Abstract

Tobacco smoke, with its complexity of constituents, damages the pancreatic organ in multiple ways. Smoke not only affects pancreatic secretion patterns via its nicotine content but induces inflammatory reactions and exerts carcinogenic effects by several other constituents. Smoke enhances ethanol-induced pancreatic injury and accelerates the development and progression of chronic pancreatitis independent of etiology. Through the process of inflammation, smoking contributes to pancreatic carcinogenesis. The experiment of Wittel and colleagues published in this issue of the American Journal of Gastroenterology sheds further light on this topic by reporting in great detail two different kinds of pancreatic damage in rats exposed to high doses of smoke.

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