Mechanisms involved in the onset of post-ERCP pancreatitis

In various prospective studies, the frequency of post-ERCP pancreatitis ranges from 1 to 14%. After exposure to trigger events, injury to the gland occurs extremely rapidly. In experimental models of acute pancreatitis, it has been suggested that digestive enzyme activation might occur within acinar cells and it has been shown that in the early stages of acute pancreatitis induced by secretagogues or by diet, there is a co-localization of digestive enzymes and lysosomal hydrolases within large cytoplasm vacuoles; this co-localization mechanism might result in activation of the digestive enzyme. In this article, we will review the trigger events which may determine the final effect of acute pancreatitis during ERCP and endoscopic sphincterotomy: mechanical, chemical, enzymatic and microbiological. Nonetheless, factors related to the patient and the physician will be considered. Finally, the hypothesis of activation of chemokines by endoscopic maneuvers as a cause of acute pancreatitis will be described.