BACKGROUND: Arterial ketone body ratio (acetoacetate/3-hydroxybutyrate, AKBR) has been reported to be a useful tool for the estimation of liver functional reserve, but a more recent report has cast doubt on the clinical significance of this redox theory. Furthermore, the effect of a diminution of liver functional reserve on AKBR has not been documented in chronic liver disease. METHODS: AKBR was measured in normal control subjects (n = 10), heavy alcohol drinkers (n = 19), patients with chronic hepatitis (n = 18) and patients with liver cirrhosis (n = 25). RESULTS: Though AKBR was lower in heavy alcohol drinkers (1.66 +/- 0. 82) than in the other noncirrhotic groups (1.97 +/- 0.93 in normal control subjects, 2.25 +/- 1.11 in patients with chronic hepatitis), this discrepancy did not reach a level of significance. AKBR in patients with liver cirrhosis (1.18 +/- 0.52) was significantly lower than that in normal controls (p < 0.01). AKBR in Child's class A, Child's class B, and Child's class C was 1.20 +/- 0.60, 1.07 +/- 0.56, and 1.27 +/- 0.45, respectively, and there were no significant differences among them. CONCLUSION: AKBR may be parallel to liver mitochondrial redox potential and hepatic functional reserve to some extent, but it does not appear to be an accurate parameter for their estimation.
BACKGROUND: Arterial ketone body ratio (acetoacetate/3-hydroxybutyrate, AKBR) has been reported to be a useful tool for the estimation of liver functional reserve, but a more recent report has cast doubt on the clinical significance of this redox theory. Furthermore, the effect of a diminution of liver functional reserve on AKBR has not been documented in chronic liver disease. METHODS: AKBR was measured in normal control subjects (n = 10), heavy alcohol drinkers (n = 19), patients with chronic hepatitis (n = 18) and patients with liver cirrhosis (n = 25). RESULTS: Though AKBR was lower in heavy alcohol drinkers (1.66 +/- 0. 82) than in the other noncirrhotic groups (1.97 +/- 0.93 in normal control subjects, 2.25 +/- 1.11 in patients with chronic hepatitis), this discrepancy did not reach a level of significance. AKBR in patients with liver cirrhosis (1.18 +/- 0.52) was significantly lower than that in normal controls (p < 0.01). AKBR in Child's class A, Child's class B, and Child's class C was 1.20 +/- 0.60, 1.07 +/- 0.56, and 1.27 +/- 0.45, respectively, and there were no significant differences among them. CONCLUSION: AKBR may be parallel to liver mitochondrial redox potential and hepatic functional reserve to some extent, but it does not appear to be an accurate parameter for their estimation.