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)