不同控制水平的支气管哮喘患者气道炎症与外周气道功能状态的研究
불동공제수평적지기관효천환자기도염증여외주기도공능상태적연구
Airway inflammation and peripheral airway function in asthmatic patients with different control levels
  • 万方数据
    中华结核和呼吸杂志 중화결핵화호흡잡지
    Chinese Journal of Tuberculosis and Respiratory Diseases
    2009年 9期 679-684 ,共6页

    潘杨%黄克武%叶青%刘学松%武宝梅%张君%常晓红%逯勇%王辰

    반양%황극무%협청%류학송%무보매%장군%상효홍%록용%왕신

    哮喘%炎症%气道阻力 哮喘%炎癥%氣道阻力
    효천%염증%기도조력
    Asthma%Inflammation%Airway resistance
    目的 了解不同临床控制水平的支气管哮喘(简称哮喘)患者的气道炎症状况及外周气道功能,观察哮喘患者诱导痰中的炎症指标能否反映外周气道功能的改变.方法 收集在北京朝阳医院就诊的哮喘患者66例,分为控制组(21例)、部分控制组(28例)、未控制组(17例)以及健康对照组(20名).所有受试者第1天进行哮喘控制测试(ACT)评分,行脉冲振荡肺功能检测气道阻力及肺功能基础值、诱导痰细胞计数和分类以及嗜酸粒细胞阳离子蛋白(ECP)浓度测定;第2天测定呼出气一氧化氮浓度(FE_(NO)),若所测得的FEV_1≥70%预测值则行乙酰甲胆碱激发试验,当气道阻力升高至基础阻力2倍或乙酰甲胆碱达到最大浓度时终止试验,3 min后行气道阻力及通气功能检测;然后嘱受试者行5次深吸气后再复测气道阻力及通气功能.比较4组受试者诱导痰细胞计数和分类、诱导痰中ECP浓度、FE_(NO)水平与ACT评分间的相关性;观察激发后以及深吸气后外周气道阻力的变化与ACT评分、诱导痰中嗜酸粒细胞(EOS)计数、痰ECP水平及FE_(NO)间的关系.结果 (1)哮喘患者诱导痰EOS计数、ECP浓度以及FE_(NO)随着控制水平的下降逐渐增高,且诱导痰EOS计数、ECP浓度均与ACT评分呈负相关(r值分别为-0.43和-0.56,均P<0.01).(2)在健康对照组,乙酰甲胆碱激发后中心气道阻力(R_(20))、外周气道阻力(R_5-R_(20))增高程度间比较差异无统计学意义(F=3.472,P>0.05),而在控制组及部分控制组激发试验后外周气道的反应强于中心气道(F值分别为18.09和14.14,均P<0.01),但激发后R_5-R_(20)的变化与ACT评分、诱导痰EOS计数、ECP、FE_(NO)水平间无相关性.(3)深吸气后,健康对照组R_5-R_(20)由(0.13±0.14)kPa·L~(-1)·s~(-1)降至(0.08±0.09)kPa·L~(-1)·s~(-1)(t=2.84,P<0.05),而控制组、部分控制组R_5-R_(20)分别由(0.24±0.15)、(0.31±0.18)kPa·L~(-1)·s~(-1)>增至(0.30±0.16)、(0.39±0.17)kPa·L~(-1)·s~(-1)(t值分别为3.90、4.68,均P<0.01),但相关分析显示,深吸气后R_5-R_(20)的变化与ACT评分、诱导痰EOS计数、ECP、FE_(NO)水平无相关性.结论 即使在控制水平的哮喘患者,仍存在气道嗜酸粒细胞炎症,且该炎症状态随着疾病控制水平的降低而逐渐加重;哮喘患者深吸气所致的外周气道舒张作用消失;检测诱导痰中的炎症指标并不能反映外周气道功能的改变.
    목적 료해불동림상공제수평적지기관효천(간칭효천)환자적기도염증상황급외주기도공능,관찰효천환자유도담중적염증지표능부반영외주기도공능적개변.방법 수집재북경조양의원취진적효천환자66례,분위공제조(21례)、부분공제조(28례)、미공제조(17례)이급건강대조조(20명).소유수시자제1천진행효천공제측시(ACT)평분,행맥충진탕폐공능검측기도조력급폐공능기출치、유도담세포계수화분류이급기산립세포양리자단백(ECP)농도측정;제2천측정호출기일양화담농도(FE_(NO)),약소측득적FEV_1≥70%예측치칙행을선갑담감격발시험,당기도조력승고지기출조력2배혹을선갑담감체도최대농도시종지시험,3 min후행기도조력급통기공능검측;연후촉수시자행5차심흡기후재복측기도조력급통기공능.비교4조수시자유도담세포계수화분류、유도담중ECP농도、FE_(NO)수평여ACT평분간적상관성;관찰격발후이급심흡기후외주기도조력적변화여ACT평분、유도담중기산립세포(EOS)계수、담ECP수평급FE_(NO)간적관계.결과 (1)효천환자유도담EOS계수、ECP농도이급FE_(NO)수착공제수평적하강축점증고,차유도담EOS계수、ECP농도균여ACT평분정부상관(r치분별위-0.43화-0.56,균P<0.01).(2)재건강대조조,을선갑담감격발후중심기도조력(R_(20))、외주기도조력(R_5-R_(20))증고정도간비교차이무통계학의의(F=3.472,P>0.05),이재공제조급부분공제조격발시험후외주기도적반응강우중심기도(F치분별위18.09화14.14,균P<0.01),단격발후R_5-R_(20)적변화여ACT평분、유도담EOS계수、ECP、FE_(NO)수평간무상관성.(3)심흡기후,건강대조조R_5-R_(20)유(0.13±0.14)kPa·L~(-1)·s~(-1)강지(0.08±0.09)kPa·L~(-1)·s~(-1)(t=2.84,P<0.05),이공제조、부분공제조R_5-R_(20)분별유(0.24±0.15)、(0.31±0.18)kPa·L~(-1)·s~(-1)>증지(0.30±0.16)、(0.39±0.17)kPa·L~(-1)·s~(-1)(t치분별위3.90、4.68,균P<0.01),단상관분석현시,심흡기후R_5-R_(20)적변화여ACT평분、유도담EOS계수、ECP、FE_(NO)수평무상관성.결론 즉사재공제수평적효천환자,잉존재기도기산립세포염증,차해염증상태수착질병공제수평적강저이축점가중;효천환자심흡기소치적외주기도서장작용소실;검측유도담중적염증지표병불능반영외주기도공능적개변.
