Published online Mar 28, 2006. doi: 10.3748/wjg.v12.i12.1949
Revised: August 2, 2005
Accepted: August 26, 2005
Published online: March 28, 2006
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.