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 l...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.展开更多
文摘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.
