Risk for gastric cancer after cholecystectomy.
BACKGROUND
It is becoming increasingly evident that chronic inflammation may predispose cancer development. In the stomach, inflammation caused by Helicobacter pylori infection is linked to gastric cancer. Cholecystectomy is regularly followed by duodenogastric bile reflux and reactive gastritis. To test whether a noninfectious long-standing inflammation impels gastric carcinogenesis as well, we assessed the risk of gastric cancer in a large, population-based cohort of cholecystectomized patients.


METHODS
We identified 251,672 individuals, in the Swedish National Inpatient Register, who had undergone cholecystectomy between 1970 and 1997. All incident cases of gastric cancer were identified through linkage to the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for comparisons with cancer rates of the general population in Sweden.


RESULTS
We found an 11% greater overall risk of distal gastric cancer (SIR=1.11, 95% CI 1.04-1.19). The risk increase was only observed among men (SIR=1.21, 95% CI 1.10-1.32), whereas no excess risk was evident for women. For men, the risk was elevated for up to 10 yr after surgery, but this elevation disappeared with longer follow-up time. There was no clear association between cholecystectomy and cardia cancer (SIR=0.95, 95% CI 0.76-1.16).


CONCLUSIONS
Inconsistency over gender strata, implausibly short induction and latency time, and disappearance of the effect over time makes a causal relationship between cholecystectomy and distal gastric cancer less likely. The findings set aside concerns of harmful long-term consequences of cholecystectomy.
Fall
Katja
K
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Ye
Weimin
W
Nyrén
Olof
O
D000368:Aged; D002299:Cardia; D002763:Cholecystectomy / Q000009:adverse effects*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D012737:Sex Factors; D013274:Stomach Neoplasms / Q000209:etiology*