Author Santhi Swaroop Vege, MD Section Editor David C Whitcomb, MD, PhD Deputy Editor Shilpa Grover, MD, MPH Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Oct 2012. | This topic last updated: Apr 18, 2012. INTRODUCTION Acute pancreatitis is an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood [1,2]. The pathogenesis of acute pancreatitis is not fully understood. Nevertheless, a number of conditions are known to induce this disorder with varying degrees of certainty, with gallstones and chronic alcohol abuse accounting for 75 percent of cases in the United States (table 1). This list will undoubtedly continue to grow, and the number of cases diagnosed as "idiopathic" will decrease as our understanding of the disease improves. This topic review will discuss the etiology of acute pancreatitis. The clinical manifestations, diagnosis, general principles of therapy, and pathogenesis of acute pancreatitis are discussed separately. (See "Predicting the severity of acute pancreatitis" and "Treatment of acute pancreatitis" and "Pancreatic debridement" and "Pathogenesis of acute pancreatitis".) INCIDENCE AND MORTALITY Accurate assessment of the incidence and mortality of acute pancreatitis is difficult as mild pancreatitis may be subclinical and deaths may occur before the diagnosis is made in severe and fulminant attacks. The reported annual incidence of acute pancreatitis has ranged from 4.9 to 35 per 100,000 population [3]. The incidence of acute pancreatitis is increasing in many European and Scandinavian countries due to increased alcohol consumption and better diagnostic capability [4]. In a retrospective study from the Netherlands, the observed incidence of acute pancreatitis increased by 28 percent between 1985 and 1995.