Helicobacter pylori infection and serum level of pepsinogen are associated with the risk of metachronous gastric neoplasm after endoscopic resection.

BACKGROUND

Patients who have undergone endoscopic resection of early gastric cancers (EGCs) are at risk for metachronous gastric neoplasm.

AIM

To determine whether serum level of pepsinogen (PG), a marker of gastric atrophy, can determine which patients who have undergone endoscopic submucosal dissection for EGC are at risk for metachronous gastric neoplasm. We also investigated the effects of Helicobacter pylori eradication on metachronous gastric neoplasm incidence.

METHODS

We performed a retrospective study of 590 consecutive patients who underwent endoscopic submucosal dissection for EGC, from January 2008 to May 2013 at a tertiary centre in South Korea; serum levels of PG were measured at the time of endoscopic submucosal dissection and H. pylori infection status were recorded. In case of proven presence of current H. pylori infection, eradication treatment was provided. Patients underwent follow-up endoscopies at 3 months, 9 months, and each year after the procedure to detect neoplasms and were tested for H. pylori infection; serum levels of PG were measured at these time points from 442 of the patients. The main and sub-cohorts were assessed for baseline characteristics, H. pylori infection, serum level of PG, and metachronous gastric neoplasm lesions.

RESULTS

During a median follow-up period of 47.7 months, 64 patients developed metachronous gastric neoplasms. In multivariate analysis of the main cohort (n = 590), risk factors for metachronous gastric neoplasm included persistent H. pylori infection (hazard ratio [HR], 2.532; P = .022) and serum ratio of PGI:PGII of three or less at the time of endoscopic submucosal dissection (HR, 1.881; P = .018). Among patients with serum PG measurements, persistent H. pylori infection (odds ratio [OR], 4.404; P = .009) and persistent decrease in mean serum ratio of PGI:PGII to 3 or less were associated with increased risk of metachronous gastric neoplasm (OR, 2.141; P = .039).

CONCLUSIONS

In a retrospective analysis of patients who underwent endoscopic resection of EGCs, eradication of H. pylori infection reduced risk for metachronous gastric neoplasm. Serum ratio of PGI:PGII of 3 or less also increase risk of metachronous gastric neoplasm after endoscopic submucosal dissection. ClinicalTrials.gov. registry number, NCT02682446.