肺泡灌洗液中SP-A水平与ARDS病情严重程度的相关性研究
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摘要
目的探讨急性呼吸窘迫综合征(ARDS)患者支气管肺泡灌洗液(BALF)中肺泡表面活性蛋白(SP-A)水平与氧合指数的相关性及临床意义。方法对入住医院RICU初次诊断为ARDS患者151例中根据入选标准和排除标准选取75例进行有创机械通气患者,以28天时患者是否存活分为存活组27例和非存活组48例。以横断面研究记录患者性别、年龄等基础指标;患者入RICU时的APACHEII评分、呼吸机参数(PIP、PEEP和VT)、血常规指标(WBC和NS)、PCT和氧合指数(PaO2/FiO2);入RICU时行纤维支气管镜肺泡灌洗使用ELISA检查BALF中SP-A的水平。结果结果显示存活组患者体重指数(BMI)高于非存活组患者(P<0.05),其余基础指标两组患者间无显著差异(P均<0.05)。入RICU时的APACHEII评分、呼吸机参数(PIP、PEEP和VT)、血常规指标(WBC和NS)、PCT、氧合指数(PaO2/FiO2)和BALF中SP-A的水平在存活组与非存活组之间均有显著差异(P均<0.05)。同时相关性分析显示BALF中SP-A水平与氧合指数有强相关性(R2=0.531)。结论临床研究表明非存活组患者的一般情况较存活组患者差,BALF中SP-A水平与ARDS患者病情严重程度呈正相关性,可作为ARDS的标记物。但仍需进一步的大样本多中心临床研究证实其价值。
Objective To investigate whether SP-A levels in bronchoalveolar lavage fluid(BALF)correlates with the severity of ARDS in adult.Methods From May 2012 to January 2018,151 adult patients(18to 75 years old)with ARDS requiring invasive mechanical ventilation from RICU in our hospital were screened in our study.Finally,75 patients were enrolled.According to whether survived in 28 days after invasive mechanical ventilation intervention,patients were divided into two groups,non-survival group(n=48)and survival group(n=27).Demographic characteristics,clinical data and the content of SP-A in BALF were recorded and measured on day 0.Correlation analysis was used to evaluate the relationship between SP-A level in BALF and PaO2/FiO2.Results Our data showed that the significant differences in body mass index(BMI),APACHEII score,PIP,PEEP,WBC,NS,PCT,PaO2/FiO2 and SP-A in BALF were found between survival group and non-survival group.Strong correlation between SP-A level in BALF and PaO2/FiO2 was observed(R2= 0.531).Conclusion The general condition of ARDS patients in non-survival group was worse than survival group.Correlation between SP-A level in BALF and PaO2/FiO2 was good.Therefore,our results indicated that SP-A level in BALF could possibly be used as a predictor of the severity of ARDS in clinical practice.However,a multiple center study with larger sample size should be carried out to further assess the value of it in future.
Objective To investigate whether SP-A levels in bronchoalveolar lavage fluid(BALF)correlates with the severity of ARDS in adult.Methods From May 2012 to January 2018,151 adult patients(18to 75 years old)with ARDS requiring invasive mechanical ventilation from RICU in our hospital were screened in our study.Finally,75 patients were enrolled.According to whether survived in 28 days after invasive mechanical ventilation intervention,patients were divided into two groups,non-survival group(n=48)and survival group(n=27).Demographic characteristics,clinical data and the content of SP-A in BALF were recorded and measured on day 0.Correlation analysis was used to evaluate the relationship between SP-A level in BALF and PaO2/FiO2.Results Our data showed that the significant differences in body mass index(BMI),APACHEII score,PIP,PEEP,WBC,NS,PCT,PaO2/FiO2 and SP-A in BALF were found between survival group and non-survival group.Strong correlation between SP-A level in BALF and PaO2/FiO2 was observed(R2= 0.531).Conclusion The general condition of ARDS patients in non-survival group was worse than survival group.Correlation between SP-A level in BALF and PaO2/FiO2 was good.Therefore,our results indicated that SP-A level in BALF could possibly be used as a predictor of the severity of ARDS in clinical practice.However,a multiple center study with larger sample size should be carried out to further assess the value of it in future.
引文
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[13]刘华君,许红波,刘文彬,等.国产牛肺表面活性剂治疗早产儿呼吸窘迫综合征的疗效观察[J].西部医学,2013,25(12):1802-1804.
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[15] Lopez-Rodriguez E,Pascual A,Arroyo R,et al.Human Pulmonary Surfactant Protein SP-A1Provides Maximal Efficiency of Lung Interfacial Films[J].Biophys J,2016,111(3):524-536.
[16] Xiao B,Xu J,Wang G,et al.Troglitazone-activated PPARγinhibits LPS-induced lung alveolar type II epithelial cells injuries via TNF-α[J].Mol Biol Rep,2011,38(8):5009-5015.
