A case of a 57-year-old farmer with a rare type of choledochal cyst (choledochocele; Alonso-Lej's type III) is described. The patient was admitted because of obstructive jaundice and acute biliary infection. Abdominal computed tomography scan showed a cystic lesion in the head of the pancreas, and endoscopic retrograde cholangiopancreatography disclosed cystic dilatation of the terminal portion of the common bile duct. It was suspected that the choledochocele could swell and compress the common bile duct, causing obstructive jaundice and acute cholangitis; therefore, it was surgically resected. We also reviewed 61 cases of choledochocele reported in Japan; the findings were similar to those reported in the English literature.

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.

To characterize liver dysfunction in patients with cirrhosis after variceal bleeding, we analyzed 50 cirrhotic patients who had bleeding esophageal varices with or without shock. Increases in serum total bilirubin levels by 1.5 times were observed within 24 h in 11 of 12 patients with shock who died > 4 days after hemorrhage but in only one of eight patients with shock who survived (p < 0.01). Increases in serum aspartate aminotransferase and alanine aminotransferase by 2.5 times were observed in six patients in the former group but in none of the latter (p < 0.05). In postmortem livers, hepatocellular degeneration with minimal inflammatory cell infiltration was observed. Ischemic hepatitis is frequently noted in cirrhotic patients with ruptured esophageal varices. Patients with increases in the serum level of total bilirubin and/or aminotransferases within 24 h from onset of hemorrhage should be carefully treated even if hemorrhage is controlled.

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