[Gastric preneoplastic changes]

Gastric cancer (GC) is the second most common cause of cancer related death worldwide. The 5-year relative survival rate ranges from 10 to 20% of cases. Therefore, it is necessary to diagnose gastric non invasive neoplasia (formerly dysplasia). Correa suggested more than 20 years ago that there was a histological cascade leading to GC: chronic active gastritis --> atrophy (AG) --> achlorydria with nitrocompounds increase --> intestinal metaplasia (IM) type I --> IM type III --> low grade dysplasia (LGD) --> high grade dysplasia (HGD) --> GC. The discovery of Helicobacter pylori infection has imposed a revision of the various pathogenetic stages: 1) GC may arise in the same context as IM and dysplasia, but without any documentable precursor. GC can develop in a context of normochloridria; 2) there are not sufficient data to support endoscopic surveillance for patients with AG; 3) there are doubts about the real necessity to operate histologically a subdivision of IM in subtypes: probably it is more important the extent of IM; 4) dysplasia is the only true histological marker of CG. In fact, LGD is associate or progressed to GC in the 9% of cases, HGD is associated or progressed to GC in the 74% of cases. It emerges the real oncologic risk of dysplasia. Such data are confirmed by immunohistochemical study of the dysplastic lesions. Therefore, an appropriate follow-up of non invasive neoplasia increases the likelihood of CG being detected in its potentially curable stage.