Use of aspirin and other nonsteroidal anti-inflammatory drugs and risk of esophageal and gastric cancer.

TLDR

Regular NSAID use is known to reduce colon cancer risk, but evidence for protective effects in other parts of the digestive tract is limited. The study examined whether NSAID use is associated with reduced risk of esophageal and gastric cancers in a large population‑based case–control design. Cases (n = 1,023) with esophageal or gastric adenocarcinomas were identified from three population‑based tumor registries, and controls (n = 695) were selected via random digit dialing and health‑care financing rosters. Current use of aspirin and nonaspirin NSAIDs was associated with a 50–60 % lower risk of esophageal adenocarcinoma, esophageal squamous cell carcinoma, and noncardia gastric adenocarcinoma, with similar reductions for nonaspirin NSAIDs, and these associations remained after excluding recent use or participants with gastrointestinal symptoms, supporting a protective effect of NSAIDs on esophageal and gastric cancer risk though causality remains uncertain.

Abstract

Regular users of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are at reduced risk of colon cancer, but the evidence for protective effects of NSAIDs elsewhere in the digestive tract is scant. We investigated the association between the use of NSAIDs and risk of esophageal and gastric cancer, using data from a large population-based, case-control study. Cases were individuals, ages 30-79 years, diagnosed with esophageal adenocarcinoma (n = 293), esophageal squamous cell carcinoma (n = 221), gastric cardia adenocarcinoma (n = 261), or noncardia gastric adenocarcinoma (n = 368) in three areas with population-based tumor registries. Controls (n = 695) were selected by random digit dialing and through the rosters of the Health Care Financing Administration. After controlling for the major risk factors, we found that current users of aspirin were at decreased risk of esophageal adenocarcinoma [odds ratio (OR), 0.37; 95% confidence interval (CI), 0.24-0.58], esophageal squamous cell carcinoma (OR, 0.49; 95% CI, 0.28-0.87), and noncardia gastric adenocarcinoma (OR, 0.46; 95% CI, 0.31-0.68), but not of gastric cardia adenocarcinoma (OR, 0.80; 95% CI, 0.54-1.19), when compared to never users. Risk was similarly reduced among current users of nonaspirin NSAIDs. The associations with current NSAID use persisted when we excluded use within 2 or 5 years of reference date, which might have been affected by preclinical disease in cases, and when we restricted analyses to subjects reporting no history of chronic gastrointestinal symptoms. Our findings add to the growing evidence that the risk of cancers of the esophagus and stomach is reduced in users of NSAIDs, although whether the association is causal in nature is not clear.