Abstract

Nearly 100 years ago, Opie [1] described gallstones impacted in the ampulla of Vater as a cause of acute pancreatitis under circumstances of a common channel formed by the common bile duct and the duct of Wirsung. In the same year, Halsted [2] suggested that retrojection of bile into the pancreas was the underlying pathophysiological event linking preampullary gallstone lodgement with consecutive acute pancreatitis. It was only during the past few decades that it became clear that biliary lithiasis and microlithiasis are responsible for about half of all cases of the disease [3–6]. Alcoholism is another major etiological factor in acute pancreatitis [7–9]. Taken together, biliary tract disease and alcoholism account for about 80% of pancreatitis etiologies in Western countries (Table 1). In contrast, other causes such as drugs, hyperparathyroidism, pregnancy, and scorpion stings are rare [7]. Acute pancreatitis following diagnostic or therapeutic procedures is increasingly observed [10–15].

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