pylori infection in the FD group was 49.7% [24]. Another study looking at the

discriminatory value of the Rome III questionnaire in dyspeptic patients found that 136 of 191 (71%) patients had FD, and H. pylori infection was present in 70 (51%) [25]. The pathophysiology of FD is multifactorial. selleckchem Although the role of H. pylori in FD remains controversial, it is possible that immune mechanisms seen in other gut infections could be involved in the pathophysiology of dyspepsia. Li et al. [26] reported increased numbers of enterochromaffin cells and mast cells in the duodenum of patients with postinfectious and nonspecific FD compared with healthy controls, in addition to higher levels of chemicals such as histamine and tryptase derived from these cells. This suggests impaired ability of the immune system to terminate the inflammatory response after infection leading to release of potent chemicals that may be involved in the pathogenesis of postinfectious FD [27]. Suzuki et al. [28] have proposed that H. pylori-associated dyspepsia might be considered an organic disease and, as such, a disease entity separated from FD. While several randomized controlled

trials in Western populations have failed to show a significant advantage of H. pylori eradication in patients with FD, a study suggested that Asian patients benefit from treatment for H. pylori infection with as much as a 13-fold increased chance of symptom GDC-0941 mouse resolution following its eradication [29]. The Second Asia Pacific Consensus Guidelines strongly recommended H. pylori eradication in H. pylori-positive patients with FD [30]. A review of current practices in diagnosis and management of functional GI disorders in the Asia-Pacific (AP) region found 58% of doctors who attended the first Asia Pacific Conference in Tokyo in November 2010 checked H. pylori status

in their patients with FD, and when positive, about half (53%) of them opted for eradication therapy [31]. The past few years have seen increased focus on histological assessment and classification of gastritis to provide better correlation with the risk of malignant transformation. The Operative Link on Gastritis Cobimetinib in vitro Assessment (OLGA) classification was introduced in 2007 [32], and placed the histological phenotypes of gastritis on a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). OLGA recommends at least five biopsy samples from: (1) the greater and lesser curvatures of the distal antrum (mucus-secreting mucosa), (2) the lesser curvature at the incisura angularis, where the earliest atrophic-metaplastic changes tend to occur, (3) the anterior and posterior walls of the proximal corpus (oxyntic mucosa).An article reviewed the histology reporting of gastritis and provides useful guidance on how to standardize gastritis histology reports in diagnostic practice [33].