Background & aims: Patients with acetaminophen-induced fulminant hepatic failure may have the capacity for recovery if sufficient liver cell mass remains to allow regeneration. We investigated the prognostic potential of the galactose elimination capacity (GEC) as a noninvasive measurement of functioning liver cell mass in severe acetaminophen-induced hepatotoxicity.
Methods: All patients admitted with acetaminophen poisoning during a 10-year period were studied retrospectively. A total of 220 patients who had at least one GEC performed were included in the study.
Results: The GEC was lower in patients with than without hepatic encephalopathy (14.5 +/- 5.6 micromol/min/kg vs. 23.2 +/- 6.7 micromol/min/kg; P < 0.0001). Among patients with hepatic encephalopathy, the GEC was significantly higher in spontaneous survivors than in nonsurvivors (16.8 +/- 5.6 micromol/min/kg vs. 12.2 +/- 4.7 micromol/min/kg; P < 0.0001). In a logistic regression analysis, GEC was associated independently with mortality (odds ratio: 1.28 per 1 micromol/min/kg decrease in GEC; 95% confidence interval: 1.14-1.45). A threshold GEC of 16.5 micromol/min/kg to identify nonsurvivors had a sensitivity of 90%, a specificity of 72%, a positive predictive value of 49%, and a negative predictive value of 96%. None of 14 patients with hepatic encephalopathy and a GEC less than 10 micromol/min/kg survived.
Conclusions: The GEC was strongly associated with development of hepatic encephalopathy and death from acetaminophen-induced fulminant hepatic failure. The GEC was too unspecific to be used alone for identification of transplantation candidates, but it may be useful as a supplement to other selection criteria.