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
46-50
,共5页
李海波%刘荣清%池淑红%张雪梅%杨丽娟
李海波%劉榮清%池淑紅%張雪梅%楊麗娟
리해파%류영청%지숙홍%장설매%양려연
肿瘤坏死因子拮抗剂%关节炎,类风湿%骨量%骨密度
腫瘤壞死因子拮抗劑%關節炎,類風濕%骨量%骨密度
종류배사인자길항제%관절염,류풍습%골량%골밀도
Tumor necrosis factor-α inhibitor%Arthritis,rheumatoid%Bone mass%Bone mineral density
目的 研究TNF-α拮抗剂治疗对已出现骨量减少的活动性RA患者骨密度的影响.方法 将62例合并骨量减少的活动性RA患者分为2组.所有患者均服用碳酸钙0.5 g/d及阿法骨化醇0.25 μg/d,试验组皮下注射重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(每周50 mg)或阿达木单抗(每2周40 mg),对照组口服甲氨蝶呤(每周10 mg),连续用药12个月.使用双能X线吸收仪测量基线时、6个月及12个月时的腰椎(L2-4)、股骨颈、大转子、Ward三角的骨密度值;同时检测骨代谢标志物Ⅰ型原胶原N-端前肽(PINP)和血清Ⅰ型胶原交联C-末端肽(CTX-Ⅰ).通过比较上述指标在治疗前后组间及组内的差异来评价TNF-α拮抗剂对骨密度的影响,统计学方法采用t检验及x2检验.结果 ①6个月时试验组腰椎、股骨颈及大转子的骨密度分别为(0.68±0.08)、(0.63±0.08)、(0.61±0.10) g/cm2,对照组上述3部位的骨密度分别为(0.65±0.06)、(0.58±0.09)、(0.56±0.07)g/cm2,试验组高于对照组(t=2.269,P=0.027;t=2.111,P=0.040; t=2.203,P=0.032).12个月时试验组的骨密度均明显高于对照组[腰椎(0.68±0.07)g/cm2和(0.62±0.08) g/cm2,t=5.115,P<0.01;股骨颈(0.63±0.08) g/cm2和(0.56±0.08) g/cm2,t=3.475,P=0.001;Ward三角(0.60±0.08) g/cm2和(0.56±0.08) g/cm2,t=2.309,P=0.025;大转子(0.61±0.10)g/cm2和(0.53±0.08) g/cm2,t=3.254,P=0.002].②与基线时对比试验组腰椎骨密度出现上升[(0.66±0.08)∥cm2和(0.68±0.07) g/cm2,t=3.411,P=O.001],而对照组腰椎骨密度表现为下降.③与基线时对比试验组CTX-Ⅰ水平明显下降,基线时CTX-Ⅰ为[(0.46±0.22) ng/ml],而6个月时为[(0.33±0.21) ng/ml] (t=5.548,P<0.01),12个月时为[(0.31±0.21) ng/ml](t=5.974,P<0.01);而对照组则没有出现下降.2组的骨形成标志物PINP在整个研究过程中无显著性变化.结论 TNF-α拮抗剂治疗表现出阻止了已出现骨量减少的活动性RA患者腰椎及髋部骨密度的继续下降.
