Abstract
Gallstone attacks accompanied by severe liver dysfunction with an elevation of serum transaminase levels above 400 IU/l were studied in this paper. Of patients with gallstone attacks admitted to our department during the past 4 years, 137 cases without complications of hepatic or cardiac diseases were analyzed. They consisted of 88 patients with cholelithiasis, 24 with choledocholithiasis and 25 with both of these lesions. Severe liver dysfunction was found in 10 (7.3%) of the total 137 cases, namely, 6 cases (6.8%) of cholelithiasis, 1 (4.2%) of choledocholithiasis and 3 (120%) of combined lithiasis. Investigation of the time course of total bilirubin, GOT, GPT, LDH and biliary tract enzymes such as LAP in these 10 cases revealed maximum elevation of GOT, GPT and LDH immediately after attack, which was followed by rapid return to normal approximately 10 days later. Biliary tract enzymes, following the course of bilirubin, frequently showed a delayed elevation to the highest level a few days later than transaminase and delayed return to normal. The ERCP and operative findings in the cholelithiasis group were featured by the presence of multiple small stones below 5mm in diameter in 4 of the 6 cases with severe liver dysfunction. The etiology of liver dysfunction in gallstone attacks has not so far been fully elucidated. We consider that the onset of liver dysfunction in cholelithiasis is triggered by an elevation of the intrabiliary pressure due to the blockage of the Ampulla, which is caused by an overflowing of small stones in the gallbladder into the common bile duct. This spontaneous migration of stones to the duodenum was presumed to contribute to a rapid normalization of the transaminase level.
