血清炎性因子水平与慢性阻塞性肺疾病继发肺动脉高压的相关性研究

The relationship between inflammatory mediators and pulmonary hypertension in patients with chronic obstructive pulmonary disease

目的通过检测血清脑钠肽、内皮素-1、C反应蛋白及肿瘤坏死因子（TNF）-α等炎性因子的水平，观察全身炎症反应与COPD继发肺动脉高压的关系。方法北京世纪坛医院呼吸科2006年1月至2010年12月收治的89例COPD患者，其中男67例，女22例，平均年龄（70±7）岁，平均FEV。占预测值％为（47＋13）％。心脏超声测定肺动脉压力；按ERS推荐的步骤行诱导痰检测，酶联免疫吸附法测定血清脑钠肽、内皮素-1、TNF-α水平；化学发光免疫法测定高敏感度血清C反应蛋白。结果89例中42例伴肺动脉高压，为肺动脉高压组；47例不伴肺动脉高压。伴肺动脉高压者血清C反应蛋白[中位51．4mg／L（20．1～92．0）mg／L]、内皮素-1[中位含量5．9ng／L（3．7—10．4）ng／L]、脑钠肽[中位303．2ng／L（112．5～824．7）ng／L]明显高于不伴肺动脉高压的患者[C反应蛋白中位含量26．7mg／L（11．5～62．9）mg／L、内皮素一1中位含量2．1ng／L（1．3—4．7）ng／L、脑钠肽中位含量143．7ng／L（85．5～306．7）ng／L]；伴肺动脉高压组TNF-α[中位含量分别为8．5ng／L（4．8～13．7）ng／L]与不伴肺动脉高压组[6．7ng／L（3．2—10．3）ng／L]比较无明显差别。多元线性回归分析结果显示，PaO：、血清C反应蛋白水平及脑钠肽水平（均P〈0．05）是收缩期肺动脉压升高的独立预测因素。结论血清C反应蛋白、内皮素-1和脑钠肽水平的升高与COPD患者中肺动脉压升高相关，提示全身炎症可能参与了COPD继发肺动脉高压的形成。

Objective The levels of C-reactive protein （CRP）, tumor necrosis factor（TNF）-ct, brain natriuretic peptide （BNP） and endothelin-1 （ET-1） were investigated to analyze the systemic inflammation in chronic obstructive pulmonary disease （COPD） patients with and without pulmonary hypertension. Methods From January 2006 to December 2010, 89 patients with COPD were enrolled in our hospital. There were 67 males and 22 females, with a mean age of （70 ＋ 7） and a mean FEV1 of （47 ＋ 13） %. Pulmonary pressure was assessed by Doppler echocardiography. The levels of plasma BNP, TNF-α and ET-1 were measured by enzyme-linked immunosorbent assay kits. High-sensitivity plasma CRP level was assessed by chemiluminescent immunoassay. Results Forty-two patients were classified as COPD with pulmonary hypertension group and 47 patients as COPD without pulmonary hypertension group. The level of CRP[51.4 mg/L （20. 1 - 92. 0） mg/L], ET-1 [5.9 ng/L （3.7 - 10. 4） ng/L] and BNP[303.2 ng/L （112. 5- 824. 7 ）ng/L] in patients with pulmonary hypertension were significantly higher than in that in patients without hypertension, CRP [ 26. 7 mg/L （ 11.5 - 62. 9 ） mg/L ], ET-1 [ 2. 1 ng/L （ 1.3 - 4. 7 ） ng/L] and BNP[ 143.7 ng/L （ 85.5 - 306. 7 ） ng/L]. The level of TNF-c~ showed no difference between the 2 groups[8.5 ng/L （4. 8 - 13.7 ） ng/L and 6. 7 ng/L （ 3.2 - 10. 3 ） ng/L], respectively. Multivariate analysis showed that PaO2 （ P 〈 0. 05 ）, CRP （ P 〈 0. 05 ） and BNP （ P 〈 0. 05 ） could predict pulmonary hypertension independently. Conclusion The level of CRP, ET-land BNP were related to pulmonary hypertension in COPD patients, suggesting that systemic inflammation play a role in the pathogenesis of pulmonary hypertension in COPD.