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
2012年
12期
892-896
,共5页
哮喘%体层摄影扫描仪,X线计算机%呼吸功能试验
哮喘%體層攝影掃描儀,X線計算機%呼吸功能試驗
효천%체층섭영소묘의,X선계산궤%호흡공능시험
Asthma%Tomography scanners,X-ray computed%Respiratory function test
目的 探讨高分辨率CT(HRCT)及诱导痰生物标志物对评估支气管哮喘(简称哮喘)控制情况的价值.方法 选择2007年7月至2008年1月就诊于山西医科大学第一医院呼吸科的哮喘患者48例作为哮喘组,体检中心健康体检者10名作为对照组,根据哮喘严重程度把哮喘组分为近似致死性哮喘发作组6例、重度哮喘组12例、中度哮喘组14例、轻度哮喘组16例,按照“支气管哮喘防治指南”规范化分级治疗6个月,达到控制和部分控制后,行HRCT、肺功能检查和诱导痰液细胞因子测定,测量气道壁面积占气道面积的百分比(WA％)、2倍气道壁厚度与气道直径比(2T/D)及吸气、呼气相肺密度值,利用酶联免疫法(ELISA)测定痰液中基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶抑制剂-1(TIMP-1)、转化生长因子(TGF)-β1的水平.结果 各组FVC占预计值％、FEV1占预计值％、FEV1/FVC和DLCO指标比较差异均有统计学意义(均P＜0.05)；在近似致死性哮喘发作组、重度哮喘组、中度哮喘组和轻度哮喘组MMP-9分别为(80±16)、(70±9)、(59 ±6)和(52±7)μg/L,TIMP-1分别为(212 ±95)、(258±167)、(128 ±51)和(98±60) μg/L,TGF-β1分别为(586±81)、(513±54)、(401±45)和(351±57) μg/L,均高于对照组[分别为(46±5)、(19±13)和(258±29)μg/L],哮喘各组随着病情的加重,水平逐渐增加(均P＜0.05)；在近似致死性哮喘发作组、重度哮喘组、中度哮喘组和轻度哮喘组痰MMP-9/TIMP-1分别为0.50±0.28、0.34±0.13、0.53 ±0.22和0.87±0.75,均低于对照组的2.93±1.13,重度哮喘组低于其他哮喘组(F =43.335,P ＜0.05).2T/D和WA％在近似致死性哮喘发作组分别为0.51 ±0.01和0.75 ±0.01,重度哮喘组分别为0.53 ±0.03和0.77±0.03,均高于中度哮喘组(分别为0.43 ±0.04和0.67±0.04)和轻度哮喘组(分别为0.42±0.04和0.66 ±0.04),而哮喘各组均高于对照组(分别为0.35±0.03和0.57±0.04)(均P＜0.05)；近似致死性哮喘发作组的吸、呼气相肺密度值均低于其他哮喘组和对照组,且吸气、呼气相肺密度差值均小于其他哮喘组和对照组(均P＜0.05)；2T/D、WA％与MMP-9、TIMP-1、TGF-β1呈正相关,而与MMP-9/TIMP-1呈负相关.结论 HRCT和诱导痰生物标志物能够准确评估哮喘控制状况,哮喘严重程度导致不同程度气道壁增厚和气道重塑,随着哮喘的加重,气体潴留更加明显,特别在近似致死性哮喘发作组尤为显著.
