中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2011年
12期
904-908
,共5页
蒋延文%庞莉%方秋红%马迎民
蔣延文%龐莉%方鞦紅%馬迎民
장연문%방리%방추홍%마영민
肺疾病,慢性阻塞性%C反应蛋白质%高血压,肺性%全身炎症反应综合征
肺疾病,慢性阻塞性%C反應蛋白質%高血壓,肺性%全身炎癥反應綜閤徵
폐질병,만성조새성%C반응단백질%고혈압,폐성%전신염증반응종합정
Pulmonary disease,chronic obstructive%C-reactive protein%Hypertension,pulmonary%Systemic inflammatory response syndrome
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FEV1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51.4 mg/L (20.1 ～92.0) mg/L]、内皮素-1[中位含量5.9 ng/L (3.7 ～10.4) ng/L]、脑钠肽[中位303.2 ng/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26.7 mg/L (11.5 ～62.9) mg/L、内皮素-1中位含量2.1 ng/L(1.3 ～4.7) ng/L、脑钠肽中位含量143.7 ng/L (85.5～306.7) ng/L]；伴肺动脉高压组TNF-α[中位含量分别为8.5 ng/L(4.8 ～13.7)ng/L]与不伴肺动脉高压组[6.7 ng/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,PaO2、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.
目的 通過檢測血清腦鈉肽、內皮素-1、C反應蛋白及腫瘤壞死因子(TNF)-α等炎性因子的水平,觀察全身炎癥反應與COPD繼髮肺動脈高壓的關繫.方法 北京世紀罈醫院呼吸科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,平均年齡(70±7)歲,平均FEV1佔預測值％為(47±13)％.心髒超聲測定肺動脈壓力；按ERS推薦的步驟行誘導痰檢測,酶聯免疫吸附法測定血清腦鈉肽、內皮素-1、TNF-α水平；化學髮光免疫法測定高敏感度血清C反應蛋白.結果 89例中42例伴肺動脈高壓,為肺動脈高壓組；47例不伴肺動脈高壓.伴肺動脈高壓者血清C反應蛋白[中位51.4 mg/L (20.1 ～92.0) mg/L]、內皮素-1[中位含量5.9 ng/L (3.7 ～10.4) ng/L]、腦鈉肽[中位303.2 ng/L( 112.5～824.7) ng/L]明顯高于不伴肺動脈高壓的患者[C反應蛋白中位含量26.7 mg/L (11.5 ～62.9) mg/L、內皮素-1中位含量2.1 ng/L(1.3 ～4.7) ng/L、腦鈉肽中位含量143.7 ng/L (85.5～306.7) ng/L]；伴肺動脈高壓組TNF-α[中位含量分彆為8.5 ng/L(4.8 ～13.7)ng/L]與不伴肺動脈高壓組[6.7 ng/L(3.2 ～ 10.3)ng/L]比較無明顯差彆.多元線性迴歸分析結果顯示,PaO2、血清C反應蛋白水平及腦鈉肽水平(均P＜0.05)是收縮期肺動脈壓升高的獨立預測因素.結論 血清C反應蛋白、內皮素-1和腦鈉肽水平的升高與COPD患者中肺動脈壓升高相關,提示全身炎癥可能參與瞭COPD繼髮肺動脈高壓的形成.
목적 통과검측혈청뇌납태、내피소-1、C반응단백급종류배사인자(TNF)-α등염성인자적수평,관찰전신염증반응여COPD계발폐동맥고압적관계.방법 북경세기단의원호흡과2006년1월지2010년12월수치적89례COPD환자,기중남67례,녀22례,평균년령(70±7)세,평균FEV1점예측치％위(47±13)％.심장초성측정폐동맥압력；안ERS추천적보취행유도담검측,매련면역흡부법측정혈청뇌납태、내피소-1、TNF-α수평；화학발광면역법측정고민감도혈청C반응단백.결과 89례중42례반폐동맥고압,위폐동맥고압조；47례불반폐동맥고압.반폐동맥고압자혈청C반응단백[중위51.4 mg/L (20.1 ～92.0) mg/L]、내피소-1[중위함량5.9 ng/L (3.7 ～10.4) ng/L]、뇌납태[중위303.2 ng/L( 112.5～824.7) ng/L]명현고우불반폐동맥고압적환자[C반응단백중위함량26.7 mg/L (11.5 ～62.9) mg/L、내피소-1중위함량2.1 ng/L(1.3 ～4.7) ng/L、뇌납태중위함량143.7 ng/L (85.5～306.7) ng/L]；반폐동맥고압조TNF-α[중위함량분별위8.5 ng/L(4.8 ～13.7)ng/L]여불반폐동맥고압조[6.7 ng/L(3.2 ～ 10.3)ng/L]비교무명현차별.다원선성회귀분석결과현시,PaO2、혈청C반응단백수평급뇌납태수평(균P＜0.05)시수축기폐동맥압승고적독립예측인소.결론 혈청C반응단백、내피소-1화뇌납태수평적승고여COPD환자중폐동맥압승고상관,제시전신염증가능삼여료COPD계발폐동맥고압적형성.
Objective The levels of C-reactive protein (CRP),tumor necrosis factor( TNF)-α,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-αand 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-α 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.
