AIM: To characterize hyperlactatemia in patients with non-acetaminophen acute liver failure (ALF) in an attempt to clarify the mechanisms implicated and the role as a prognosis factor. METHODS: In the setting of liver transplantation, 63 consecutive patients with non-acetaminophen acute liver failure were studied in relation to tissue oxygenation, hemodynamic and metabolic parameters. Before and after transplantation, the number of infected patients and outcome were registered. RESULTS: Acute ALF showed higher levels of lactate than subacute ALF (5.4+/- 1 mmol/L versus 2.2+/- 0.6 mmol/L, P=0.01). Oxygenation parameters were within the normal range. Lactate levels showed good correlation with respiratory quotient (r=0.759, P< 0.005), mean glucose administration (r=0.664, P=0.01) and encephalopathy (r=0.698, P=0.02), but not with splanchnic arteriovenous difference in PCO2, pH and the presence of infection (P=0.1). Portal vein lactate was higher (P< 0.05) than arterial and mixed venous lactate, suggesting its production of hyperlactatemia in the intestine and spleen. The presence of infection was an independent predictor of survival. CONCLUSION: Hyperlactatemia is not a prognosis factor due to byproduct of the overall acceleration in glycolysis.
AIM: To characterize hyperlactatemia in patients with non-acetaminophenacute liver failure (ALF) in an attempt to clarify the mechanisms implicated and the role as a prognosis factor. METHODS: In the setting of liver transplantation, 63 consecutive patients with non-acetaminophenacute liver failure were studied in relation to tissue oxygenation, hemodynamic and metabolic parameters. Before and after transplantation, the number of infectedpatients and outcome were registered. RESULTS: Acute ALF showed higher levels of lactate than subacute ALF (5.4+/- 1 mmol/L versus 2.2+/- 0.6 mmol/L, P=0.01). Oxygenation parameters were within the normal range. Lactate levels showed good correlation with respiratory quotient (r=0.759, P< 0.005), mean glucose administration (r=0.664, P=0.01) and encephalopathy (r=0.698, P=0.02), but not with splanchnic arteriovenous difference in PCO2, pH and the presence of infection (P=0.1). Portal vein lactate was higher (P< 0.05) than arterial and mixed venous lactate, suggesting its production of hyperlactatemia in the intestine and spleen. The presence of infection was an independent predictor of survival. CONCLUSION:Hyperlactatemia is not a prognosis factor due to byproduct of the overall acceleration in glycolysis.
Authors: E E Douzinas; P D Tsidemiadou; M T Pitaridis; I Andrianakis; A Bobota-Chloraki; K Katsouyanni; D Sfyras; K Malagari; C Roussos Journal: Am J Respir Crit Care Med Date: 1997-01 Impact factor: 21.405
Authors: J O Clemmesen; A L Gerbes; V Gülberg; B A Hansen; F S Larsen; C Skak; N Tygstrup; P Ott Journal: Hepatology Date: 1999-02 Impact factor: 17.425