1型肝肾综合征患者内毒素和内皮素1水平分析

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

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)pg/ml和0.6±0.6(P<0.05)。实验室指标中,HRS组血清尿素、肌酐、半胱氨酸蛋白酶抑制剂及钾水平高于非HRS组,差异有统计学意义(P<0.05);而HRS组的Na、Cl水平低于非HRS组,差异有统计学意义(P<0.05),两组间ALT、AST差异无统计学意义(P>0.05)。结论内毒素诱导ET-1表达增加,ET-1强烈收缩肾血管引发肾灌注不足,导致1型HRS的产生。内毒素和ET-1与1型HRS发生关系密切。

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 develop- ment 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 arteri- al 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 compari- son 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%） （X2 = 11.91, P 〈 0.05 ）. The PCT and ET - l 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/mi, 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 C1 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 vasocon-striction, thus leading to type 1 HRS. Endotoxin and ET - 1 are closely associated with the development of type 1 HRS.