1型肝肾综合征患者内毒素和内皮素1水平分析

高宝秀; 聂鑫; 贺勇; 杨正兵; 罗通行; 宋昊岚; 李贵星

doi:10.3969/j.issn.1001-5256.2014.01.016

1型肝肾综合征患者内毒素和内皮素1水平分析

DOI: 10.3969/j.issn.1001-5256.2014.01.016

1. 四川大学华西医院实验医学科
2. 四川大学华西医院消化内科

基金项目:

四川省科技支撑项目(2010SZ0252)；

详细信息

中图分类号: R575.2
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出版历程
- 收稿日期: 2013-05-13
- 出版日期: 2014-01-20

Analysis of endotoxin and endothelin-1 levels in patients with type 1 hepatorenal syndrome

Department of Laboratory Medicine, West China Hospital, Sichuan University

Research funding:

摘要

摘要:
目的分析肝硬化腹水伴1型肝肾综合征（HRS）患者的临床资料、实验室指标、感染发生率、血清降钙素原（PCT）和内皮素1（ET-1）水平,探讨内毒素和ET-1在HRS发生中的作用。方法纳入本院2009年1月至2012年10月住院的肝硬化腹水伴1型HRS患者56例（HRS组）及肝硬化伴腹水且肾功能正常患者60例（非HRS组）,收集2组患者的一般资料、肝硬化病因、感染发生率及类型、Child-Pugh分级、全身炎症反应综合征（SIRS）评分及平均动脉压（MAP）;同时采集2组患者血液,分析肝肾功能、电解质、PCT、ET-1水平。比较2组患者的临床资料和检测指标。计数资料采用χ2检验,正态分布计量资料组间比较采用成组t检验,非正态分布计量资料组间比较采用Wilcoxon秩和检验。结果 HRS组感染发生率为75.0%,显著高于非HRS组的28.4%（χ2=11.91,P<0.05）。HRS组PCT、ET-1和SIRS分别为8.72（3.14,31.68）ng/L、（13.04±2.82）pg/ml和2.1±1.1,高于非HRS组的0.11（0.04,0.45）ng/L、（5.76±1.68）...
- 肝肾综合征 /
- 肝硬化 /
- 内毒素类 /
- 内皮缩血管肽1
Abstract:
Objective To analyze the clinical data, laboratory parameters, infection rate, and serum procalcitonin ( PCT) and ET- 1 levels of patients with cirrhotic ascites and type 1 hepatorenal syndrome ( HRS) and to investigate the roles of endotoxin and ET- 1 in the development of HRS. Methods Between January 2009 and October 2012, 56 inpatients with cirrhotic ascites and type 1 HRS ( HRS group) and 60 inpatients with cirrhotic ascites who had normal renal function ( non- HRS group) were included in the study. Their general data, causes of liver cirrhosis, infection rates and types, Child- Pugh classification, systemic inflammatory response syndrome ( SIRS) score, and mean arterial pressure ( MAP) were recorded; blood samples were collected to evaluate liver and renal function and measure serum electrolyte, PCT, and ET- 1 levels. The clinical data and laboratory parameters were compared between the two groups. Categorical data were analyzed by chi-square test; comparison of normally distributed continuous data between the two groups was made by independent- samples t test, and comparison of non- normally distributed continuous data between the two groups was made by Wilcoxon rank sum test. Results The infection rate of HRS group ( 75. 0%) was significantly higher than that of non- HRS group ( 28. 4%) ( χ2= 11. 91, P < 0. 05) . The PCT and ET- 1 levels and SIRS score of HRS group [8. 72 ( 3. 14, 31. 68) ng / L, 13. 04 ± 2. 82 pg / ml, and 2. 1 ± 1. 1]were significantly higher than those of non-HRS group [0. 11 ( 0. 04, 0. 45) ng / L, 5. 76 ± 1. 68 pg / ml, and 0. 6 ± 0. 6] ( P < 0. 05) . In addition, the HRS group had significantly higher serum urea, creatine, cystatin C, and K levels than the non- HRS group ( P < 0. 05) , while the HRS group had significantly lower Na and Cl levels than the non- HRS group ( P < 0. 05) . There were no significant differences in ALT and AST levels between the two groups ( P > 0. 05) . Conclusion Endotoxin causes elevated expression of ET- 1, and ET- 1 induces renal perfusion deficiency by intense renal vasoconstriction, thus leading to type 1 HRS. Endotoxin and ET- 1 are closely associated with the development of type 1 HRS.
- hepatorenal syndrome /
- liver cirrhosis /
- endotoxins /
- endothelin-1

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参考文献(23)

[1]WONG F.Hepatorenal syndrome:current management[J].Curr Gastroenterol Rep, 2008, 10 (1) :22-29.

[2]ANGELI P, MERKEL C.Pathogenesis and management of hepatorenal syndrome in patients with cirrhosis[J].J Hepatol, 2008, 42 (Suppl 1) :s93-s103.

[3]ZHANG HQ, NIE X, WU B, et al.Correlation of endotoxin and hepatorenal syndrome in patients with decompensated liver cirrhosis[J].J Clin Hepatol, 2012, 15 (6) :539-541. (in Chinese) 张焕强, 聂鑫, 吴斌, 等.内毒素血症与肝肾综合征的关系研究[J].实用肝脏病杂志, 2012, 15 (6) :539-541.

