Korean Journal of Medicine (대한내과학회지), Vol.85(2) : 111~115, 2013
Acute pancreatitis is an inflammatory disease that is caused by various etiologies including gallstone, alcohol or hypertriglyceridemia. Although most cases of acute pancreatitis show self-limiting course, severe cases are still associated with significant morbidity and mortality. The pathogenic mechanisms of acute pancreatitis are not fully understood. However, it is a central dogma that premature intracellular activation of trypsinogen is the earliest pathologic event. Even though it remains unknown how intracellular trypsinogen activation can be caused by such diverse etiologies, this initial insult in pancreatic acinar cells lead to local inflammatory complications and a systemic response or death. Pathophysiologic mechanisms related to the progression of acute pancreatitis include microcirculatory injury, chemoattraction of inflammatory cells, release of pro-inflammatory cytokines, and bacterial translocation to pancreas and systemic circulation. Recently, several interesting transgenic mice model experiments shed a light in trypsin independent mechanism of local and systemic inflammation for progression of acute pancreatitis.