B型脑钠肽、超敏C反应蛋白、纤维蛋白原、D-二聚体及血气分析在慢性阻塞性肺疾病急性加重期合并肺动脉高压患者中的表达

Expressions of brain natriuretic peptide,fibrinogen,hypersensitive C-reactive protein,D-Dimer and arterial blood gas analysis in acute exacerbation of chronic obstructive pulmonary disease patients complicated with pulmonary hypertension

目的探讨血浆B型脑钠肽(BNP)、超敏C反应蛋白(hs-CRP)、纤维蛋白原(Fib)、D-二聚体(D-Dimer)水平及血气分析在慢性阻塞性肺病急性加重期(AECOPD)合并肺动脉高压(PH)患者中的表达及临床意义。方法选取135例AECOPD住院患者,分为单纯AECOPD组75例和AECOPD+PH组60例。采用超声心动图测定肺动脉收缩压力(PASP)值。比较2组患者血清BNP、D-Dimer、hs-CRP、Fib及动脉血气分析指标。结果 AECOPD+PH组患者hs-CRP、BNP、D-Dimer、动脉血二氧化碳分压[p(CO_2)]均显著高于AECOPD组(P<0.05),而AECOPD+PH组患者动脉血氧分压[p(O_2)]显著低于AECOPD组(P<0.05)。多元线性回归分析结果显示,hs-CRP、Fib、BNP、D-Dimer、p(CO_2)水平与肺动脉压呈正相关(P<0.05),p(O_2)与PASP呈负相关(P<0.05),hs-CRP、Fib、D-Dimer与BNP呈正相关(P<0.05)。结论 hs-CRP、Fib、BNP、D-Dimer参与了AECOPD合并肺动脉高压的形成,全身炎症在AECOPD继发肺动脉高压的发病中发挥重要作用。

Objective To explore the expressions and significance of brain natriuretic peptide(BNP),hypersensitive C-reactive protein(hs-CRP),human fibrinogen(Fib),D-Dimer and blood gas analysis in patients with acute exacerbation of chronic obstructive pulmonary disease(AECOPD)and pulmonary hypertension(PH).Methods Totally 135 patients with AECOPD were divided into single AECOPD group(n=75)and AECOPD+PH group(n=60).The value of pulmonary systolic pressure(PASP)was measured by echocardiography.Serum BNP,hs-CRP,D-Dimer,Fib levels and arterial blood gas analysis indexes such as p(CO 2)and p(O 2)were compared between two groups.Results The levels of hs-CRP,BNP,D-Dimer and p(CO 2)in AECOPD+PH group were significantly higher than those in AECOPD group(P<0.05),while p(O 2)in AECOPD+PH group was significantly lower than that in AECOPD group.Multiple linear regression analysis showed that the levels of hs-CRP,Fib,BNP,D-Dimer and p(CO 2)were positively correlated with pulmonary artery pressure(P<0.05),and p(O 2)was negatively correlated with PASP(P<0.05).Conclusion The hs-CRP,Fib,BNP,and D-Dimer participate in the formation of AECOPD complicated with pulmonary hypertension,and systemic inflammation plays an important role in the pathogenesis of AECOPD complicated with pulmonary hypertension.