組比較,Infliximab可使RA患者外週血骨保護素/RANKL比值下降趨勢減緩.雖然,經甲氨蝶呤或Infliximab+甲氨蝶呤治療後,對照組[0週:(238±15)pg/ml;18週:(118±l0)pg/ml]和Infliximab治療組[0週:(223±6)pg/ml;18週:(162±6)pg/ml)]患者血清中骨保護素水平均下降(P＞0.05),但Infliximab治療組患者血清骨保護素下降趨勢得以減緩.結論 RA患者經Infliximab聯閤甲氨蝶呤治療後,骨破壞受到抑製,其作用機製可能是部分通過對RANK/RANKL/骨保護素繫統的調節來行使的.
목적 탐토중조항종류배사인자(TNF)-α인서감합단극륭항체(Infliximab)대류풍습관절염(RA)환자외주혈핵인자κB수체인자(RANK)/핵인자κB수체활화인자(RANKL)/골보호소계통적영향.방법 50례경엄격사선적류풍습관절염(RA)환자안수궤분배원칙분위2조.일조환자접수Infliximab(3 mg/kg)+갑안접령치료;일조환자접수갑안접령단독치료작위대조,분별우0、2、6、14주급약.관찰0주여18주Infliximab치료조여대조조환자상관림상지표적개변,대비외주혈중RANK、RANKL mRNA표체정황이급혈청중골보호소단백수평적변화.용t검험화x2검험주통계학분석.결과 경Infliximab치료후,재RA환자관절방사성상중,가이관찰도골파배정도유감완추세.여대조조비교,Infliximab치료조(병사＞1년)환자골주실정황득도공제;Infliximab치료조(0주:80.25;18주:63.2)여대조조(0주:83.37;18주:30.87)환자외주혈중RANK、RANKL mRNA표체수평균하강(P＞0.05);여대조조비교,Infliximab가사RA환자외주혈골보호소/RANKL비치하강추세감완.수연,경갑안접령혹Infliximab+갑안접령치료후,대조조[0주:(238±15)pg/ml;18주:(118±l0)pg/ml]화Infliximab치료조[0주:(223±6)pg/ml;18주:(162±6)pg/ml)]환자혈청중골보호소수평균하강(P＞0.05),단Infliximab치료조환자혈청골보호소하강추세득이감완.결론 RA환자경Infliximab연합갑안접령치료후,골파배수도억제,기작용궤제가능시부분통과대RANK/RANKL/골보호소계통적조절래행사적.
Objective Infliximab is a kind of recombinant human mouse chimeric anti-tumor necrosis factor monoclonal antibody. Here we aimed to examine the impact of infliximab therapy on RANK/RANKL/OPG system in the peripheral blood of rheumatoid arthritis (RA) patients. Methods Fifty patients with RA were rigorously screened and randomly divided into 2 groups. One group was treated with infliximab (3 mg/kg)and methotrexate (MTX). As control, the other group was treated with MTX alone. Infliximab was administered at weeks 0, 2, 6 and 14. The expression of RANK, RANKL mRNA in the peripheral blood, serum OPG and clinical indicators changes at week 0 and 18 were compared.x2-test or t-test were used for statistical analysis.Results After treated with infliximab, bone damage of joints were slowed down when examined by radiography in RA patients compared with the control group. And the ratio of OPG/RANKL was also decreased in RA peripheral blood (w0: 80.25;w 18: 63.2); (control group w0: 83.37; w18: 30.87)(P＞0.05). Although after the treatment with either MTX alone [w0: (238±15) pg/ml; w18: (118±10) pg/ml] or infliximab combined with MTX [(w0: (223.1±6.2) pg/ml; w18:(162.4±5.5) pg/ml], the serum levels of OPG were all decreased (P＞0.05), the level of OPG in infliximab treatment group was declined slower than those in the control group. Conclusion RA bone destruction can be inhibited by the combination therapy of infliximab and MTX. The mechanism may be partly through the RANK/RANKL/OPG system.