目的 研究TNF-α拮抗劑治療對已齣現骨量減少的活動性RA患者骨密度的影響.方法 將62例閤併骨量減少的活動性RA患者分為2組.所有患者均服用碳痠鈣0.5 g/d及阿法骨化醇0.25 μg/d,試驗組皮下註射重組人Ⅱ型腫瘤壞死因子受體-抗體融閤蛋白(每週50 mg)或阿達木單抗(每2週40 mg),對照組口服甲氨蝶呤(每週10 mg),連續用藥12箇月.使用雙能X線吸收儀測量基線時、6箇月及12箇月時的腰椎(L2-4)、股骨頸、大轉子、Ward三角的骨密度值;同時檢測骨代謝標誌物Ⅰ型原膠原N-耑前肽(PINP)和血清Ⅰ型膠原交聯C-末耑肽(CTX-Ⅰ).通過比較上述指標在治療前後組間及組內的差異來評價TNF-α拮抗劑對骨密度的影響,統計學方法採用t檢驗及x2檢驗.結果 ①6箇月時試驗組腰椎、股骨頸及大轉子的骨密度分彆為(0.68±0.08)、(0.63±0.08)、(0.61±0.10) g/cm2,對照組上述3部位的骨密度分彆為(0.65±0.06)、(0.58±0.09)、(0.56±0.07)g/cm2,試驗組高于對照組(t=2.269,P=0.027;t=2.111,P=0.040; t=2.203,P=0.032).12箇月時試驗組的骨密度均明顯高于對照組[腰椎(0.68±0.07)g/cm2和(0.62±0.08) g/cm2,t=5.115,P<0.01;股骨頸(0.63±0.08) g/cm2和(0.56±0.08) g/cm2,t=3.475,P=0.001;Ward三角(0.60±0.08) g/cm2和(0.56±0.08) g/cm2,t=2.309,P=0.025;大轉子(0.61±0.10)g/cm2和(0.53±0.08) g/cm2,t=3.254,P=0.002].②與基線時對比試驗組腰椎骨密度齣現上升[(0.66±0.08)∥cm2和(0.68±0.07) g/cm2,t=3.411,P=O.001],而對照組腰椎骨密度錶現為下降.③與基線時對比試驗組CTX-Ⅰ水平明顯下降,基線時CTX-Ⅰ為[(0.46±0.22) ng/ml],而6箇月時為[(0.33±0.21) ng/ml] (t=5.548,P<0.01),12箇月時為[(0.31±0.21) ng/ml](t=5.974,P<0.01);而對照組則沒有齣現下降.2組的骨形成標誌物PINP在整箇研究過程中無顯著性變化.結論 TNF-α拮抗劑治療錶現齣阻止瞭已齣現骨量減少的活動性RA患者腰椎及髖部骨密度的繼續下降.
목적 연구TNF-α길항제치료대이출현골량감소적활동성RA환자골밀도적영향.방법 장62례합병골량감소적활동성RA환자분위2조.소유환자균복용탄산개0.5 g/d급아법골화순0.25 μg/d,시험조피하주사중조인Ⅱ형종류배사인자수체-항체융합단백(매주50 mg)혹아체목단항(매2주40 mg),대조조구복갑안접령(매주10 mg),련속용약12개월.사용쌍능X선흡수의측량기선시、6개월급12개월시적요추(L2-4)、고골경、대전자、Ward삼각적골밀도치;동시검측골대사표지물Ⅰ형원효원N-단전태(PINP)화혈청Ⅰ형효원교련C-말단태(CTX-Ⅰ).통과비교상술지표재치료전후조간급조내적차이래평개TNF-α길항제대골밀도적영향,통계학방법채용t검험급x2검험.결과 ①6개월시시험조요추、고골경급대전자적골밀도분별위(0.68±0.08)、(0.63±0.08)、(0.61±0.10) g/cm2,대조조상술3부위적골밀도분별위(0.65±0.06)、(0.58±0.09)、(0.56±0.07)g/cm2,시험조고우대조조(t=2.269,P=0.027;t=2.111,P=0.040; t=2.203,P=0.032).12개월시시험조적골밀도균명현고우대조조[요추(0.68±0.07)g/cm2화(0.62±0.08) g/cm2,t=5.115,P<0.01;고골경(0.63±0.08) g/cm2화(0.56±0.08) g/cm2,t=3.475,P=0.001;Ward삼각(0.60±0.08) g/cm2화(0.56±0.08) g/cm2,t=2.309,P=0.025;대전자(0.61±0.10)g/cm2화(0.53±0.08) g/cm2,t=3.254,P=0.002].②여기선시대비시험조요추골밀도출현상승[(0.66±0.08)∥cm2화(0.68±0.07) g/cm2,t=3.411,P=O.001],이대조조요추골밀도표현위하강.③여기선시대비시험조CTX-Ⅰ수평명현하강,기선시CTX-Ⅰ위[(0.46±0.22) ng/ml],이6개월시위[(0.33±0.21) ng/ml] (t=5.548,P<0.01),12개월시위[(0.31±0.21) ng/ml](t=5.974,P<0.01);이대조조칙몰유출현하강.2조적골형성표지물PINP재정개연구과정중무현저성변화.결론 TNF-α길항제치료표현출조지료이출현골량감소적활동성RA환자요추급관부골밀도적계속하강.
