Intestinal Metaplasia Related to Gastric Cancer: An Outcome Analysis of Biomarkers for Early Detection

Abstract

First of all, H. pylori should be absolutely eradicated for the prevention of MGC develop‐ ment. The efficacy of standard 7-14 day triple therapies is decreasing, mainly due to increas‐ ing primary bacterial resistance to antibiotics. Currently, the most effective treatments are either the sequential regimen or the concomitant therapy. The sequential therapy was first introduced in Italy in 2000 (Zullo et al., 2000). This regimen is a 10-day therapy, including a simple dual therapy with a proton pump inhibitor (PPI) plus amoxicillin 1 g (both twice dai‐ ly) given for the first 5 days, followed by a triple therapy including a PPI, clarithromycin 500 mg, and tinidazole 500 mg (all given twice daily) for the remaining 5 days. Different antibi‐ otic combinations, administered together with a PPI, have been proposed in the last deca‐ des. Unfortunately, no available therapy is able to eradicate H. pylori in all treated patients. Therefore, new drugs and novel therapeutic approaches are needed. It has been recently re‐ ported by a randomized clinical trial that simvastatin as adjuvant to standard therapy im‐ proves significantly the H. pylori eradication rate (Nseir et al., 2012). The search for novel antibacterial therapies against H. pylori is a “work in progress” driven by the goal of pre‐ venting gastric cancer, and by worldwide increasing antibiotic resistance (Fiorini et al., 2012). We believe that MSI and mAb Das-1 reactivity may be reliable biomarkers to identify a sub‐ group of patients at sufficiently high risk of MGC after endoscopic resection to justify endo‐ scopic surveillance. According to recent reports, H. pylori eradication is able to significantly reduce gene methylation thus delaying or reversing H. pylori-induced-gastric carcinogenesis (Chan et al., 2006; Leung et al., 2006; Perri et al., 2007). It has been also reported that sonic hedgehog methylation was detected more frequently in the high-risk group for gastric can‐ cer after H. pylori treatment (Shiotani et al., 2012). Further studies on genetic and epigenetic alterations, are necessary to clarify the credibility of the markers in different regional popu‐ lations