Acute-on-chronic liver failure(ACLF) is increasingly recognized as a complex syndrome that is reversiblein many cases. It is characterized by an acute deterioration of liver function in the background of a pre-existin...Acute-on-chronic liver failure(ACLF) is increasingly recognized as a complex syndrome that is reversiblein many cases. It is characterized by an acute deterioration of liver function in the background of a pre-existing chronic liver disease often associated with a high short-term mortality rate. Organ failure(OF) is always associated, and plays a key role in determining the course, and the outcome of the disease. The definition of ACLF remains controversial due to its overall ambiguity, with several disparate criteria among various associations dedicated to the study of liver diseases. Although the precise pathogenesis needs to be clarified, it appears that an altered host response to injury might be a contributing factor caused by immune dysfunction, ultimately leading to a pro-inflammatory status, and eventually to OF. The PIRO concept(Predisposition, Insult, Response and Organ Failure) has been proposed to better approach the underlying mechanisms. It is accepted that ACLF is a different and specific form of liver failure, where a precipitating event is always involved, even though it cannot always be ascertained. According to several studies, infections and active alcoholism often trigger ACLF. Viral hepatitis, gastrointestinal haemorrhage, or drug induced liver injury, which can also provoke the syndrome. This review mainly focuses on the physiopathology and prognostic aspects. We believe these features are essential to further understanding and providing the rationale for improveddisease management strategies.展开更多
目的探讨肝豆状核变性、乙型肝炎不同肝功能状态时血浆铜蓝蛋白水平的差异及其临床意义。方法用终末期肝病模型(model for end-stage liver disease,MELD)评分衡量肝功能损害的严重性,采用散射比浊法检测并比较分析肝豆状核变性、慢加...目的探讨肝豆状核变性、乙型肝炎不同肝功能状态时血浆铜蓝蛋白水平的差异及其临床意义。方法用终末期肝病模型(model for end-stage liver disease,MELD)评分衡量肝功能损害的严重性,采用散射比浊法检测并比较分析肝豆状核变性、慢加急性肝衰竭极期以及恢复期、慢性乙型肝炎患者的血浆铜蓝蛋白水平。结果肝豆状核变性(n=50)、慢加急性肝衰竭极期和恢复期(n=30)、慢性乙型病毒性肝炎患者(n=50)的MELD评分分别为11.1±6.5、20.4±4.2、10.9±4.9、9.6±9.8,血浆铜蓝蛋白分别为(0.065±0.036)g/L、(0.176±0.037)g/L、(0.210±0.056)g/L、(0.197±0.038)g/L;血浆铜蓝蛋白水平4组之间的两两比较存在差异(F=111.4,P<0.001),肝豆状核变性患者低于其他3组(P<0.001)。结论肝豆状核变性血浆铜蓝蛋白水平显著降低。相对于肝豆状核变性,没有肝衰竭的慢性乙型肝炎血浆铜蓝蛋白水平几乎正常。慢加急性肝衰竭极期血浆铜蓝蛋白水平仅轻度下降,随着肝功能衰竭的恢复,血浆铜蓝蛋白恢复正常。展开更多
