A high incidence of inflammation and carcinoma of the biliary tract in patients with anomalous pancreaticobiliary ductal junction has been well documented. The change in biliary phospholipids as a result of the reflux of pancreatic juice into the biliary tract through anomalous pancreaticobiliary ductal junction may be responsible for it. We developed a new method of analysis of phospholipid classes using aminopropyl Bond Elut cartridge for extraction and highperformance liquid chromatography for separation. Satisfactory recovery was achieved (i.e., more than 95% for both phosphatidylcholine and lysophosphatidylcholine). With this method, the bile of 11 patients with anomalous pancreaticobiliary ductal junction was examined. The concentration and proportion of lysophosphatidylcholine in bile were much higher in the presence of anomalous pancreaticobiliary ductal junction than in controls (3.44 ± 1.50 mmol/L vs. 0.52 ± 0.25 mmol/L, 60.0% ± 31.0% vs. 2.3% ± 1.4% in gallbladder bile; p <0.001). In contrast, the concentration of phosphatidylcholine and the sum of phosphatidylcholine and lysophosphatidylcholine in gallbladder bile significantly decreased (p <0.001), but in hepatic bile they did not. An inverse correlation was found between the proportion of lysophosphatidylcholine and phospholipid concentration in gallbladder bile. Phospholipase A2 and amylase activities in bile were markedly high. Increased total fatty acid concentration and proportion of unsaturated fatty acid in bile were found. Total bile acid concentration in gallbladder bile was significantly lower than in controls. These results suggest that a considerable amount of lysophosphatidylcholine, which is known to have a cytotoxic effect, is produced by phospholipase A2 in refluxing pancreatic juice, and an increased concentration of lysophosphatidylcholine gives rise to cell damage causing mucosal hyperplasia and metaplasia. This condition may be one of the factors responsible for the occurrence of carcinoma of the biliary tract. (HEPATOLOGY 1991;13:s438–444.)
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