Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation

Murphy, Nick; Kodakat, Sadik K.; Wendon, Julia; Jooste, C. A.; Muiesan, Paolo; Rela, Mohamed; Heaton, Nigel

doi:10.1097/00003246-200111000-00011

Cited by 90 publications

(62 citation statements)

References 36 publications

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“…The measurements of lactate concentration are considered to be one of the most reliable biochemical parameters to determine the severity and outcome of acute liver failure and reflect the severity of liver injury (33). Hyperlactatemia develops under clinical conditions in approximately 80% of patients suffering from fulminant liver failure, for example, due to hepatitis-induced enhancement of hepatic and extrahepatic anaerobic glycolytic activity with higher lactate generation together with a reduced hepatocyte capacity and function to clear lactate, altogether resulting in a net hepatic lactate production (34,35). In control, the hepatocellular integrity in the absence of Con A (sham) was not affected by hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Critical Role of Hypoxia and A2A Adenosine Receptors in Liver Tissue-Protecting Physiological Anti-Inflammatory Pathway

Choukèr

Thiel

Lukashev

et al. 2008

Mol Med

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Section: Discussionmentioning

confidence: 99%

Critical Role of Hypoxia and A2A Adenosine Receptors in Liver Tissue-Protecting Physiological Anti-Inflammatory Pathway

Choukèr

Thiel

Lukashev

et al. 2008

Mol Med

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“…Hyperglycaemia may contribute to raised ICP because increased glucose influx leads to cerebral lactic acid accumulation. 71 Hence it may be prudent to keep blood glucose within the normal limits.…”

Section: Nutritional and Metabolic Supportmentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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Acute liver failure (ALF) is a rare, potentially fatal complication of severe hepatic illness resulting from various causes. In a clinical setting, severe hepatic injury is usually recognised by the appearance of jaundice, encephalopathy and coagulopathy. The central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique and multifactorial. Ammonia plays a central role in the pathogenesis. The role of newer ammonia lowering agents is still evolving. Liver transplant is the only effective therapy that has been identified to be of promise in those with poor prognostic factors, whereas in the others, aggressive intensive medical management has been documented to salvage a substantial proportion of patients. A small fraction of patients undergo liver transplant and the remaining are usually treated with medical therapy. Therefore, identification of the complications and causes of death in such patients, and use of appropriate prognostic models to identify those who need liver transplant and those who can be managed with medical treatment is a vital component of therapeutic strategy. In this review, we discuss the various pathogenetic mechanisms and treatment options available. ( J CLIN EXP HEPATOL 2015;5:S104-S115)A cute liver failure (ALF) can be a fatal complication of acute hepatic injury and occurs unpredictably. It is a rare clinical entity marked by the sudden loss of hepatic function and a severe life-threatening course in a person with no prior history of liver disease. ALF represents a syndrome rather than a specific disease, having multiple causes that vary in course and outcome. ALF is difficult to identify in its early stages, resulting in frequent delays in initiation of treatment. The causes of ALF include viral hepatitis, drug induced and toxin-induced liver damage, metabolic errors, ischemia, and miscellaneous rare causes.ALF is defined by three criteria: (1) rapid development of hepatocellular dysfunction (jaundice, coagulopathy), (2) encephalopathy, and (3) absence of a prior history of liver disease. 1 However, the interval between onset of acute hepatic injury (jaundice) and onset of liver failure (encephalopathy with or without coagulopathy) in such patients (icterus-encephalopathy interval; IEI) has been described to be between 4 weeks (Indian definition) 2-4 to 24 weeks (AASLD-ALF study group). 5 Further, due to the diverse natural course, ALF has been sub-classified as hyperacute (IEI # 7 day), acute (IEI # 4 weeks) and sub-acute ALF (IEI $ 5 week to #12 weeks) by British authors. 6 Despite these differences in definitions, the central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique an...

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“…indicated by slightly abnormal coagulation tests and elevated transaminase levels). It has been shown that patients with acute liver failure actually have a splanchnic release of lactate [8], thought to be due to accelerated splanchnic glycolysis and defects in hepatic pyruvate metabolism [9]. In healthy individuals, hepatic lactate clearance is estimated to be up to 70% of the whole body clearance.…”

Section: Discussionmentioning

confidence: 99%

Unexplained severe lactic acidosis in emergency medicine

Ulvin¹

2013

JOURNAL OF CASE REPORTS AND STUDIES

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Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation

Cited by 90 publications

References 36 publications

Critical Role of Hypoxia and A2A Adenosine Receptors in Liver Tissue-Protecting Physiological Anti-Inflammatory Pathway

Critical Role of Hypoxia and A2A Adenosine Receptors in Liver Tissue-Protecting Physiological Anti-Inflammatory Pathway

Management in Acute Liver Failure

Unexplained severe lactic acidosis in emergency medicine

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