Alcohol abuse and the risk of pancreatic cancer
Background: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. Methods: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer...
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Published in | Gut Vol. 51; no. 2; pp. 236 - 239 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and British Society of Gastroenterology
01.08.2002
BMJ BMJ Publishing Group Ltd BMJ Publishing Group LTD Copyright 2002 by Gut |
Subjects | |
Online Access | Get full text |
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Summary: | Background: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. Methods: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. Results: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2–1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9–4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8–10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3–2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6–2.2). Conclusions: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking. |
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Bibliography: | local:0510236 Correspondence to: Dr W Ye, Department of Medical Epidemiology, Karolinska Institutet, Box 281, SE 171 77, Stockholm, Sweden; weiye@mbox.ki.se ark:/67375/NVC-L7QZL9ND-J istex:CEB5C6EB9DA118DC86C06A2D8D20833A5B62E048 href:gutjnl-51-236.pdf PMID:12117886 Correspondence to: Dr W Ye, Department of Medical Epidemiology, Karolinska Institutet, Box 281, SE 171 77, Stockholm, Sweden; weiye@mbox.ki.se |
ISSN: | 0017-5749 1468-3288 1458-3288 |
DOI: | 10.1136/gut.51.2.236 |