首页> 外文期刊>Annals of the Rheumatic Diseases: A Journal of Clinical Rheumatology and Connective Tissue Research >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.
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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.

机译:肿瘤坏死因子α阻滞降低活动性类风湿关节炎患者的循环N末端脑钠肽水平:一项前瞻性队列研究的结果。

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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.
机译:背景:类风湿关节炎(RA)患者的心力衰竭和血管事件的风险增加。循环N末端脑钠肽(NT-proBNP)的少量增加与心血管事件的风险增加相关,并且高水平的信号表示左心功能不全。关于活动性RA患者中肿瘤坏死因子α(TNFalpha)阻断剂对循环NT-proBNP水平影响的数据尚缺乏,但可能是有益的。方法:计划连续171名无充血性心力衰竭(NYHA III或IV级)的RA(28关节疾病活动评分> 3.2)患者每两周接受一次阿达木单抗治疗。在储存的基线和16周样本中同时测量血清NT-proBNP浓度。配对样本t检验用于观察阿达木单抗给药前后的生物标志物差异。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,并进行相关性的多变量线性回归分析(正向选择程序)。结果:阿达木单抗给药16周后,NT-proBNP的循环水平显着下降(NT-proBNP中位数为83.0 pg / ml对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)的变化有关。在多变量分析中,脉压和红细胞沉降率的变化仍与循环NT-proBNP水平的变化独立相关。结论:这些观察结果表明,在没有明显心力衰竭的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,也没有潜在的心血管风险。

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