[1]刘锋锋,郑建杰,刘淼淼.体外膜肺氧合治疗对成人暴发性心肌炎患者细胞因子表达谱的影响[J].陕西医学杂志,2022,51(4):429-432,436.[doi:DOI:10.3969/j.issn.1000-7377.2022.04.010]
　LIU Fengfeng,ZHENG Jianjie,LIU Miaomiao.Influence of extracorporeal membrane oxygenation therapy on cytokine expression profile in adult patient with fulminant myocarditis[J].,2022,51(4):429-432,436.[doi:DOI:10.3969/j.issn.1000-7377.2022.04.010]
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体外膜肺氧合治疗对成人暴发性心肌炎患者细胞因子表达谱的影响
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
51
期数:
2022年4期
页码:
429-432,436
栏目:
临床研究
出版日期:
2022-04-05

文章信息/Info

Title:
Influence of extracorporeal membrane oxygenation therapy on cytokine expression profile in adult patient with fulminant myocarditis
作者:
刘锋锋; 郑建杰; 刘淼淼
(西安交通大学第一附属医院心血管外科,陕西 西安 710061)
Author(s):
LIU Fengfeng; ZHENG Jianjie; LIU Miaomiao
(Department of Cardiovascular Surgery, the First Affiliated Hospital of Xi'an Jiaotong Unviersity,Xi'an 710061,China)
关键词:
体外膜肺氧合;  暴发性心肌炎;  细胞因子;  白细胞介素;  炎症;  预后
Keywords:
Extracorporeal membrane oxygenation;  Fulminant myocarditis;  Cytokine;  Interleukin;  Inflammation;  Prognosis
分类号:
R 542.2
DOI:
DOI:10.3969/j.issn.1000-7377.2022.04.010
文献标志码:
A
摘要:
目的:分析暴发性心肌炎患者血清细胞因子表达谱,观察体外膜肺氧合(ECMO)治疗对暴发性心肌炎患者细胞因子水平的影响。方法:纳入暴发性心肌炎患者28例和19例对照者,采集基线和ECMO撤除后的外周血,分离血清,液相芯片分析法检测14种细胞因子水平,观察暴发性心肌炎患者血清细胞因子变化及其对生存结局的预测效能。结果:暴发性心肌炎组和对照组血清中均未检测到白细胞介素-3(IL-3)表达。干扰素-α(IFN-α)、IFN-γ、IL-1α、IL-1β、IL-1ra、IL-4、IL-10、IL-33和血管内皮细胞生长因子(VEGF)水平在暴发性心肌炎组和对照组之间比较差异无统计学意义(均P>0.05)。暴发性心肌炎患者血清IL-2[(5400.00±2181.00)pg/ml]、IL-6[714.6(521.0,1071.0)pg/ml]、IL-7[269.7(169.4,402.5)pg/ml]和IL-15[105.7(50.5,186.5)pg/ml]水平均显著高于对照组(均P<0.05)。暴发性心肌炎组存活者和死亡者血清IL-6水平的受试工作者特征曲线分析示,曲线下面积为0.871,95%可信区间为0.740～1.002,生存结局预测效能良好(P=0.006)。但IL-2、IL-7和IL-15的生存结局预测效能较差(均P>0.05)。暴发性心肌炎存活者血清IL-6水平在ECMO撤除后显著低于基线[337.8(212.5,432.7)pg/ml与635.8(327.4,893.7)pg/ml,P=0.0014],但IL-2、IL-7和IL-15水平在基线和ECMO撤除后的比较差异无统计学意义(均P>0.05)。结论:IL-2、IL-6、IL-7和IL-15可能参与了暴发性心肌炎的发病,ECMO治疗通过降低血清IL-6水平抑制患者炎症应答。
Abstract:
Objective:To analyze serum cytokine expression profile,and to investigate the influence of extracorporeal membrane oxygenation(ECMO)therapy on cytokine expression in patients with fulminant myocarditis.Methods:Twenty-eight patients with fulminant myocarditis and nineteen controls were enrolled.Blood samples were collected at baseline and post ECMO therapy,and serum was isolated.Fourteen cytokine levels in the serum were measured by luminex performance assay.Changes of cytokine levels and prognostic values for survival were assessed.Results:IL-3 was not detected in the serum of either fulminant myocarditis patients or controls.There was no significant difference in serum interferon-α(IFN-α),IFN-γ,interleukin-1α(IL-1α),IL-1β,IL-1ra,IL-4,IL-10,IL-33 or vascular endothelial growth factor level between fulminant myocarditis patients and controls(all P>0.05).The levels of IL-2 [(5400.00±2181.00)pg/ml],IL-6 [714.6(521.0,1071.0)pg/ml],IL-7 [269.7(169.4,402.5)pg/ml] and IL-15[105.7(50.5,186.5)pg/ml] were remarkably increased in fulminant myocarditis patients compared with controls(all P<0.05).Serum IL-6 in survival and death groups of fulminant myocarditis patients was analyzed by receiver operating characteristic curve,and the area under the curve was 0.871,and 95% confidence interval was 0.740 to 1.002,indicating the better prognostic value for survival(P=0.006).However,IL-2,IL-7 or IL-15 had worse prognostic values for survival(all P>0.05).Serum IL-6 level was robustly reduced post ECMO therapy compared with baseline in survival patients of fulminant myocarditis [337.8(212.5,432.7)pg/ml vs.635.8(327.4,893.7)pg/ml,P=0.0014].However,there was no statistical difference in IL-2,IL-7 or IL-15 between baseline and post ECMO therapy(all P>0.05).Conclusion:IL-2,IL-6,IL-7 and IL-15 might take part in the pathogenesis of fulminant myocarditis.ECMO therapy reduced inflammatory response of fulminant myocarditis patients through reduction of IL-6.

