高迁移率族蛋白B1对细菌性脓毒血症患者生存状况评价的临床意义

doi:10.3969/j.issn.1673-8640.2021.01.016

摘要/Abstract

摘要：

目的探讨高迁移率族蛋白B1（HMGB1）对预测细菌性脓毒血症患者生存状况的临床意义。方法选取2015年6月—2017年6月细菌性脓毒血症患者110例,根据患者生存情况分为生存组（84例）和死亡组（26例）。采用酶联免疫吸附试验（ELISA）检测患者血浆HMGB1水平,分析病原菌的分布和构成,以及患者的生存状况与HMGB1的关系。结果生存组和死亡组患者入院第1天HMGB1水平分别为（36.26±23.57）和（42.67±24.86）pg/mL,急性生理与慢性健康评分Ⅱ（APACHEⅡ）分别为（16.52±6.35）和（26.37±6.74）分,差异有统计学意义（P<0.05）;入院7 d内,生存组患者血浆HMGB1水平逐渐降低,而死亡组患者HMGB1水平没有明显变化。HMGB1水平越高,脓毒血症患者感染革兰阴性菌的风险越大。结论 HMGB1水平能有效预测细菌性脓毒血症患者的病情发展,可用于评估其生存状况。

关键词: 高迁移率族蛋白B1, 脓毒血症, 细菌感染, 生存状况

Abstract:

Objective To observe the predictive role of high mobility group box 1 protein（HMGB1）in the survival status of patients with bacterialsepsis. Methods A total of 110 patients with sepsis caused by bacteria confirmed from June 2015 to June 2017were recruited in this study. They were divided into survival group（n=84）and death group（n=26）according to survival status. The plasma level of HMGB1 was measured using ELISA method. The distribution and composition of pathogenic bacteria were analyzed. The relationship between living status and HMGB1 level was investigated. Results HMGB1 leveland APACHEⅡ scorein the survival group were significantly lower than those in the death group were[（36.26±23.57）pg/mL vs（42.67±24.86）pg/mL,16.52±6.35vs26.37±6.74,P<0.05] on the first day after admission.HMGB1 level of the survival group decreased gradually within 7 days after after admission,while HMGB1 level of the death group was unchanged. The higherHMGB1 level,the greaterinfectedrisk of Gram-negative bacteria in sepsis patients. Conclusion HMGB1 can effectively predict the progression of patients with sepsisand evaluate the survival status.

Key words: High mobility group box 1 protein, Sepsis, Bacterial infection, Living status

中图分类号:

R521

付晶, 凃星. 高迁移率族蛋白B1对细菌性脓毒血症患者生存状况评价的临床意义[J]. 检验医学, 2021, 36(1): 80-83.

FU Jing, TU Xing. Serum high mobility group box-1 expression in patients with sepsis caused by bacteria and its clinical significant[J]. Laboratory Medicine, 2021, 36(1): 80-83.

