医药前沿
醫藥前沿
의약전연
YIAYAO QIANYAN
2012年
35期
38-39
,共2页
慢性阻塞性肺疾病%肺动脉高压%C 反应蛋白%炎性因子
慢性阻塞性肺疾病%肺動脈高壓%C 反應蛋白%炎性因子
만성조새성폐질병%폐동맥고압%C 반응단백%염성인자
COPD%pulmonary hypertention%C-reactive protein%systemic inflammatory response
目的探讨系统性炎症反应与慢性阻塞性肺疾病(COPD)继发肺动脉高压的关系.方法69例 COPD 患者行心脏彩色多普勒超声,根据安静状态下收缩期的肺动脉压(SPAP)分为肺动脉高压组(SPAP ≥30mmHg)和单纯 COPD 组(SPAP<30mmHg),分别测定两组患者的血浆 C 反应蛋白、内皮素-1(ET-1)及肿瘤坏死因子(TNF)-α.结果肺动脉高压组(n=36)患者血浆 C 反应蛋白为7.5mg/L[(5.0~10.8)mg/L],内皮素-1为52.6pg/mL[(48.6~54.5)pg/mL],肿瘤坏死因子-α为35.9 pg/mL[(24.1~54.3)pg/mL],均明显高于单纯 COPD 组(n=33):C 反应蛋白为4.0mg/L[(1.5~5.5)mg/L],内皮素为46.0pg/mL[(44.8~53.7)pg/mL],肿瘤坏死因子-α为27.8 pg/mL[(19.7~40.1)pg/mL].肺动脉高压组患者 C 反应蛋白、内皮素-1、肿瘤坏死因子-α与收缩期的肺动脉压呈正相关(r 分别为0.45、0.61、0.56,P 均<0.05).结论 C 反应蛋白、内皮素-1及肿瘤坏死因子-α与 COPD 患者肺动脉压力升高有关,提示炎症反应是慢性阻塞性肺疾病(COPD)继发肺动脉高压形成的重要因素.
目的探討繫統性炎癥反應與慢性阻塞性肺疾病(COPD)繼髮肺動脈高壓的關繫.方法69例 COPD 患者行心髒綵色多普勒超聲,根據安靜狀態下收縮期的肺動脈壓(SPAP)分為肺動脈高壓組(SPAP ≥30mmHg)和單純 COPD 組(SPAP<30mmHg),分彆測定兩組患者的血漿 C 反應蛋白、內皮素-1(ET-1)及腫瘤壞死因子(TNF)-α.結果肺動脈高壓組(n=36)患者血漿 C 反應蛋白為7.5mg/L[(5.0~10.8)mg/L],內皮素-1為52.6pg/mL[(48.6~54.5)pg/mL],腫瘤壞死因子-α為35.9 pg/mL[(24.1~54.3)pg/mL],均明顯高于單純 COPD 組(n=33):C 反應蛋白為4.0mg/L[(1.5~5.5)mg/L],內皮素為46.0pg/mL[(44.8~53.7)pg/mL],腫瘤壞死因子-α為27.8 pg/mL[(19.7~40.1)pg/mL].肺動脈高壓組患者 C 反應蛋白、內皮素-1、腫瘤壞死因子-α與收縮期的肺動脈壓呈正相關(r 分彆為0.45、0.61、0.56,P 均<0.05).結論 C 反應蛋白、內皮素-1及腫瘤壞死因子-α與 COPD 患者肺動脈壓力升高有關,提示炎癥反應是慢性阻塞性肺疾病(COPD)繼髮肺動脈高壓形成的重要因素.
목적탐토계통성염증반응여만성조새성폐질병(COPD)계발폐동맥고압적관계.방법69례 COPD 환자행심장채색다보륵초성,근거안정상태하수축기적폐동맥압(SPAP)분위폐동맥고압조(SPAP ≥30mmHg)화단순 COPD 조(SPAP<30mmHg),분별측정량조환자적혈장 C 반응단백、내피소-1(ET-1)급종류배사인자(TNF)-α.결과폐동맥고압조(n=36)환자혈장 C 반응단백위7.5mg/L[(5.0~10.8)mg/L],내피소-1위52.6pg/mL[(48.6~54.5)pg/mL],종류배사인자-α위35.9 pg/mL[(24.1~54.3)pg/mL],균명현고우단순 COPD 조(n=33):C 반응단백위4.0mg/L[(1.5~5.5)mg/L],내피소위46.0pg/mL[(44.8~53.7)pg/mL],종류배사인자-α위27.8 pg/mL[(19.7~40.1)pg/mL].폐동맥고압조환자 C 반응단백、내피소-1、종류배사인자-α여수축기적폐동맥압정정상관(r 분별위0.45、0.61、0.56,P 균<0.05).결론 C 반응단백、내피소-1급종류배사인자-α여 COPD 환자폐동맥압력승고유관,제시염증반응시만성조새성폐질병(COPD)계발폐동맥고압형성적중요인소.
Objective To investigate the relationship between systemic inflammatory response and pulmonary hypertention in chronic obstructive pulmonary disease(COPD). Methods Sixty-nine COPD patients were enroled in this study. Al subjects were divided into two groups according to color Doppler ultrasound of the heart, which defined as pulmonary hypertention and non pulmonary hypertention group.The plasma CRP,ET-1 and TNF-α were completed on each COPD patient. Results CRP, ET-1 and TNF-α showed significantly higher values in pulmonary hypertention group(7.5mg/L[(5.0 ~ 10.8)mg/L],52.6pg/mL[(48.6 ~ 54.5)pg/mL],35.9 pg/mL[(24.1 ~ 54.3)pg/mL],respectively) compared with non pulmonary hypertention group(4.0mg/L[(1.5 ~ 5.5)mg/L], 46.0pg/mL[(44.8 ~ 53.7)pg/mL], 27.8 pg/mL[(19.7 ~ 40.1)pg/mL],respectively).In pulmonary hypertention group SPAP was positively correlated with CRP,ET-1 and TNF-α respectively (r=0.45,0.61,0.56,P<0.05). Conclusion inflammatory response is one of the factors which related to pulmonary hypertention in COPD patients.
