Characteristics and predictors of gastric cancer after Helicobacter pylori eradication

Abstract

Helicobacter pylori (H. pylori) eradication can reduce gastric cancer. However, gastric cancer still develops after eradication, and cases who received eradication therapy are increasing. In this study, we have reviewed the characteristics and predictors of primary gastric cancer developing after H. pylori eradication. In terms of the characteristics, endoscopic, histologic, and molecular characteristics are reported. Endoscopically, gastric cancer after eradication is often depressed-type and shows a gastritis-like appearance, which sometimes makes the diagnosis difficult. Histologically, most gastric cancer after eradication is intestinal type, and non-neoplastic epithelium, also called epithelium with low-grade atypia, is frequently seen over the tumor, which is presumably the cause of the endoscopic gastritis-like appearance. As for molecular characteristics, some markers, such as Ki67, MUC2, and Wnt5a expression, are lower in cancer from patients in whom H. pylori has been eradicated. In terms of predictors, several Japanese studies have reported that severe endoscopic atrophy at eradication is a risk factor for gastric cancer development. Histologic intestinal metaplasia, especially in the corpus, and long-term use of proton pump inhibitors, are also reported as risk factors for gastric cancer after H. pylori eradication. These studies on the characteristics and predictors of gastric cancer development will become the cornerstone for establishing a novel surveillance program based on the gastric cancer risk stratification specific to H. pylori-eradicated patients.

Gastric microbes associated with gastric inflammation, atrophy and intestinal metaplasia 1 year afterHelicobacter pylorieradication

“…The development of gastric atrophy and IM leads to loss of acid-secreting parietal cell 38. This may favour the proliferation of gastric microbes or colonisation of the stomach by oral microbes 39. We recognised that the emergence of atrophy or IM was associated with increased abundance of Granulicatella , Actinomyces , Rothia , Peptostreptococcus , Streptococcus , Abiotrophia and Parvimonas , in the absence of H. pylori .…”

Assessment of Endoscopic Gastric Atrophy according to the Kimura-Takemoto Classification and Its Potential Application in Daily Practice

“…As successful eradication of H. pylori could not eliminate the risk of GC, [28][29][30][31][32][33][34] it is important to identify high-risk individuals who still need surveillance after eradication. Several studies have consistently confirmed that the severity of EGA at baseline is associated with not only the current presence of GC but also the risk for GC development (Table 1).…”

“…41 However, eradication therapy can make the detection of metachronous GC very challenging, as post-eradication GC lesions often have a depressed-type and gastritis-like appearance. 32 Some studies have reported that moderate-to-severe EGA is a risk factor for metachronous GC (Table 2). 26,42,43 Therefore, endoscopists should also carefully search for subtle suspicious lesions in patients with this endoscopic finding.…”

Prevention of gastric cancer by Helicobacter pylori eradication: A review from Japan

“…It has also been reported that the incidence of primary EGC increases 5 years after H pylori has been eradicated . Moreover, this new form has been observed not only in MGC but also in primary EGC after H pylori eradication (Figure ) …”

“…21 Moreover, this new form has been observed not only in MGC but also in primary EGC after H pylori eradication (Figure 4). [22][23][24][25] Because this form of EGC is different from that of gastric cancer that occurs in the conventional H pylori-infected stomach, there is a possibility that this form of cancer may be misdiagnosed or diagnosed after it has progressed to a later stage. In addition, the belief among endoscopists that gastric cancer is less likely to develop after H pylori eradication may lead to a detection bias.…”