目的:总结乙型肝炎病毒(hepatitis B virus,HBV)相关的慢加急性肝衰竭(acute on chronic liver failure,ACLF)患者发生急性肾损伤(acute kidney injury,AKI)的临床特点和预后情况。方法:回顾性分析2010年9月至2019年9月住院治疗的HBV相...目的:总结乙型肝炎病毒(hepatitis B virus,HBV)相关的慢加急性肝衰竭(acute on chronic liver failure,ACLF)患者发生急性肾损伤(acute kidney injury,AKI)的临床特点和预后情况。方法:回顾性分析2010年9月至2019年9月住院治疗的HBV相关的ACLF基础上合并AKI的患者150例,总结患者的性别、发病年龄、实验室检查、Child-pugh分级、MELD评分,并随访患者的生存情况,分析患者的生存时间、影响预后的因素。结果:在发生AKI时,93%患者合并腹水,81%患者合并自发性腹膜炎,65%患者合并肝性脑病,58.7%患者合并肺部感染。AKI 1期90例(60.0%)、2期44例(29.3%)、3期16例(10.7%)。在诊断AKI时合并低钠血症患者,白蛋白水平更低(t=2.571,P=0.011),而尿素氮、血钾及白细胞水平更高(t=3.184,P=0.002;t=2.069,P=0.040;t=2.251,P=0.026)。74.7%患者在30天内死亡,90天生存率为16.7%。在诊断AKI时合并低钠血症患者30天或90天的死亡率均显著高于不合并低钠血症患者(χ^(2)=4.11,P=0.044;χ^(2)=3.901,P=0.0497)。Kaplan-Meier生存分析显示,发生AKI前尿酸异常、发生AKI时存在低钠血症、合并心或肺功能损伤、代谢性酸中毒、上消化道出血、肝性脑病等因素的患者,生存明显差。Cox回归分析显示,存在肝肾以外的脏器功能严重损伤、合并代谢性酸中毒以及高龄,是ACLF发生AKI患者死亡的独立危险因素,死亡风险增加约2~3倍。结论:HBV相关的ACLF患者在发生AKI时大多合并有腹水和自发性腹膜炎,AKI 1期患者多见。合并肝肾以外的脏器功能严重损伤、代谢性酸中毒以及高龄的患者死亡风险高。展开更多
文摘Acute-on-chronic liver failure(ACLF) is increasingly recognized as a complex syndrome that is reversiblein many cases. It is characterized by an acute deterioration of liver function in the background of a pre-existing chronic liver disease often associated with a high short-term mortality rate. Organ failure(OF) is always associated, and plays a key role in determining the course, and the outcome of the disease. The definition of ACLF remains controversial due to its overall ambiguity, with several disparate criteria among various associations dedicated to the study of liver diseases. Although the precise pathogenesis needs to be clarified, it appears that an altered host response to injury might be a contributing factor caused by immune dysfunction, ultimately leading to a pro-inflammatory status, and eventually to OF. The PIRO concept(Predisposition, Insult, Response and Organ Failure) has been proposed to better approach the underlying mechanisms. It is accepted that ACLF is a different and specific form of liver failure, where a precipitating event is always involved, even though it cannot always be ascertained. According to several studies, infections and active alcoholism often trigger ACLF. Viral hepatitis, gastrointestinal haemorrhage, or drug induced liver injury, which can also provoke the syndrome. This review mainly focuses on the physiopathology and prognostic aspects. We believe these features are essential to further understanding and providing the rationale for improveddisease management strategies.
文摘目的探讨肝豆状核变性、乙型肝炎不同肝功能状态时血浆铜蓝蛋白水平的差异及其临床意义。方法用终末期肝病模型(model for end-stage liver disease,MELD)评分衡量肝功能损害的严重性,采用散射比浊法检测并比较分析肝豆状核变性、慢加急性肝衰竭极期以及恢复期、慢性乙型肝炎患者的血浆铜蓝蛋白水平。结果肝豆状核变性(n=50)、慢加急性肝衰竭极期和恢复期(n=30)、慢性乙型病毒性肝炎患者(n=50)的MELD评分分别为11.1±6.5、20.4±4.2、10.9±4.9、9.6±9.8,血浆铜蓝蛋白分别为(0.065±0.036)g/L、(0.176±0.037)g/L、(0.210±0.056)g/L、(0.197±0.038)g/L;血浆铜蓝蛋白水平4组之间的两两比较存在差异(F=111.4,P<0.001),肝豆状核变性患者低于其他3组(P<0.001)。结论肝豆状核变性血浆铜蓝蛋白水平显著降低。相对于肝豆状核变性,没有肝衰竭的慢性乙型肝炎血浆铜蓝蛋白水平几乎正常。慢加急性肝衰竭极期血浆铜蓝蛋白水平仅轻度下降,随着肝功能衰竭的恢复,血浆铜蓝蛋白恢复正常。
