Uwe A Wittel1, Ulrich T Hopt, Surinder K Batra. 1. Departement of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany. uwe.wittel@uniklinik-freiburg.de
Abstract
BACKGROUND AND AIMS: Epidemiological data clearly indicate that cigarette smoking is associated with an increased risk for developing chronic pancreatitis and pancreatic cancer. Despite of this clear epidemiological correlation, cigarette smoke-induced pancreatic damage has only been investigated in a small number of experimental studies. METHODS: Experimental studies examining the effect of cigarette smoke or cigarette smoke constituents on the pancreas were reviewed. RESULTS: Recent data indicate that smoking also induces chronic pancreatic inflammation in rodents within a period of 12 weeks upon exposure with environmental cigarette smoke. Supported by the finding that morphologic pancreatic damage is also induced by nicotine treatment, cigarette smoke-induced pancreatic damage is likely to be caused by a disturbance of regulation of exocrine pancreas. The morphological alterations, however, induced by nicotine, are less pronounced and therefore, other substances and pathophysiologic mechanisms, such as carcinogen action or cigarette smoke-induced reduction of anti-protease activity, are likely to aggravate pancreatic damage upon cigarette smoke inhalation. CONCLUSION: These data indicate that several constituents of cigarette smoke induce a disturbance of pancreatic function. This multifactorial event induces morphologic pancreatic damage upon cigarette smoke exposure in rodents.
BACKGROUND AND AIMS: Epidemiological data clearly indicate that cigarette smoking is associated with an increased risk for developing chronic pancreatitis and pancreatic cancer. Despite of this clear epidemiological correlation, cigarette smoke-induced pancreatic damage has only been investigated in a small number of experimental studies. METHODS: Experimental studies examining the effect of cigarette smoke or cigarette smoke constituents on the pancreas were reviewed. RESULTS: Recent data indicate that smoking also induces chronic pancreatic inflammation in rodents within a period of 12 weeks upon exposure with environmental cigarette smoke. Supported by the finding that morphologic pancreatic damage is also induced by nicotine treatment, cigarette smoke-induced pancreatic damage is likely to be caused by a disturbance of regulation of exocrine pancreas. The morphological alterations, however, induced by nicotine, are less pronounced and therefore, other substances and pathophysiologic mechanisms, such as carcinogen action or cigarette smoke-induced reduction of anti-protease activity, are likely to aggravate pancreatic damage upon cigarette smoke inhalation. CONCLUSION: These data indicate that several constituents of cigarette smoke induce a disturbance of pancreatic function. This multifactorial event induces morphologic pancreatic damage upon cigarette smoke exposure in rodents.
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