Serum pepsinogen levels can quantify the risk of development of metachronous gastric cancer after endoscopic resection

Abstract

We have previously reported that serum pepsinogen (PG) can quantify the level of gastric mucosal atrophy, and that H. pylori eradication reduces cancer development in subjects with mild atrophy identified by serum PG levels. The aim of this study was to elucidate the predictive ability of serum PG levels for the development of metachronous gastric cancer (MGC) after endoscopic resection (ER) of primary cancer in association with H. pylori eradication. A retrospective chart review was performed, and 330 patients who underwent ER for initial early gastric cancer were enrolled. Presence or absence of H. pylori, serum PG levels, and endoscopic atrophy at ER were evaluated. H. pylori eradication was performed at the patient's request after ER. The incidence of MGC in these patients was analyzed. Of 330 patients, 47 developed MGC. Endoscopic extensive atrophy was observed more frequently in patients with MGC (p 5 0.001). Although PG I or PG II alone did not significantly differ according to development of MGC, the proportion of PG I/II 3.0, which is one of the criteria of PG test-positive, was significantly higher in patients with MGC (83 vs. 69%, p 5 0.04). H. pylori eradication after ER did not affect MGC development (p 5 0.2). On multivariate analysis, serum PG I/II ratio 3.3 was significantly associated with the development of MGC (hazard ratio: 3.66, 95% confidence interval: 1.47-12.25, p 5 0.004). The risk of MGC after ER could be quantitatively predicted by the PG I/II ratio regardless of H. pylori status.The International Agency for Research on Cancer (IARC) GLOBOCAN indicated that an estimated 1 million new cases of gastric cancer occurred worldwide in 2012, and it was the third most common cause of cancer death, accounting for 723,000 deaths. 1,2 In Japan, gastric cancer is the second most common cause of cancer death, accounting for 49,000 deaths per year.Accompanied by improvements in and increased use of endoscopy, detection of early stage gastric cancer has become more frequent. With improvement in endoscopic resection (ER) technique, represented by endoscopic submucosal dissection (ESD), ER has been widely accepted for local tumor resection. One of the merits of ER is that it can preserve the entire stomach. However, the procedure inevitably leaves stomach encompassing atrophic gastric mucosa, which is considered to be a hazardous region for cancer development. Hence, follow-up endoscopy for detecting metachronous gastric cancer (MGC) after ER is important.H. pylori infection causes chronic gastritis, which results in gastric atrophy, intestinal metaplasia, dysplasia and cancer. [3][4][5] In 1994, the IARC categorized H. pylori as a Group 1 carcinogen for gastric cancer. Recently, several meta-analyses reported the preventive effect of H. pylori eradication on gastric cancer development, [6][7][8][9] and the effect appears to be influenced by the background gastric mucosal status to some extent. Chen et al. reported that H. pylori eradication reduced the risk of gastric cancer in patients with non-atrop...

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

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