参考文献/References:

[1] Sharma AN,Stultz JR,Bellamkonda N,et al.Fulminant myocarditis:Epidemiology,pathogenesis,diagnosis,and management[J].Am J Cardiol,2019,124(12):1954-1960.
[2] 李 梅,李晓丽.卡托普利联合小剂量胺碘酮对病毒性心肌炎合并室性心律失常患儿心电图、心肌损伤标志物和新功能的影响[J].陕西医学杂志,2018,47(11):1496-1499.
[3] Hang W,Chen C,Seubert JM,et al.Fulminant myocarditis:A comprehensive review from etiology to treatments and outcomes[J].Signal Transduct Target Ther,2020,5(1):287.
[4] Maisch B.Cardio-immunology of myocarditis:Focus on immune mechanisms and treatment options[J].Front Cardiovasc Med,2019,6:48.
[5] 中国医学会心血管病学分会精准医学学组,中华心血管病杂志编辑委员会,成人暴发性心肌炎工作组.成人暴发性心肌炎诊断与治疗中国专家共识[J].中华心血管病杂志,2017,45(9):742-752.
[6] Lee EP,Chu SC,Huang WY,et al.Factors associated with in-hospital mortality of children with acute fulminant myocarditis on extracorporeal membrane oxygenation[J].Front Pediatr,2020,8:488.
[7] Park H,Lim Y,Kim MC,et al.Case report:Fulminant myocarditis successfully treated with extracorporeal membrane oxygenation in ikeda strain orientia tsutsugamushi infection[J].Front Cardiovasc Med,2021,8:795249.
[8] 台 适,孙佳星,唐建军,等.体外膜肺氧合在成人暴发性心肌炎合并心原性休克患者中的应用价值[J].中华心力衰竭和心肌病杂志,2020,4(3):175-180.
[9] 唐素美,侯新蕊,胡 鑫,等.应用体外膜肺氧合辅助治疗成人爆发性心肌炎的疗效观察[J].北京医学,2018,40(11):1019-1021.
[10] Zhao F,Shi G,Wu Z,et al.A successful rescue of juvenile fulminant myocarditis by extracorporeal membrane oxygenation combined with intra-aortic balloon pump:A case report[J].Ann Transl Med,2021,9(16):1355.
[11] 周 雪.基于Bcl-2/Bax/Caspase-3信号通路探讨三七总皂苷对自身免疫性心肌炎模型大鼠心肌凋亡影响[J].陕西中医,2021,42(11):1504-1511.
[12] Zeng JH,Liu YX,Yuan J,et al.First case of COVID-19 complicated with fulminant myocarditis:A case report and insights[J].Infection,2020,48(5):773-777.
[13] Ishikura H,Maruyama J,Hoshino K,et al.Coronavirus disease(COVID-19)associated delayed-onset fulminant myocarditis in patient with a history of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection[J].J Infect Chemother,2021,27(12):1760-1764.
[14] Rivadeneyra L,Charó N,Kviatcovsky D,et al.Role of neutrophils in CVB3 infection and viral myocarditis[J].J Mol Cell Cardiol,2018,125:149-161.
[15] Fontes JA,Barin JG,Talor MV,et al.Complete freund's adjuvant induces experimental autoimmune myocarditis by enhancing IL-6 production during initiation of the immune response[J].Immun Inflamm Dis,2017,5(2):163-176.
[16] Coppola C,Hopkins B,Huhn S,et al.Investigation of the impact from IL-2,IL-7,and IL-15 on the growth and signaling of activated CD4+ T cells[J].Int J Mol Sci,2020,21(21):7814.
[17] Tan MCC,Ortega-Legaspi JM,Cheng SF,et al.Acute myocarditis following high-dose interleukin-2 treatment[J].J Cardiol Cases,2016,15(1):28-31.
[18] Kubin N,Richter M,Sen-Hild B,et al.Macrophages represent the major pool of IL-7Ralpha expressing cells in patients with myocarditis[J].Cytokine,2020,130:155053.
[19] Guo L,Liu MF,Huang JN,et al.Role of interleukin-15 in cardiovascular diseases[J].J Cell Mol Med,2020,24(13):7094-7101.
[20] Wei X,Fang Y,Hu H.Immune-mediated mechanism in coronavirus fulminant myocarditis[J].Eur Heart J,2020,41(19):1855.

备注/Memo

备注/Memo:
基金项目:陕西省自然科学基础研究一般项目(S2020-JC-QN-2798)
更新日期/Last Update: 2022-04-07