Objective To explore the effect of tumor necrosis factor (TNF)-α inhibitors therapy on bone mineral density (BMD) in active rheumatoid arthritis (RA) patients with low bone mass.Methods Sixtytwo active RA patients with low bone mass were treated with a standard treatment of calcium carbonate 0.5 g/d and alfacalcidol 0.25 μg/d,and were divided into two groups.Patients of the control group were treated with methotrexate 10 mg per week,while patients of the experimental group were treated with combined recombinant human type Ⅱ tumor necrosis factor receptor-antibody fusion protein 50 mg per week or adalimumab 40 mg/2 week subcutaneously for 12 months with methotrexate.BMD of lumbar spine (L2-4),femoral neck,trochanter and Ward's triangle region by dual energy X-ray absorptiometry (DEXA),as well as the bone turnover markers serum C telopeptide of type-Ⅰ collagen (CTX-Ⅰ) and serum procollagen type-Ⅰ N propeptide (PINP) were measured by enzyme-linkedimmunosorbent assay (ELISA) in both groups at the baseline,treatment for six-month and twelve-month.T test and Chi-square test was used to process the data.Results ① After 6 months of treatment,the BMD of lumbar spine,femoral neck and trochanter in the group with TNF-α inhibitors were higher than the control group [(0.68±0.08) g/cm2 vs (0.65±0.06) g/cm2,t=2.269,P=0.027; (0.63±0.08) g/cm2 vs (0.58±0.09) g/cm2,t=2.111,P=0.040; (0.61±0.10) g/cm2 vs (0.56±0.07) g/cm2,t=2.203,P=0.032; respectively].And after 12 months,the BMD of all regions were significantly higher thanthe control group [spine,(0.68±0.07) g/cm2 vs (0.62±0.08) g/cm2,t=5.115,P=0.000; femoral neck,(0.63±0.08)g/cm2 vs (0.56±0.08) g/cm2,t=3.475,P=0.001; Ward's triangle region (0.60±0.08) g/cm2 vs (0.56±0.08) g/cm2,t=2.309,P=0.025; trochanter,(0.61±0.10) g/cm2 vs (0.53±0.08) g/cm2,t=3.254,P=0.002; respectively].② Compared to the baseline,BMD of lumbar spine was significantly decreased in the control group after 12 months.While in the group of TNF-α inhibitors,BMD of lumbar spine was increased[(0.66±0.08) g/cm2 vs (0.68±0.07)g/cm2,t=3.411,P=0.001].③ Compared to the baseline,CTX-Ⅰ,a marker of bone resorption was significantly decreased at 6 months and 12 months in the group with TNF-αinhibitors [6 months,(0.33±0.2) ng/ml vs (0.46±0.22) ng/ml,t=5.548,P<0.01; 12 months,(0.31±0.21) ng/ml vs (0.46±0.22) ng/ml,t=5.974,P<0.01],while this decline was not found in the control group.PINP,a marker of bone formation was stable in both 2 groups during the study.Conclusion In active RA patients with low bone mass,loss of BMD in the spine and hip can be arrested by the treatmentof TNF-α inhibitors.