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Gut 2005;54:446-447; doi:10.1136/gut.2004.048785
Copyright © 2005 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2005;54:446-447
© 2005 by BMJ Publishing Group Ltd & British Society of Gastroenterology

COMMENTARY

Chronic pancreatitis

Where there’s smoke there’s not necessarily fire

M V Apte, R C Pirola, J S Wilson

Pancreatic Research Group, The University of New South Wales, Sydney, Australia

Correspondence to:
Correspondence to:
Professor J Wilson
South Western Sydney Clinical School, The University of New South Wales, Level 2, Thomas and Rachel Moore Education Centre, Liverpool Hospital, Liverpool, NSW 2170, Australia; js.wilson@unsw.edu.au


The role of smoking in alcoholic pancreatitis

Keywords: chronic alcoholic pancreatitis; diabetes; calcification; tobacco smoking

The first 150 words of the full text of this article appear below.

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 . . . [Full text of this article]


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Gut 2005 54: 510-514. [Abstract] [Full Text] [PDF]

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