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Pathogenesis of acute pancreatitis

Santhi Swaroop Vege, MD
Section Editor
David C Whitcomb, MD, PhD
Deputy Editor
Shilpa Grover, MD, MPH


Acute pancreatitis is an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood. A number of conditions are known to induce this disorder with varying degrees of certainty. However, the pathogenesis of this disorder is not fully understood.

This topic review will focus on the current understanding of the pathogenesis of acute pancreatitis. The etiologic conditions associated with this disorder are discussed separately. (See "Etiology of acute pancreatitis".)


A number of animal models have been developed to understand the pathogenesis of acute pancreatitis [1]. None is strictly comparable to the human condition. Gallstones and alcohol abuse, for example, are responsible for 75 percent of cases of acute pancreatitis in humans, but none of the animal models duplicates these situations. In addition, the commonly used agents for inducing pancreatitis in animal models, such as cerulein and a choline-deficient ethionine-supplemented diet, are not recognized causes of human acute pancreatitis.

Nevertheless, the structural and biochemical changes seen in early phases of acute pancreatitis are remarkably constant in different animal models, and similar changes have been demonstrated in human acute pancreatitis. Furthermore, the clinical and pathologic features of human acute pancreatitis, regardless of the inciting event, are very similar.

Thus, despite the limitations of animal models, the data suggest that a similar cascade of events occurs once pancreatitis begins that is independent of the inciting event or initial mechanism. Animal studies have shown that this cascade cannot be halted successfully unless therapy is initiated either prophylactically or within a few hours of the inciting event. It is not clear from these studies why some individuals experience only interstitial or edematous pancreatitis, while others go on to develop the necrotizing form of the disease.


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Literature review current through: Sep 2016. | This topic last updated: Aug 10, 2016.
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