Where there’s smoke there’s not necessarily fire
Apte, M. V., Pirola, R. C., & Wilson, J. S. (2005). Where there’s smoke there’s not necessarily fire. Gut, 54(4), 446-447. doi:10.1136/gut.2004.048785
Although alcohol abuse is a major association of chronic pancreatitis, it is well known that only a minority of heavy drinkers develop clinically evident pancreatitis.1,2 This observation has led to a sustained effort to identify factors that may increase the susceptibility of alcoholics to the development and progression of the disease.
One of the candidate susceptibility factors is smoking. The interest in smoking as a risk factor for the development and accelerated progression of alcoholic pancreatitis is understandable given that a number of smoking/nicotine related effects on the pancreas have been described in the literature. High concentrations of nicotine have been shown to increase pancreatic protein synthesis in isolated acini.3 Nicotine has also been shown to induce vacuolisation and nuclear pyknosis in acinar cells.4 Serum levels of pancreatic enzymes are reported to be significantly increased in smokers after intravenous secretin.5–7 In addition, in vivo and in vitro studies have demonstrated that smoking significantly inhibits pancreatic secretion.8,9 The concept that smoking enhances the toxic effects of alcohol on the pancreas was examined in a recent experimental study where cigarette smoke was administered to anaesthetised rats receiving intravenous ethanol; the …