New Insights Into the Mechanisms of Pancreatitis

A number of discrete pathologic events contribute to the initiation and perpetuation of acute pancreatitis.1 These processes are sequential and often interrelated. An emerging theme is that genetic or environmental factors, such as ethanol, may sensitize the gland to injury.1 For example, mice exposed to the coxsackie A virus are dramatically sensitized to the development of ethanol-induced pancreatitis.2 Further, chronic ethanol feeding alone does not cause pancreatitis in rodents, but it does cause animals to develop acute pancreatitis when they receive physiologic concentrations of cholecystokinin (CCK) or cholinergic agonists such as carbachol.1 Remarkably, such noxious stimuli was recently shown to block normal secretion at the apical pole of the pancreatic acinar cell, redirecting the release of digestive enzymes across basolateral membrane into the interstitial space. Insults that target the pancreatic acinar cell often seem to initiate disease.