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肿瘤坏死因子-α 阻断治疗可降低活动期类风湿关节炎患者的循环 N 末端脑利钠肽前体水平:一项前瞻性队列研究的结果。

Tumour necrosis factor {alpha} blockade reduces circulating N-terminal pro-brain natriuretic peptide levels in patients with active rheumatoid arthritis: results from a prospective cohort study.

机构信息

Correspondence to Dr Mike Peters, VU University Medical Centre, P O Box 7057, 1007 MB Amsterdam, The Netherlands.

出版信息

Ann Rheum Dis. 2010 Jul;69(7):1281-5. doi: 10.1136/ard.2009.119412. Epub 2009 Nov 23.

Abstract

BACKGROUND

Patients with rheumatoid arthritis (RA) are at increased risk of heart failure and vascular events. Small increases in circulating N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with an increased risk of a cardiovascular event, and high levels signal left ventricular dysfunction. Data on the effects of tumour necrosis factor alpha(TNFalpha) blocking agents on circulating NT-proBNP levels in patients with active RA are lacking but may be informative.

METHODS

171 consecutive patients with RA (28-joint disease activity score >3.2) without congestive heart failure (NYHA class III or IV) were scheduled to receive adalimumab once every 2 weeks. Serum NT-proBNP concentrations were measured simultaneously on stored baseline and 16-week samples. Paired sample t tests were used to observe differences in biomarkers before and after adalimumab administration. Correlations between the biomarkers and changes in circulating log NT-proBNP levels were evaluated with the Pearson test and multivariable linear regression analyses of correlates were performed (forward selection procedure).

RESULTS

Circulating levels of NT-proBNP decreased significantly after 16 weeks of adalimumab administration (median NT-proBNP 83.0 pg/ml vs 69.5 pg/ml, p=0.004). Changes in NT-proBNP levels were associated with changes in pulse pressure (r=0.18, p=0.02), systolic blood pressure (r=0.16, p=0.04) and erythrocyte sedimentation rate (r=0.18, p=0.02). On multivariable analysis, changes in pulse pressure and erythrocyte sedimentation rate remained independently associated with changes in circulating NT-proBNP levels.

CONCLUSIONS

These observations show that blocking TNFalpha in patients with RA without evident heart failure decreases NT-proBNP levels by about 18%. This suggests no treatment-induced deterioration in cardiac function and a potential cardiovascular risk benefit.

摘要

背景

类风湿关节炎(RA)患者发生心力衰竭和血管事件的风险增加。循环 N 末端脑利钠肽前体(NT-proBNP)的小幅度升高与心血管事件风险增加相关,而高水平则提示左心室功能障碍。缺乏关于肿瘤坏死因子-α(TNFα)阻断剂对活动期 RA 患者循环 NT-proBNP 水平影响的数据,但可能具有信息性。

方法

171 例连续 RA 患者(28 关节疾病活动评分>3.2)无充血性心力衰竭(纽约心脏协会[NYHA]III 或 IV 级),计划每 2 周接受阿达木单抗一次。同时测量储存的基线和 16 周样本中的血清 NT-proBNP 浓度。采用配对样本 t 检验观察阿达木单抗给药前后生物标志物的差异。采用 Pearson 检验评估生物标志物与循环 log NT-proBNP 水平变化之间的相关性,并进行多变量线性回归分析(正向选择程序)。

结果

阿达木单抗治疗 16 周后,循环 NT-proBNP 水平显著降低(中位数 NT-proBNP 83.0 pg/ml 比 69.5 pg/ml,p=0.004)。NT-proBNP 水平的变化与脉压(r=0.18,p=0.02)、收缩压(r=0.16,p=0.04)和红细胞沉降率(r=0.18,p=0.02)的变化相关。多变量分析显示,脉压和红细胞沉降率的变化与循环 NT-proBNP 水平的变化独立相关。

结论

这些观察结果表明,在无明显心力衰竭的 RA 患者中阻断 TNFα 可使 NT-proBNP 水平降低约 18%。这表明没有治疗引起的心脏功能恶化,并可能具有心血管风险获益。

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