Oesophageal and Proximal Gastric Adenocarcinomas Are Rare After Detection of Helicobacter pylori Infection

Shria Kumar; David C. Metz; Gregory G. Ginsberg; David E. Kaplan; David S. Goldberg

Disclosures

Aliment Pharmacol Ther. 2020;51(8):781-788. 

In This Article

Results

We identified 36 803 patients who had H pylori identified by pathology, stool antigen, or urea breath test between 01 January 1994 and 31 December 2018. Median age of the cohort was 60.4 years; 91.8% were male. Of these, 108 (0.29%) developed oesophageal and proximal gastric cancers. Table 1 compares those patients who did and did not develop oesophageal and proximal gastric cancers. Those who had future oesophageal and proximal gastric cancers were older, 64.5 vs 61.6 years, P < 0.001 and more likely to be male, 97.2% vs 91.8%, P = 0.04. There were no significant differences in race, but patients with future oesophageal and proximal gastric cancers were more likely to be non-Hispanic/Latino (4.6% vs 11.3%, P = 0.01). They were more likely to have a history of smoking, 35.2% vs 25.5%, P = 0.02.

The cumulative incidence of oesophageal and proximal gastric cancers at 5, 10 and 15 years after detection of H pylori was 0.15%, 0.26% and 0.34%, respectively. When compared to the development of distal gastric adenocarcinomas in the same cohort (persons with detected H pylori infection), where the incidence of non-proximal gastric adenocarcinomas at 5, 10 and 20 years was 0.37%, 0.5% and 0.65%, respectively, the development of oesophageal and proximal gastric cancers is markedly lower, as seen in Figure 1.

Figure 1.

The development of oesophageal and proximal gastric cancers versus the development of distal gastric adenocarcinomas after detection of Helicobacter pylori infection

We then evaluated for factors associated with future oesophageal and proximal gastric cancers using the multivariable competing risk time to event model (Table 2). Increasing age was associated with an increased risk of future oesophageal and proximal gastric cancers SHR: 1.17; 95% CI: 1.09–1.25, P < 0.001 (for each 5-year increase in age at time of H pylori detection). Black, Asian, and Native Hawaiian/Pacific Islanders were less likely to develop future oesophageal and proximal gastric cancers as compared to white patients, P < 0.001, while patients with a history of smoking were more likely to develop future oesophageal and proximal gastric cancers, SHR: 2.06; 95% CI: 1.33–3.18, P = 0.001. Those of Hispanic or Latino ethnicity were less likely to develop future oesophageal and proximal gastric cancers compared to those of non-Hispanic or Latino ethnicity, 0.57 (0.22–1.46), P = 0.06. Figure 2 displays cumulative incidence curves. Importantly, in the multivariable model, whether the patient received prescription for an eradication regimen for H pylori was not found to be significant, and was not included in the final model.

Figure 2.

Cumulative incidence curves for oesophageal and proximal gastric cancers by A) race; B) ethnicity; C) smoking, adjusted for other covariates

A secondary analysis limited to those patients who were prescribed treatment for H pylori evaluated the association of H pylori eradication status with future oesophageal and proximal gastric cancers. Among the 27 748 patients who received a prescription for H pylori eradication, 8474 (30.5%) underwent subsequent re-testing. Of these 8474, 7541 (89.0%) had confirmed H pylori eradication and 933 (11.0%) had persistent H pylori infection. Of the 27 748 patients who received a prescription for H pylori eradication, eradication status was unknown in 19 274 (69.5%). During model building, eradication status was not significant and not included in the final model. Figure 3 displays the difference in future oesophageal and proximal gastric cancers by H pylori eradication status. As compared to those with persistent infection, there was no significant difference in future oesophageal and proximal gastric cancers among those with confirmed eradication of H pylori (SHR 3.28, 95% CI: 0.45–24.10) or unknown eradication status (SHR 2.29, 95% CI: 0.32–16.46). The difference between groups was not significant (P = 0.22) and as such, was not included in the final multivariable model. Results of the final multivariable analysis of this secondary analysis are displayed in Table S1. To note, among this same cohort, persons with both confirmed eradication and unknown eradication status had a markedly lower risk of future non-proximal gastric adenocarcinoma, versus those with persistent infection (SHR for those with confirmed eradication 0.24, 95% CI: 0.15–0.41 and for those with unknown eradication status 0.16, 95% CI: 0.10–0.25, P < 0.001).[19]

Figure 3.

Cumulative incidence curves for the development of future oesophageal and proximal gastric cancers by Helicobacter pylori eradication status

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