图/表 3

参考文献 17

[1]	HAWIGER J,VEACH R A,ZIENKIEWICZ J.New paradigms in sepsis:from prevention to protection of failing microcirculation[J]. J Thromb Haemost,2015,13(10):1743-56.
[2]	YUKI K,MURAKAMI N.Sepsis pathophysiology and anesthetic consideration[J]. Cardiovasc Hematol Disord Drug Targets,2015,15(1):57-69.
[3]	WEISS S L,FITZGERALD J C,PAPPACHAN J,et al.Global epidemiology of pediatric severe sepsis:the sepsis prevalence,outcomes,and therapies study[J]. Am J Respir Crit Care Med,2015,191(10):1147-1157.
[4]	RIVERS E P,JAEHNE A K,NGUYEN H B,et al.Early biomarker activity in severe sepsis and septic shock and a contemporary review of immunotherapy trials:not a time to give up,but to give it earlier[J]. Shock,2013,39(2):127-137.
[5]	LEE W,KU S,YOO H,et al.Andrographolide inhibits HMGB1-induced inflammatory responses in human umbilical vein endothelial cells and in murine polymicrobial sepsis[J]. Acta Physiol(Oxf),2014,211(1):176-187.
[6]	ZHANG Y G,ZHU X,LU R,et al.Intestinal epithelial HMGB1 inhibits bacterial infection via STAT3 regulation of autophagy[J]. Autophagy,2019,15(11):1935-1953.
[7]	YANG R,ZOU X,TENHUNEN J,et al.HMGB1 neutralization is associated with bacterial translocation during acetaminophen hepatotoxicity[J]. BMC Gastroenterol,2014,14:66.
[8]	CHIRICO V,LACQUANITI A,LEONARDI S,et al. Acute pulmonary exacerbation and lung function decline in patients with cystic fibrosis：high-mobility group box 1（HMGB1） between inflammation and infection[J]. Clin Microbiol Infect,2015,21(4):368.e1-368.e9.
[9]	HAAK B W,WIERSINGA W J.The role of the gut microbiota in sepsis[J]. Lancet Gastroenterol Hepatol,2017,2(2):135-143.
[10]	CLAUSHUIS T A M,DE VOS A F,NIESWANDT B,et al. Platelet glycoprotein Ⅵ aids in local immunity during pneumonia-derived sepsis caused by gram-negative bacteria[J]. Blood,2018,131(8):864-876.
[11]	MAGGIO S D,MILANO G,MARCHIS F D,et al.Non-oxidizable HMGB1 induces cardiac fibroblasts migration via CXCR4 in a CXCL12-independent manner and worsens tissue remodeling after myocardial infarction[J]. Biochim Biophys Acta Mol Basis Dis,2017,1863(11):2693-2704.
[12]	ZHENG Y,ZHU G.HMGB1 suppresses colon carcinoma cell apoptosis triggered by co-culture with dendritic cells via an ER stress-associated autophagy pathway[J]. Mol Med Rep,2018,17(2):3123-3132.
[13]	张冬燕. 细菌性脂多糖诱导骨细胞凋亡及释放HMGB1[J]. 济南:山东大学,2012.
[14]	杨婉,张平安,韩瑞玲. 脓毒症休克患者血浆高迁移率族蛋白B1表达水平动态变化及临床意义[J]. 国际检验医学杂志,2017,38(4):433-435.
[15]	孙诚,江稳强,陈纯波,等. 脓毒症患者血浆高迁移率族蛋白-1的变化及意义[J]. 实用医学杂志,2012,28(11):1806-1808.
[16]	ABDULMAHDI W,PATEL D,RABADI M M,et al.HMGB1 redox during sepsis[J]. Redox Biol,2017,13:600-607.
[17]	GRÉGOIRE M,TADIÉ J M,UHEL F,et al. Frontline science:HMGB1 induces neutrophil dysfunction in experimental sepsis and in patients who survive septic shock[J]. J Leukoc Biol,2017,101(6):1281-1287.

细菌种类	菌株数/株	构成比/%
革兰阳性菌	44	44
表皮葡萄球菌	14	14
金黄色葡萄球菌	21	21
溶血性葡萄球菌	4	4
腐生葡萄球菌	2	2
肺炎链球菌	3	3
革兰阴性菌	56	56
大肠埃希菌	26	26
鲍曼不动杆菌	9	9
肺炎克雷伯菌	7	7
铜绿假单胞菌	5	5
奇异变形菌	6	6
脑膜炎坏血性黄杆菌	2	2
阴沟肠杆菌	1	1
合计	100	100

细菌种类	菌株数/株	构成比/%
革兰阳性菌	44	44
表皮葡萄球菌	14	14
金黄色葡萄球菌	21	21
溶血性葡萄球菌	4	4
腐生葡萄球菌	2	2
肺炎链球菌	3	3
革兰阴性菌	56	56
大肠埃希菌	26	26
鲍曼不动杆菌	9	9
肺炎克雷伯菌	7	7
铜绿假单胞菌	5	5
奇异变形菌	6	6
脑膜炎坏血性黄杆菌	2	2
阴沟肠杆菌	1	1
合计	100	100

病原菌	例数	HMGB1/（pg/mL）
病原菌	例数	<4.10	4.10~25.60	25.60~34.50	>34.50
革兰阳性菌	48
例数		0	7	30	11
阳性率/%		0.00	14.58	62.50	22.92
革兰阴性菌	62
例数		0	8	16	38
阳性率/%		0.00	12.90	25.81	61.29
χ²值			0.034	16.35	25.37
P值			>0.05	<0.001	<0.001

病原菌	例数	HMGB1/（pg/mL）
病原菌	例数	<4.10	4.10~25.60	25.60~34.50	>34.50
革兰阳性菌	48
例数		0	7	30	11
阳性率/%		0.00	14.58	62.50	22.92
革兰阴性菌	62
例数		0	8	16	38
阳性率/%		0.00	12.90	25.81	61.29
χ²值			0.034	16.35	25.37
P值			>0.05	<0.001	<0.001

组别	HMGB1水平/（pg/mL）				APACHEII评分
组别	第1天	第3天	第5天	第7天	APACHEII评分
生存组	36.26±23.57	32.27±14.85	21.42±13.28	10.87±3.74	16.52±6.35
死亡组	42.67±24.86	39.60±21.34	36.57±18.95	43.87±19.28	26.37±6.74
t值	2.024	2.214	2.527	2.985	2.351
P值	<0.05	<0.05	<0.01	<0.01	<0.05