出 处:《中国综合临床》2009年第6期614-617,共4页Clinical Medicine of China
摘 要:目的探讨慢性阻塞性肺疾病(COPD)相关性肺动脉高压(PAH)的发生率及其与诱导痰炎症细胞、血清超敏C-反应蛋白(hs—CRP)、IL-8及TNF—α之间的关系。方法对COPD稳定期患者68例和健康体检者30例常规行肺动脉、动脉血气分析、X线胸片等检查。对诱导痰进行炎症细胞分类计数,免疫比浊法测定血清hs-CRP,ELISA法测定血清IL-8与TNF-α。COPD组行超声心动图检查推算肺动脉收缩压(PASP),并测量心脏有关腔室大小。根据PASP〉30mmHg,将COPD患者分为PAH组和单纯COPD组。结果COPD组患者PAH发生率53%(36/68),分层研究发现轻、中、重度COPD患者PAH发生率分别为27%(3/11)、38%(5/13)和64%(28/44),差异具有统计学意义(χ^2=6.020,P〈0.05)。PAH组PASP与右心室游离壁厚度(RVWT)显著高于单纯COPD组,差异具有统计学意义[PASP:PAH组(52±15)mmHg,单纯COPD组(23±12)mmHg。t=3.32,P〈0.01;PVWT:PAH组(5.03±1.04)mm,单纯COPD组(3.78±0.57)mm,t=2.36,P〈0.05)]。PAH组诱导痰炎症细胞总数、中性粒细胞计数、血清hs—CRP、IL-8及TNF-α水平明显高于单纯COPD组和健康对照组,差异具有统计学意义[痰炎症细胞总数:PAH组(2.84±0.56)×10^9/L,单纯COPD组(1.73±0.42)×10^9/L,健康对照组(0.68±0.23)×10^9/L;中性粒细胞计数:PAH组(2.78±0.52)×10^9/L,单纯COPD组(2.57±0.26)×10^9/L,健康对照组(0.63±0.21)×10^9/L;血清hs—CRP:PAH组(32±12)mg/L,单纯COPD组(23±11)mg/L,健康对照组(11±4)mg/L;IL-8:PAH组(113±34)ng/L,单纯COPD组(69±24)ng/L,健康对照组(38±11)ng/L;TNF—α:PAH组(206±63)ng/L;单纯COPD组(153±54)ng/L,健康对照组(75±26)ng/L](P均〈0.05)。PAH组PASP与第1秒用力呼气量占预计值%(FEV.%)呈负�Objective To explore the relationship between pulmonary arterial hypertension (PAH) associated with chronic obstructive pulmonary disease (COPD) and inflammatory reaction(inflammatory cell, hs CRP, IL-8 and TNF-α). Methods According to echocardiography results, the patients ( systolic pulmonary artery pressure, SPAP 〉30 mm Hg) were divided into PAH group(n =36) ,single COPD group(n =32) . All of the patients and 30 healthy subjects( control group) were recruited into the study. Lung function, arterial blood gases, cell differentials in induced sputum, and the levels of serum high sensitivity CRP(hs-CRP) ,IL-8 ,TNF-α were determined . Results The incidence of PAH associated with COPD were 53% (36/68), including 27% (3/11) of mild PAH,38% (5/13) of moderate PAH and 64% (28/44) of severe PAH and there were significantly differences in the severity of the spirometric abnormality (χ^2 = 6. 020, P 〈 0.05 ). The mean PASP and right ventricle wall thickness (RVWT) in PAH group were significantly greater in the patients compared to single COPD [ PASP: (52±15)mmHg in PAH group and (23 ± 12) mm Hg in single COPD group, t = 3.32, P 〈 0.01 ; PVWT: ( 5.03 ± 1.04 )mm in PAH group and (3.78 ± 0.57 )mm in single COPD group,t = 2.36 ,P 〈 0.05 ]. The levels of total cell count and neutrophils in induced sputum ,hs-CRP, IL-8 and TNF-α in PAH group were higher than those in single COPD group and healthy subjects [ toal cell count : (2.84 ± 0.56) × 10^9/L in PAH group and ( 1.73 ± 0.42) × 10^9/L in single COPD group and (0.68 ±0.21) × 10^9/L in control group;neutrophils: (2.78 ±0.52) × 10^9/L in PAH group and (2.57 ±0.26) × 10^9/L in single COPD group and (0.63 ± 0.21 ) × 10^9/L in control group ; hs CRP: (32 ± 12) mg/L in PAH group and (23 ±11)mg/L in single COPD group and (11 ±4)mg/L in control group; IL-8:(113 ±34) ng/L in PAH group and ( 69 ± 24 ) ng/L in single COPD grou
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