Page last updated: Tuesday, November 18, 2008
Alcohol and pancreatic cancer
It has never been established whether or not alcohol is casually related with pancreatic cancer (PC), with most studies addressing this relationship showing negative results. However, heavy drinking may cause chronic pancreatitis, which is a known PC risk. By mechanisms other than alcohol-related pancreatitis, alcohol may also alter pancreatic function, which in turn may predispose to PC. If alcohol is a PC risk factor, this association should be easiest to document in long-term heavy drinkers, notably alcoholics.

In this population -based cohort study by Ye W, Lagergren J, Weiderpass E, Nyren O, Adami H-Q and Ekbom A., the risk of PC was undertaken in patients with a discharge diagnosis of alcoholism, alcoholic chronic pancreatitis or alcoholic liver cirrhosis. PC risk was also evaluated in cohorts of patients hospitalised for non-alcoholic chronic pancreatitis or non-alcoholic liver cirrhosis.

In a retrospective cohort based on the Swedish Inpatients Register the risk of PC was analysed in patients admitted between 1965-1994 to the hospital for alcoholism (n= 78,688) patients with alcoholic chronic pancreatitis (n=3500), patients with non-alcoholic pancreatitis (n= 4952), patients with alcoholic liver cirrhosis (n=13,553) and patients with non-alcoholic liver cirrhosis (n=7057) Through linkage with nationwide registers follow-up continued until 1995. Standardised incidence ratios (SIRs) expressed the relative risk by taking the Swedish population at large as reference .Relative to non-alcoholics, alcoholics had just a modest excess risk of PC (SIR 1.4, 95% CI 1.2 -1.5). The over representation of smokers in the alcoholic cohort might confound a true SIR of unity. The risk of PC was considerably lower in the patients with non-alcoholic (SIR 2.2, 95% CI 0.9-4.5) than in patients with alcoholic chronic pancreatitis (SIR 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 reserved causation from undiagnosed cancers. The excess risk was moderate in patients with alcoholic liver cirrhosis (SIR 1.9, 95% 1.3-2.8) while no excess was found for non-alcoholic liver cirrhosis (SIR 1.2, 95% CI 0.6-2.2).

Among alcoholics the excess risk for pancreatic cancer is small and might be attributable to confounding smoking. Even amongst alcoholics who had developed complications such as chronic pancreatitis or liver cirrhosis, the excess risk of pancreatic cancer was modest. Therefore it is unlikely that alcohol plays a casual role in the aetiology of pancreatic cancer.

Source. Ye W, Lagergren J, Weiderpass E, Nyren O, Adami H-Q, Ekbom A. Alcohol abuse and the risk of pancreatic cancer. Gut 51 (2002) 236- 239.

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