Abstract
BackgroundPancreaticobiliary reflux (PBR) causes chronic inflammation of the gallbladder mucosa and changes in the bile components, which are known to promote gallstone formation. This study aimed to investigate the bile biochemistry changes in gallstone patients with PBR and provide new clues for research on the involvement of PBR in gallstone formation.MethodsPatients undergoing surgery for gallstones between December 2020 and May 2021 were eligible for inclusion. The bile biochemistry (including amylase, lipase, triglyceride, cholesterol, free fatty acids [FFAs], alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], and γ-glutamyl transferase [γ-GT]) of the included gallstone patients was analysed to determine correlations with PBR.ResultsIn this study, 144 gallstone patients who underwent surgery were enrolled. Overall, 15.97 % of the patients had an increased bile amylase level, which was associated with older age and significantly higher bile levels of ALP, lipase, triglyceride, and FFAs. Positive correlations were observed between amylase and lipase, triglyceride, FFAs levels in the gallbladder bile. However, the bile levels of triglyceride, FFAs, and lipase were positively correlated with each other only in the PBR group and showed no significant correlation in the control (N) group. In addition, elevated bile FFAs levels were found to be an independent risk factor for gallbladder wall thickening.ConclusionsIn conclusion, PBR-induced increase in FFAs and triglyceride in the gallbladder bile is a cause of gallstone formation, and an increase in bile ALP suggests the presence of cholestasis in PBR.
Highlights
Pancreaticobiliary reflux (PBR) causes chronic inflammation of the gallbladder mucosa and changes in the bile components, which are known to promote gallstone formation
Table 2; Fig. 3A show that the bile levels of lipase, free fatty acids (FFAs), triglyceride and alkaline phosphatase (ALP) were significantly higher in the PBR group than in the N group
The reflux of pancreatic enzymes into the biliary tract and gallbladder, which is induced by PBR, causes chronic inflammation of gallbladder mucosa and changes in the bile components, eventually resulting in the formation of gallstones [7, 24, 26, 27]
Summary
Pancreaticobiliary reflux (PBR) causes chronic inflammation of the gallbladder mucosa and changes in the bile components, which are known to promote gallstone formation. The mechanism of gallstone formation due to PBR is still unclear, and may be related to the hydrolysis of phospholipids and induction of chronic inflammation of gallbladder mucosa. The derivatives of PC hydrolysis by PLA2, such as lysophosphatidylcholine (lysoPC), have been reported to cause biliary epithelial cell damage, leading to chronic mucosal inflammation, hyperplasia, and metaplasia, which are responsible for gallstone formation, gallbladder cancer and biliary tract cancer [6, 12, 13, 17, 18]. In animal models and gallstone patients, gallstone formation is preceded by inflammatory changes in the gallbladder wall, including increased gallbladder wall thickness [1, 19]. Lee et al even found that inflammation is a necessary factor for cholesterol gallstone formation in a model of gallstone formation in prairie dogs [20]
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