pylori and nonmalignant disease. This paper reviews RAD001 the literature from the past year on this association. For more than a decade, the histologic classification of gastritis remained unchanged, and histologic assessment of the presence of gastritis was customarily performed by means of the Sydney system
[2]. However, over the past three years, there has been a revival of interest for this subject. For a better correlation with the risk of neoplastic progression, the Operative Link on Gastritis Assessment (OLGA) classification has been introduced [3]. In this staging system, the presence of atrophic gastritis and its topography is graded into stages I to IV. A recent study showed that interobserver agreement of this classification can be improved by grading intestinal metaplasia instead of atrophic gastritis, as in this study the overall agreement between pathologists increased from 0.64 (kappa value) for atrophic gastritis to 0.87 (kappa value) for intestinal metaplasia [4]. All together, this leads to a classification system that allows rapid evaluation of the risk of neoplastic progression in terms of the severity and distribution of intestinal metaplasia, based on the combination of antrum and corpus biopsy specimens. (Table 1) This approach is supported by cohort studies focusing on cancer
risk in patients with different grades of premalignant changes of the gastric lining [5]. Over the past years, evidence is accumulating on the potential association Selleckchem AZD9668 between H. pylori and autoimmune gastritis [6–8]. This association is thought to 3-mercaptopyruvate sulfurtransferase be explained by H. pylori infection as a trigger of gastric autoimmunity, with subsequent development
of autoimmune gastritis and pernicious anemia [6,9]. In this hypothetical process, molecular mimicry plays a central role, which means that a cross-activation occurs between H. pylori derived antigens and autoantigens of the gastric mucosa inducing a process of auto-immunity [10]. Unfortunately, the confirmation of an etiologic link between longstanding H. pylori infection and pernicious anemia is hindered by several factors, the low grade of colonization or even disappearance of H. pylori in the presence of gastric atrophy, a negative serology several years after clearance of H. pylori infection, the low incidence of autoimmune gastritis, and the asymptomatic onset explaining why autoimmune gastritis is rarely diagnosed at an early stage. Very large cohort studies of H. pylori-positive subjects are required to investigate this association, and their results should be awaited. As H. pylori-related peptic ulcer disease (PUD) is the cause of symptoms in only a minority of patients with dyspepsia, recommendations on H. pylori testing and subsequent eradication in all patients with dyspeptic symptoms vary greatly [11–13]. The effect of H.