Shimada K, Yanagisawa J, Nakayama F
Department of Surgery I, Kyushu University Faculty of Medicine, Japan.
Hepatology. 1991 Mar;13(3):438-44.
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 high-performance 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 less than 0.001). In contrast, the concentration of phosphatidylcholine and the sum of phosphatidylcholine and lysophosphatidylcholine in gallbladder bile significantly decreased (p less than 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, isp reduced by phospholipase A2 in refluxing pancreatic juice, and an increased concentration of lysophosphatidylcholine gives rise to cell damage causing mucosal hyperplasia and metaplasia.(ABSTRACT TRUNCATED AT 250 WORDS)
胰胆管连接异常患者中胆管炎和胆管癌的高发病率已有充分记录。胰液通过异常的胰胆管连接反流至胆道导致的胆汁磷脂变化可能是其原因。我们开发了一种新的磷脂类分析方法,使用氨丙基键合硅胶柱进行提取,高效液相色谱进行分离。回收率令人满意(即磷脂酰胆碱和溶血磷脂酰胆碱的回收率均超过95%)。用这种方法检测了11例胰胆管连接异常患者的胆汁。存在胰胆管连接异常时,胆汁中溶血磷脂酰胆碱的浓度和比例远高于对照组(胆囊胆汁中分别为3.44±1.50 mmol/L vs. 0.52±0.25 mmol/L,60.0%±31.0% vs. 2.3%±1.4%;p<0.001)。相比之下,胆囊胆汁中磷脂酰胆碱的浓度以及磷脂酰胆碱和溶血磷脂酰胆碱的总和显著降低(p<0.001),但肝胆汁中未降低。胆囊胆汁中溶血磷脂酰胆碱的比例与磷脂浓度呈负相关。胆汁中磷脂酶A2和淀粉酶活性明显升高。胆汁中总脂肪酸浓度增加,不饱和脂肪酸比例升高。胆囊胆汁中总胆汁酸浓度显著低于对照组。这些结果表明,已知具有细胞毒性作用的大量溶血磷脂酰胆碱在反流的胰液中被磷脂酶A2降解,溶血磷脂酰胆碱浓度升高导致细胞损伤,引起黏膜增生和化生。(摘要截选至250字)