    Objective To observe the airway inflammation and peripheral airway function in asthmatic patients with different control levels, and to investigate whether the airway inflammation profile detected by induced sputum reflects the peripheral airway dysfunction. Methods The recruited asthmatic subjects (n=66) were divided into 3 groups: asthma controlled (8 male and 13 female), asthma partly controlled (12 male and 16 female), asthma uncontrolled (6 male and 11 female). Twenty healthy subjects served as the control group (9 male and 11 female). On the 1st day, all the subjects were required to take asthma control test (ACT), and to receive measurement of lung function by osciilometry and spirometry as well as inflammatory cell profile of induced sputum and the concentration of eosinophil cationic protein (ECP). Exhaled nitric oxide (Feso) was measured on the 2nd day, and oscillometry methacholine provocation was conducted for patients whose baseline FEV_1 was ≥70% predicted. The provocation process was terminated when airway resistance was increased by twice of the basic value, or when the mcthacholine reached the highest concentration. Then airway resistance and lung function were examined after 3 minutes. Finally, airway resistance and lung function were measured again after the subjects had 5 consecutive deep inspirations (DI). Correlation analysis was conducted between ACT scores and inflammatory cells count, ECP concentrations of induced sputum and FE_(NO) among different groups. The correlations were also made between the change of peripheral airway resistance triggered by provocation or DI and ACT scores, total eosinophil, ECP level of induced sputum, FE_(NO) respectively. Results The total eosinophil count and ECP level in induced sputum and FE_(NO) in asthmatic patients increased with the decline of control level. Negative correlations between ACT scores and total eosinophil count as well as the ECP level were observed (r = -0.43, -0.56, P < 0.01). In the healthy control group, the percentage of increase in peripheral airway resistance (R_5-R_(20)) and central airway resistance (R_(20)) did not show significant difference (F = 3.472, P > 0.05) with methacholine provocation, while the percentage of increase in R_5-R_(20) was greater than in R_(20) in both controlled and partly controlled asthmatic patients with provocation (F=18.09 and 14.14, P< 0.01), though the change of R_5-R_(20) showed no correlations with ACT scores, eosinophil count of induced sputum, ECP level and FE_(NO). After DI, R_5-R_(20), decreased from (0. 13 ±0. 14) kPa · L~(-1) · s~(-1) to (0. 08 ± 0. 09) kPa · L~(-1) · s~(-1) (t = 2. 84, P < 0. 05) in the healthy control group, while R_5-R_(20), increased from (0. 24 ±0. 15) kPa · L~(-1) · s~(-1) to (0.30 ±0. 16) kPa · L~(-1) · s~(-1) in the controlled asthma group, from (0.31 ±0. 18) kPa · L~(-1) · s~(-1) to (0. 39 ±0. 17) kPa · L~(-1) · s~(-1) in the partly controlled asthma group (t =3.90 and 4. 68, P <0. 01, respectively). No correlations were observed between the change of R_5-R_(20) after DI and ACT scores, total eosinophil counts, ECP level as well as FE_(NO)(r= -0. 07, 0. 28, -0. 14, 0. 14, P >0. 05). Conclusions Even in asthma patients with controlled disease, eosinophilic inflammation in the airway was still present, and the eosinophilic inflammation became more severe with the decline of control level. Bronchodilatory effect caused by DI disappeared in asthmatic patients. The inflammation profile detected by induced sputum did not reflect the dysfunction of peripheral airways.
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