Journal
PANCREAS
Volume 41, Issue 8, Pages 1219-1224Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPA.0b013e31825de97d
Keywords
tobacco consumption; chronic alcoholism; chronic pancreatitis; natural course; risk factors of pancreatitis
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Objectives: Smoking has been shown to affect the course of alcoholic chronic pancreatitis (ACP). However, a dose- dependent relationship between ACP course and the amount of tobacco consumption has not been studied. Methods: All consecutive smokers with ACP were included prospectively. Thresholds were defined at 10, 15, 20, and 30 pack- years (p. y.) to assess the relationship between tobacco intake and ACP complications. Statistical adjustment on alcohol intake was performed. Results: One hundred eight patients (male, 86%) were included. The median tobacco intake was 30 p. y. (range, 3Y90 p. y.) Pancreatic calcifications and duct abnormalities were observed in 70% and 73%, respectively. Pancreatic exocrine insufficiency and diabetes mellitus were observed in 36% and 30%, respectively. No differences in ACP outcome were seen at 10- p. y. threshold. At a 15- p. y. threshold, ACP diagnosis was made earlier (36 versus 46 years; P = 0.0036). At a 20- p. y. threshold, ACP occurred earlier (P = 0.0002), and the patients hadmore often calcifications (P = 0.05). Similar results were observed at the 30- p. y. threshold, but additionally pancreatic exocrine insufficiency occurred earlier (P = 0.04). Conclusion: Tobacco intake accelerates the course of ACP in a dosedependent fashion, apart from the amount of alcohol intake. A major threshold effect is seen in 20 p. y.
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