[4]Chinese Society of Hepatology and Chinese Society of Infectious Diseases, Chinese Medical Association.The guideline of prevention and treatment for chronic hepatitis B[J].J Clin Hepatol, 2006, 22 (1) :3-15. (in Chinese) 中华医学会肝病学分、感染病学分会.慢性乙型肝炎防治指南[J].临床肝胆病杂志, 2006, 22 (1) :3-15.

[5] SALERNO F, GERBES A, GINS P, et al.Diagnosis, prevention and treatment of hepatorenal syndrome with cirrhosis[J].Gut, 2007, 56 (9) :1310-1318.

[6] GARCIA-PAGN JC, CACA K, BUREAU C, et al.Early use of TIPS in patients with cirrhosis and variceal bleeding[J].N Engl J Med, 2010, 362 (25) :2370-2379.

[7]CRDENAS A, GINES P.Hepatorenal syndrome[J].Clin Liver Dis, 2006, 10 (2) :371-385.

[8]WEN Y, WANG DL, LIU P.Activated protein kinase C alpha participates in the decreased glomerular filtration rate in hepatorenal syndrome induced by tumor necrosis factor alpha[J].J Med Res, 2013, 42 (3) :120-123. (in Chinese) 闻颖, 王冬蕾, 刘沛.蛋白激酶Cα激活参与肿瘤坏死因子α引起的肝肾综合征肾小球滤过率下降[J].医学研究杂志, 2013, 42 (3) :120-123.

[9]KRAG A, BENDTSEN F, HENRIKSEN JH, et al.Low cardiac output predicts development of hepatorenal syndrome and survival in patients with cirrhosis and ascites[J].Gut, 2010, 59 (1) :105-110.

[10]MOORE KP, AITHAL GP.Guidelines on the management of ascites in cirrhosis[J].Gut, 2006, 55 (Suppl 6) :vi1-2.

[11]RUNYON BA.AASLD Practice Guidelines Committee.Management of adult patients with ascites due to cirrhosis:an update[J].Hepatology, 2009, 49 (6) , 2087-2107.

[12] European Association for the Study of the Liver.EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis[J].J Hepatology, 2010, 53 (3) , 397-417.

[13]HARBARTH S, HOLECKOVA K, FROIDEVAUX C, et al.Diagnostic value of procalcitonin, interleukin-6 and interleukin-8 in critically ill patients admitted with suspected sepsis[J].Am J Respire Crit Care Med, 2001, 164 (3) :396-402.

[14]XU XY, ZHENG YY.Hepatorenal syndrome-vasoconstrictor or vasodilator?[J].J Clin Hepatol, 2011, 27 (8) :801-803. (in Chinese) 徐小元, 郑颖颖.肝肾综合征——缩血管还是扩血管?[J].临床肝胆病杂志, 2011, 27 (8) :801-803.

[15] GINSP, SCHRIER RW.Renal failure in cirrhosis[J].N Engl J Med, 2009, 361 (13) :1279-1290.

[16]TURBAN S, THULUVATH PJ, ATTA MG.Hepatorenal syndrome[J].World J Gastroenterol, 2007, 13 (30) :4046-4055.

[17]THABUT D, MASSARD J, GANGLOFF A, et al.Model for endstage liver disease score and systemic inflammatory response are major prognostic factors in patients with cirrhosis and acute functional renal failure[J].Hepatology, 2007, 46 (6) :1872-1882.

[18]GAO BX, NIE X, WU B, et al.Implications of elevated levels of prostagtandin I2 and thromboxane A2 in type I Hepatorenal syndrome[J].J Clin Hepatol, 2012, 28 (11) :860-862. (in Chinese) 高宝秀, 聂鑫, 吴斌, 等.Ⅰ型肝肾综合征患者前列腺素I2和血栓素A2水平分析[J].临床肝胆病杂志, 2012, 28 (11) :860-862.

[19]FENHAMMAR J, ANDERSSON A, FORESTIER J, et al.Endothelin receptor a antagonism attenuates renal medullary blood flow impairment in endotoxemic pigs[J].PLoS ONE, 2011, 6 (7) :e21534.

[20]DIVINO JN, CHAWLA KS, da SILA CM, et al.Endothelin-1production by the canine macrophage cell line DH82:Enhanced production in response to microbial challenge[J].Vet Immunol Immunopathol, 2010, 136 (1-2) :127-132.

[21]HOSHINO K, TAKEUCHI O, KAWAI T, et al.Cutting edge:Toll-like receptor 4 (TLR4) -deficient mice are hyporesponsive to lipopolysaccharide:evidence for TLR4 as the Lps gene product[J].J Immunol, 1999, 162 (7) :3749-3752.

[22]SAWAL H, UEDAL T, TAKEYAMA Y, et al.Role of toll-like receptor 4 in the pathophysiology of severe acute pancreatitis in mice[J].Surg Today, 2007, 37 (10) :867-873.

[23]RAKONCZAY Z Jr, HEGYI P, TAKCS T, et al.The role of NF-kB activation in the pathogenesis of acute pancreatitis[J].Gut, 2008, 57 (2) :259-267.

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