目的 探討高分辨率CT(HRCT)及誘導痰生物標誌物對評估支氣管哮喘(簡稱哮喘)控製情況的價值.方法 選擇2007年7月至2008年1月就診于山西醫科大學第一醫院呼吸科的哮喘患者48例作為哮喘組,體檢中心健康體檢者10名作為對照組,根據哮喘嚴重程度把哮喘組分為近似緻死性哮喘髮作組6例、重度哮喘組12例、中度哮喘組14例、輕度哮喘組16例,按照“支氣管哮喘防治指南”規範化分級治療6箇月,達到控製和部分控製後,行HRCT、肺功能檢查和誘導痰液細胞因子測定,測量氣道壁麵積佔氣道麵積的百分比(WA％)、2倍氣道壁厚度與氣道直徑比(2T/D)及吸氣、呼氣相肺密度值,利用酶聯免疫法(ELISA)測定痰液中基質金屬蛋白酶-9(MMP-9)、基質金屬蛋白酶抑製劑-1(TIMP-1)、轉化生長因子(TGF)-β1的水平.結果 各組FVC佔預計值％、FEV1佔預計值％、FEV1/FVC和DLCO指標比較差異均有統計學意義(均P＜0.05)；在近似緻死性哮喘髮作組、重度哮喘組、中度哮喘組和輕度哮喘組MMP-9分彆為(80±16)、(70±9)、(59 ±6)和(52±7)μg/L,TIMP-1分彆為(212 ±95)、(258±167)、(128 ±51)和(98±60) μg/L,TGF-β1分彆為(586±81)、(513±54)、(401±45)和(351±57) μg/L,均高于對照組[分彆為(46±5)、(19±13)和(258±29)μg/L],哮喘各組隨著病情的加重,水平逐漸增加(均P＜0.05)；在近似緻死性哮喘髮作組、重度哮喘組、中度哮喘組和輕度哮喘組痰MMP-9/TIMP-1分彆為0.50±0.28、0.34±0.13、0.53 ±0.22和0.87±0.75,均低于對照組的2.93±1.13,重度哮喘組低于其他哮喘組(F =43.335,P ＜0.05).2T/D和WA％在近似緻死性哮喘髮作組分彆為0.51 ±0.01和0.75 ±0.01,重度哮喘組分彆為0.53 ±0.03和0.77±0.03,均高于中度哮喘組(分彆為0.43 ±0.04和0.67±0.04)和輕度哮喘組(分彆為0.42±0.04和0.66 ±0.04),而哮喘各組均高于對照組(分彆為0.35±0.03和0.57±0.04)(均P＜0.05)；近似緻死性哮喘髮作組的吸、呼氣相肺密度值均低于其他哮喘組和對照組,且吸氣、呼氣相肺密度差值均小于其他哮喘組和對照組(均P＜0.05)；2T/D、WA％與MMP-9、TIMP-1、TGF-β1呈正相關,而與MMP-9/TIMP-1呈負相關.結論 HRCT和誘導痰生物標誌物能夠準確評估哮喘控製狀況,哮喘嚴重程度導緻不同程度氣道壁增厚和氣道重塑,隨著哮喘的加重,氣體潴留更加明顯,特彆在近似緻死性哮喘髮作組尤為顯著.
목적 탐토고분변솔CT(HRCT)급유도담생물표지물대평고지기관효천(간칭효천)공제정황적개치.방법 선택2007년7월지2008년1월취진우산서의과대학제일의원호흡과적효천환자48례작위효천조,체검중심건강체검자10명작위대조조,근거효천엄중정도파효천조분위근사치사성효천발작조6례、중도효천조12례、중도효천조14례、경도효천조16례,안조“지기관효천방치지남”규범화분급치료6개월,체도공제화부분공제후,행HRCT、폐공능검사화유도담액세포인자측정,측량기도벽면적점기도면적적백분비(WA％)、2배기도벽후도여기도직경비(2T/D)급흡기、호기상폐밀도치,이용매련면역법(ELISA)측정담액중기질금속단백매-9(MMP-9)、기질금속단백매억제제-1(TIMP-1)、전화생장인자(TGF)-β1적수평.결과 각조FVC점예계치％、FEV1점예계치％、FEV1/FVC화DLCO지표비교차이균유통계학의의(균P＜0.05)；재근사치사성효천발작조、중도효천조、중도효천조화경도효천조MMP-9분별위(80±16)、(70±9)、(59 ±6)화(52±7)μg/L,TIMP-1분별위(212 ±95)、(258±167)、(128 ±51)화(98±60) μg/L,TGF-β1분별위(586±81)、(513±54)、(401±45)화(351±57) μg/L,균고우대조조[분별위(46±5)、(19±13)화(258±29)μg/L],효천각조수착병정적가중,수평축점증가(균P＜0.05)；재근사치사성효천발작조、중도효천조、중도효천조화경도효천조담MMP-9/TIMP-1분별위0.50±0.28、0.34±0.13、0.53 ±0.22화0.87±0.75,균저우대조조적2.93±1.13,중도효천조저우기타효천조(F =43.335,P ＜0.05).2T/D화WA％재근사치사성효천발작조분별위0.51 ±0.01화0.75 ±0.01,중도효천조분별위0.53 ±0.03화0.77±0.03,균고우중도효천조(분별위0.43 ±0.04화0.67±0.04)화경도효천조(분별위0.42±0.04화0.66 ±0.04),이효천각조균고우대조조(분별위0.35±0.03화0.57±0.04)(균P＜0.05)；근사치사성효천발작조적흡、호기상폐밀도치균저우기타효천조화대조조,차흡기、호기상폐밀도차치균소우기타효천조화대조조(균P＜0.05)；2T/D、WA％여MMP-9、TIMP-1、TGF-β1정정상관,이여MMP-9/TIMP-1정부상관.결론 HRCT화유도담생물표지물능구준학평고효천공제상황,효천엄중정도도치불동정도기도벽증후화기도중소,수착효천적가중,기체저류경가명현,특별재근사치사성효천발작조우위현저.