[17] Mittal N,Sanyal SN.Cycloxygenase inhibition enhances the effects of surfactant therapy in endotoxin-induced rat model of ARDS[J].Inflammation,2011,34(2):92-8.
[18] Xiao M,Zhu T,Zhang W,et al.Emodin Ameliorates LPS-Induced Acute Lung Injury,Involving the Inactivation of NF-κB in Mice[J].Int J Mol Sci,2014,15(11):19355-19368.
[19]宋振举,白春学.急性肺损伤/急性呼吸窘迫综合征分子标记物:从单一到联合[J].中华急诊医学杂志,2014,23(003):245-247.
[20] Qi D,Tang X,He J,et al.Omentin protects against LPS-induced ARDS through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt/eNOS-dependent mechanism[J].Cell Death Dis,2016,7(9):2360.
[2] Blank R,Napolitano LM.Epidemiology of ARDS and ALI[J].Crit Care Clin,2011,27(3):439-58.
[3] Zhu T,Wang DX,Zhang W,et al.Andrographolide Protects Against LPS-induced Acute Lung Injury by Inactivation of NF-κB[J].PLOS ONE,2013,8(2):56407.
[4]朱涛,管弦,张维,等.脱氢穿心莲内酯琥珀酸半酯通过抑制iNOS减轻LPS诱导的急性肺损伤导致的氧化应激[J].南方医科大学学报,2012,32(9):1238-1241.
[5] Dechert RE,Park PK,Bartlett RH.Evaluation of the oxygenation index in adult respiratory failure[J].J Trauma Acute Care Surg,2014,76(2):469-73.
[6] Zhu B,Zheng F,Liu N,et al.Diagnostic value of surfactant protein-a in severe acute pancreatitis-induced acute respiratory distress syndrome[J].Med Sci Monit,2014,20:1728-1734.
[7] ARDS Definition Task Force,Ranieri VM,Rubenfeld GD,et al.Acute respiratory distress syndrome:the Berlin Definition[J].JAMA,2012,307(23):2526-33.
[8] Zhu T,Zhang W,Wang DX.Insulin up-regulates epithelial sodium channel in LPS-induced acute lung injury model in rats by SGK1activation[J].Injury,2012,43(8):1277–1283.
[9]任凯旋,涂岳圣,朱涛,等.大黄素通过PPARγ/NF-κB信号通路抑制LPS诱导的RAW264.7细胞炎症反应[J].西部医学,2018(01):12-15,20.
[10]朱涛,肖敏,文富强,等.脱氢穿心莲内酯琥珀酸半酯上调水通道蛋白5减轻LPS诱导的急性肺损伤肺水肿的实验研究[J].西部医学,2014,26(01):16-18,22.
[11]傅萱,林锦乐,张文武,等.ARDS生物标志物的研究进展[J].中华危重病急救医学,2017,29(7):656-661.
[12]贾子毅,刘晓伟,刘志.机械通气氧合指数对ARDS患者预后评估的价值:附228例回顾性分析[J].中华危重病急救医学,2017,29(1):45-50.
[13]刘华君,许红波,刘文彬,等.国产牛肺表面活性剂治疗早产儿呼吸窘迫综合征的疗效观察[J].西部医学,2013,25(12):1802-1804.
[14] Whitsett JA,Wert SE,Weaver TE.Diseases of pulmonary surfactant homeostasis[J].Annu Rev Pathol,2015,10:371-393.
[15] Lopez-Rodriguez E,Pascual A,Arroyo R,et al.Human Pulmonary Surfactant Protein SP-A1Provides Maximal Efficiency of Lung Interfacial Films[J].Biophys J,2016,111(3):524-536.
[16] Xiao B,Xu J,Wang G,et al.Troglitazone-activated PPARγinhibits LPS-induced lung alveolar type II epithelial cells injuries via TNF-α[J].Mol Biol Rep,2011,38(8):5009-5015.
[17] Mittal N,Sanyal SN.Cycloxygenase inhibition enhances the effects of surfactant therapy in endotoxin-induced rat model of ARDS[J].Inflammation,2011,34(2):92-8.
[18] Xiao M,Zhu T,Zhang W,et al.Emodin Ameliorates LPS-Induced Acute Lung Injury,Involving the Inactivation of NF-κB in Mice[J].Int J Mol Sci,2014,15(11):19355-19368.
[19]宋振举,白春学.急性肺损伤/急性呼吸窘迫综合征分子标记物:从单一到联合[J].中华急诊医学杂志,2014,23(003):245-247.
[20] Qi D,Tang X,He J,et al.Omentin protects against LPS-induced ARDS through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt/eNOS-dependent mechanism[J].Cell Death Dis,2016,7(9):2360.