Molecular mechanisms of alcohol associated pancreatitis

Figure 1 Proposed model for the development of alcoholic chronic pancreatitis. This proposed model incorporated alcohol abuse into the seminal acute pancreatitis event (SAPE) model proposed by Whitcomb. Alcohol metabolism results in biochemical and molecular changes in acinar cells that sensitizes the pancreas to injury. A secondary trigger initiates an initial episode of acute pancreatitis. This is the SAPE. Repeated clinical or subclinical episodes of pancreatitis coupled with ethanol-induced aberrant repair and regeneration of the damaged pancreas leads to fibrotic scarring which eventually results in chronic pancreatitis.