AIM:To characterize hyperlactatemia in patients withnon-acetaminophen acute liver failure(ALF)in anattempt to clarify the mechanisms implicated and therole as a prognosis factor.METHODS:In the setting of liver transplantation,63consecutive patients with non-acetaminophen acute liverfailure were studied in relation to tissue oxygenation,hemodynamic and metabolic parameters.Before andafter transplantation,the number of infected patientsand outcome were registered.RESULTS:Acute ALF showed higher levels of lactatethan subacute ALF(5.4±1 mmol/L versus 2.2±0.6mmol/L,P=0.01).Oxygenation parameters were withinthe normal range.Lactate levels showed good correlationwith respiratory quotient(r=0.759,P<0.005),meanglucose administration(r=0.664,P=0.01)andencephalopathy(r=0.698,P=0.02),but not withsplanchnic arteriovenous difference in PCO2,pH and thepresence of infection(P=0.1).Portal vein lactate washigher(P<0.05)than arterial and mixed venous lactate,suggesting its production of hyperlactatemia in theintestine and spleen.The presence of infection was anindependent predictor of survival.CONCLUSION:Hyperlactatemia is not a prognosisfactor due to byproduct of the overall acceleration inglycolysis. AIM: To characterize hyperlactatemia in patients with non-acetaminophenic acute liver failure (ALF) in anattempt to clarify the mechanisms implicated and therole as a prognosis factor. METHODS: In the setting of liver transplantation, 63 consecutive patients with non-acetaminophen acute liver failure were studied in relational 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 lactatethan subacute ALF (5.4 ± 1 mmol / L versus 2.2 ± 0.6 mmol / L, P = 0.01) .Oxygenation parameters were withinthe normal range. Lactate levels showed good correlationwith respiratory quotient (r = 0.759, P <0.005), meanglucose administration (r = 0.664, but not withsplanchnic arteriovenous difference in PCO2, pH and the presence of infection (P = 0.1) .Portal vein lactate washigher (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 inglycolysis.