Objective To explore the significance of assessing asthma control by high-resolution computed tomography (HRCT) and biological markers in induced sputum.Methods Forty-eight patients with asthma (asthma group) and 10 healthy subjects (control group) were retrospectively analyzed.The asthma patients were divided into 4 groups based on severity:6 with near-fatal attacks,12 with severe,14 with moderate and 16 with mild asthma.These patients received step therapy for 6 months based on the guidelines for the prevention and treatment of asthma.After achieving asthma control or partial control,HRCT,lung function and cytokine levels in induced sputum were measured.The ratio of wall area to total airway area (WA％),the ratio of 2 airway wall thickness to outer diameter (2T/D) and lung densities in both the inspiratory and expiratory phases were measured.Matrix metalloproteinase-9 (MMP-9),tissue inhibitor of metalloproteinases-1 (TIMP-1),and transformation growth facter-β1 (TGF-β1) levels in the sputum were assessed by enzyme-linked immunosorbent assay.Results There were significant differences in forced vital capacity and forced expiratory volume in 1 second as the percentage of predicted value (FVC％ and FEV1％,respectively),the ratio of FEV1/FVC,and diffusing capacity of the lung for carbon monoxide(DLCO) among groups (F=5.526,15.064,16.326,2.945,respectively,P ＜0.05).Sputum levels of MMP-9,TIMP-1 and TGF-β1 were significantly increased in the near-fatal asthma,severe asthma,moderate asthma and mild asthma groups [MMP-9:(80 ± 16),(70 ± 9),(59 ± 6),and (52 ± 7) μg/L,respectively; TIMP-1:(212 ±95),(258 ± 167),(28 ± 51),and 98 ± 60 μg/L,respectively; TGF-β1:(586 ±81),(513 ±54),(401 ±45) and (351 ±57) μg/L,respectively]compared with the control group [MMP9:(46 ±5) μg/L; TIMP:(19 ± 13) μg/L; and TGF-β1:(258 ±29) μg/L].These parameters were progressively increased in the asthma groups with the severity of disease (F =11.179,49.914,9.286,respectively,P ＜0.05).The ratio of MMP-9 /TIMP-1 in sputum was decreased in the near-fatal attack,severe,moderate and mild asthma groups (0.50 ± O.28,0.34 ± 0.13,0.53 ± 0.22,and 0.87 ± 0.75,respectively) compared with the control group (2.93 ± 1.13).The MMP-9/TIMP-1 ratio in the severe asthma group was lowest among the asthma groups (F =43.335,P ＜ 0.05).2T/D and WA％ were higher in both the near-fatal asthma group (0.51 ± 0.01 and 0.75 ± 0.01,respectively) and the severe asthma group (0.53 ± 0.03 and 0.77 ± 0.03,respectively) as compared to the moderate asthma group (0.43 ±0.04 and 0.67 ± 0.04,respectively) or the mild group (0.42 ± 0.04 and 0.66 ± 0.04,respectively).2T/D and WA％ were higher in the asthma groups than in the control group (0.35 ±0.03 and 0.57 ±0.04,respectively),(F =40.224,41.294,respectively,P ＜ 0.05).Lung densities in both the inspiratory and expiratory phases were lower in the near-fatal attack group as compared to those in the other asthma groups or the control group; and the lung density differences between the two phases in the near-fatal attack group were smaller than those in the other asthma groups or the control group (F =5.048,13.247,11.541,respectively,P ＜ 0.05).2T/D and WA％ were correlated positively with MMP-9,TIMP-1 and TGFβ1 levels,but negatively with the MMP-9/TIMP-1 ratio,respectively.Conclusions HRCT and biological markers in induced sputum could be used to accurately evaluate asthma control.These findings suggest that the severity of asthma,especially,near-fatal attack of asthma,is correlated not only with the degree of airway remodeling,but also with the degree of air trapping.
