C-reactive protein and risk of venous thromboembolism: results from a population-based case-crossover study.

C-reactive protein and risk of venous thromboembolism: results from a population-based case-crossover study.
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DOI:
10.3324/haematol.2017.186957
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发表时间:
2018-07
期刊:
影响因子:
10.1
通讯作者:
Hansen JB
Hansen JB
中科院分区:
医学1区
文献类型:
--
作者:
Grimnes G;Isaksen T;Tichelaar YIGV;Brox J;Brækkan SK;Hansen JB

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长期低度炎症似乎不是静脉血栓栓塞症的危险因素。无论原因如何,急性炎症对静脉血栓栓塞症风险的影响很少被研究。我们的目的是通过C反应蛋白评估急性炎症对静脉血栓栓塞症的短期风险的影响。我们对从普通人群招募的静脉血栓栓塞症患者(n=707)进行了病例交叉研究。从事件发生前90天(危险期)和之前4个90天控制期的医院记录中检索有关诱因和C反应蛋白水平的信息。条件Logistic回归用于获得自然对数(Ln)转化的C反应蛋白从控制期到危险期变化的β系数,并确定相应的静脉血栓栓塞症的优势比。C反应蛋白中位数危险期为107 mg/L,控制期为7 mg/L~16 mg/L。C反应蛋白水平在危险期比控制期高58%(95%可信区间39-77%)。Ln-C-反应蛋白增加一个单位与静脉血栓栓塞症风险增加相关(OR 1.79,95%CI 1.48-2.16)。在对制动和感染进行调整后,风险估计值仅略有减弱。在分层分析中,在有(OR 1.55,95%CI 1.01-2.38)和无感染(OR 1.77,95%CI 1.22-2.57)的病例中,ln-C-反应蛋白与静脉血栓栓塞症的风险增加相关。总而言之,我们发现C反应蛋白评估的急性炎症是静脉血栓栓塞症的触发因素。
Long-term, low-grade inflammation does not seem to be a risk factor for venous thromboembolism. The impact of acute inflammation, regardless of cause, on risk of venous thromboembolism is scarcely studied. We aimed to investigate the impact of acute inflammation, assessed by C-reactive protein, on short-term risk of venous thromboembolism. We conducted a case-crossover study of patients with venous thromboembolism (n=707) recruited from a general population. Information on triggers and C-reactive protein levels were retrieved from hospital records during the 90 days before the event (hazard period) and in four preceding 90-day control periods. Conditional logistic regression was used to obtain β coefficients for change in natural log (ln) transformed C-reactive protein from control to hazard periods and to determine corresponding odds ratios for venous thromboembolism. Median C-reactive protein was 107 mg/L in the hazard period, and ranged from 7 mg/L to 16 mg/L in the control periods. The level of C-reactive protein was 58% (95% CI 39-77%) higher in the hazard period than in the control periods. A one-unit increase in ln-C-reactive protein was associated with increased risk of venous thromboembolism (OR 1.79, 95% CI 1.48-2.16). The risk estimates were only slightly attenuated after adjustment for immobilization and infection. In stratified analyses, ln-C-reactive protein was associated with increased risk of venous thromboembolism in cases with (OR 1.55, 95% CI 1.01-2.38) and without infection (OR 1.77, 95% CI 1.22-2.57). In conclusion, we found that acute inflammation, assessed by C-reactive protein, was a trigger for venous thromboembolism.
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