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Chronic gastritis caused by Helicobacter pylori infection increases risk for developing adenocarcinoma of the gastric body. Chronic mucosal inflammation also occurs because of bile reflux after cholecystectomy, but whether this chronic inflammation also increases risk for gastric cancer is unclear.
To evaluate this question, investigators in Sweden studied a cohort of 251,672 patients who underwent cholecystectomy from 1970 through 1997 and who were identified in the Swedish National Inpatient Register. All cases of gastric cancer in the same population were identified using the Swedish Cancer Registry and were linked to the cholecystectomy cohort through unique record numbers. The incidence of gastric cancer in the cholecystectomy cohort was compared to its incidence in the general Swedish population.
Compared with the general population, cholecystectomy patients had increased risk for noncardia gastric cancer during the first year after surgery (standardized incidence ratio [SIR], 1.41; 95% CI, 1.13–1.73). After excluding occurrences during the first year, the incidence was still 11% higher in the cholecystectomy group (SIR, 1.11; 95% CI, 1.04–1.19). Increased risk remained for 10 years after surgery; after that, the cohort and the general population had equivalent risk. After excluding the first postoperative year, no increase was noted in risk for cancer of the cardia. Sex did not influence risk for cancer of the cardia.
The authors noted that these data are inconsistent with known characteristics of gastric cancer, which include a higher incidence in men and a long latency time between the initiation of inflammation and the development of cancer. Because risk for post-cholecystectomy gastric cancer was the same in both sexes, and because the association was attenuated over time (instead of increasing over time), the investigators concluded that cholecystectomy is unlikely to cause gastric cancer.
Fall K et al. Risk for gastric cancer after cholecystectomy. Am J Gastroenterol 2007 Jun; 102:1180-4.
Comment
This study demonstrates an important issue that arises with large population-based studies. The presence of a statistically significant association does not prove causation. Such studies potentially have many confounding factors that can cause weak, but statistically significant, associations, as seen here. The data must be interpreted in the light of known characteristics of the disease. If the data conflict with these characteristics, as in this case, one should be skeptical of a causative effect. A caveat here, however, is that bile actually might act as a carcinogen, and cholecystectomy might slightly increase risk for cancer in a manner that is different from that of H. pylori infection.