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Scand J Clin Lab Invest. 2013;73(4):293-9. doi: 10.3109/00365513.2013.773591. Epub 2013 Mar 20.

Lactate metabolism in chronic liver disease.

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  • 1a Center of Functional and Diagnostic Imaging and Research, Department of Clinical Physiology and Nuclear Medicine 239.
  • 2b Gastro Unit, Medical Division 360 Hvidovre Hospital, Faculty of Health Sciences, University of Copenhagen , Hvidovre, Denmark.



In the healthy liver there is a splanchnic net-uptake of lactate caused by gluconeogenesis. It has previously been shown that patients with acute liver failure in contrast have a splanchnic release of lactate caused by a combination of accelerated glycolysis in the splanchnic region and a reduction in hepatic gluconeogenesis.


The aims of the present study were to investigate lactate metabolism and kinetics in patients with chronic liver disease compared with a control group with normal liver function.


A total of 142 patients with chronic liver disease and 14 healthy controls underwent a liver vein catheterization. Blood samples from the femoral artery and the hepatic and renal veins were simultaneously collected before and after stimulation with galactose.


The fasting lactate levels, both in the hepatic vein and in the femoral artery, were higher in the patients than in the controls (P < 0.001) and there were a hepatic net-uptake of lactate in both groups. Fasting lactate concentrations correlated directly with the portal pressure, mean arterial blood pressure, and SaO2 and negatively with ICG clearance.


Lactate levels are elevated in cirrhotic patients compared to controls relating to portal pressure and aspects of liver dysfunction and the lactate levels seem to increase with the severity of cirrhosis. This may not be caused by decreased gluconeogenesis but merely be due to accelerated glycolysis in the splanchnic region. Future studies should focus on the impact of chronic liver disease on lactate kinetics.


Cirrhosis; Swan-Ganz catheterization; galactose; kinetics; portal hypertension

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