摘要目的 探讨急性肺损伤(ALI)患者血清白细胞介素-17(IL-17)及白细胞介素-33(IL-33)水平与急性生理学与慢性健康状况Ⅱ(APACHEⅡ)评分的相关性,分析其对ALI的预后评估价值。方法 选取2017年1月至2018年10月海口市第三人民医院收治的ALI患者128例,根据ALI患者生存情况分为存活组( n =82)和死亡组( n =46)。采用APACHEⅡ评分标准将ALI患者分为低危组( n =30)、中危组( n =46)和高危组( n =52)。采用酶联免疫吸附法检测各组血清IL-17及IL-33水平。应用ROC曲线分析血清IL-17及IL-33水平预测ALI患者死亡的价值,Pearson相关分析ALI患者血清IL-17及IL-33水平与APACHEⅡ评分的相关性。结果 死亡组血清IL-17(ng/L:27.83±7.36 vs. 14.60±4.25)及IL-33(ng/L:46.37±11.30 vs. 30.28± 8.46)均明显高于存活组( P <0.05)。高危组血清IL-17(ng/L:26.20± 7.48 vs. 18.70±6.24, 13.18±4.25)、IL-33(ng/L:42.50±11.62 vs. 36.25±9.13,27.40± 7.34 )及APACHEⅡ评分(分:29.60±3.70 vs.18.90±3.20, 9.70±1.80)、病死率(63.5% vs. 26.1%、6.7 %)均明显高于中危组和低危组( P < 0.05)。受试者工作特征(ROC)曲线分析显示,血清IL-17及 IL- 33水平预测ALI患者死亡的最佳截断值分别为18.45 ng/L及34.20 ng/L,两项联合预测ALI患者死亡的ROC曲线下面积(AUC)[0.890(95%CI 0.832~0.951)]明显高于单项,其敏感度和特异度为89.4%和84.7%。相关分析显示,死亡组血清IL-17及IL-33水平与APACHEⅡ评分均呈正相关( r =0.816、0.730 ,P < 0.01)。结论 血清IL-17及IL-33水平与ALI患者病情严重程度及预后相关,IL-17及IL-33联合检测对预测ALI患者预后效果更好。
黄一桂,陈钰,梁勇,许俊旭,吴挺实,钟婉红. IL-17及IL-33对急性肺损伤患者病情及预后的评估价值[J]. 中国急救医学, 2019, 39(8): 744-748.
Huang Yi-gui, Chen Yu, Liang Yong, Xu Jun-xu, Wu Ting-shi, Zhong Wan-hong. Value of IL-17 and IL-33 in evaluating the condition and prognosis of patients with acute lung injury. Chinese Journal of Critical Care Medicine, 2019, 39(8): 744-748.
[1]Santa Cruz R, Alvarez LV, Heredia R, et al. Acute respiratory distress syndrome: mortality in a single center according to different〖JP〗 definitions[J]. J Intensive Care Med, 2017, 32(5): 326-332.
[2]Brandenberger C, Kling KM, Vital M, et al. The role of pulmonary and systemic immunosenescence in acute lung injury[J]. Aging Dis, 2018, 9(4): 553-565.
[3]Ding Q, Liu GQ, Zeng YY, et al. Role of IL-17 in LPS-induced acute lung injury: an in vivo study[J]. Oncotarget, 2017, 8(55): 93 704-93 711.
[4]Zhang Y, Lv R, Hu X, et al. The role of IL-33 on LPS-induced acute lung injury in mice[J]. Inflammation, 2017, 40(1): 285-294.
[5]Dey S, Karim HMR, Yunus M, et al. Relationship of on Admission Hypocalcaemia and Illness Severity as Measured by APACHE-Ⅱ and SOFA Score in Intensive Care Patients[J]. J Clin Diagn Res, 2017, 11(3): UC01-UC03.
[6]Jiang Z, Zhou Q, Gu C, et al. Depletion of circulating monocytes suppresses IL-17 and HMGB1 expression in mice with LPS-induced acute lung injury[J]. Am J Physiol Lung Cell Mol Physiol, 2017, 312(2): L231-L242.
[7]Lin SH, Fu J, Wang CJ, et al. Inflammation elevated IL-33 originating from the lung mediates inflammation in acute lung injury[J]. Clin Immunol, 2016, 28(16): 30 535-30 536.
[8]丁琦, 黄建安. Th17/IL-17在急性肺损伤中的研究进展[J]. 临床肺科杂志, 2018, 23(11): 2111-2113.
[9]Rathnakar SK, Vishnu VH, Muniyappa S, et al. Accuracy and predictability of PANC-3 scoring system over APACHEⅡ in acute pancreatitis: a prospective study[J]. J Clin Diagn Res, 2017, 11(2): PC10-PC13.
[10]周洪, 綦俊, 张奇, 等. 外周血Th17细胞对脓毒症急性肺损伤病情严重程度及预后的评估价值[J]. 现代免疫学, 2016, 36(2): 113-117.
[11]杨霞, 张景鸿, 陈威, 等. IL-17、RORγt在百草枯中毒小鼠急性肺损伤中的表达[J]. 实用医学杂志, 2017, 33(11): 1757-1761.
[12]Luzina IG, Kopach P, Lockatell V, et al. Interleukin-33 potentiates bleomycin-induced lung injury[J]. Am J Respir Cell Mol Biol, 2013, 49(6): 999-1008.
[13]Chhangani NP, Amandeep M, Choudhary S, et al. Role of acute physiology and chronic health evaluation Ⅱ scoring system in determining the severity and prognosis of critically ill patients in pediatric intensive care unit[J]. Indian J Crit Care Med, 2015, 19(8): 462-465.
[14]Ding Q, Liu G, Zeng Y, et al. Glycogen synthase kinase-3β inhibitor reduces LPS induced acute lung injury in mice[J]. Mol Med Rep, 2017, 16(5): 6715-6721.
[15]Wang L, Wang X, Tong L, et al. Recovery from acute lung injury can be regulated via modulation of regulatory T cells and Th17 cells[J]. Scand J Immunol, 2018, 88(5): e12 715.
[16]Zhao J, Zhao Y. Interleukin-33 and its receptor in pulmonary inflammatory diseases[J]. Crit Rev Immunol, 2015, 35(6): 451-461.