However, a large majority progress

to chronic active gastritis, where from thenceforth the fork in the road develops. A proportion of patients will develop antral predominant gastritis which may subsequently be complicated by duodenal ulcer(s) and/or rarely Acalabrutinib in vivo lymphoma, whilst another proportion will develop multifocal atrophic gastritis and subsequently become at risk for developing gastric ulcer(s), gastric cancer and rarely lymphoma. Why one individual during the course of their HP infection should clear the infection without the use of antibiotics is uncertain, and why individuals should arrest at any stage of this “pathway” without progressing to develop complications again is unresolved. The nature of acute infections with HP are understood due to a small number of cases where investigators and/or volunteers have been intentionally infected with the bacteria.29,30 Acute gastritis results histologically in a neutrophilic gastritis followed by a gradual infiltration by all classes

of inflammatory cells, including prominently lymphocytes and coupled with a transient hypochlorhydria. Post-acute gastritis, two patterns of chronic gastritis are observed and this difference in topography is associated with different diseases. Antral predominant gastritis is seen usually in conjunction with little or no gastric atrophy in duodenal selleck chemical ulcer disease, with normal or increased acid secretion.30–33 This is in comparison to the extensive pattern of gastritis with corpus (usually with antral) atrophy which tends to progress through intestinal metaplasia, to intestinal-type gastric cancer with hypochlorhydria, or achlorhydria. Carbohydrate The location of a peptic ulcer, when considered in association with HP infection gives the clinician the pattern and topography of HP-associated inflammation in the stomach. Duodenal ulcers are associated with antral predominant gastritis of the non-atrophic variety, hypergastrinaemia and hypersecretion of acid.30 Patients with duodenal ulcer virtually never develop body atrophic gastritis and consequently retain robust acid secretion.34,35

Conversely, gastric ulcers are thought to be associated with a chronic non-atrophic gastritis initially which progresses to chronic atrophic gastritis which involves both corpus and, invariably, the antrum and decreased acid output.36,37 Importantly, in patients with CAG, some studies have found that eradication of HP infection partially reverses the hypochlorhydria/achlorhydria seen resulting in an improvement in inflammation histologically.38–43 Annibale et al. report only 20% of their study patients reversed gastric body atrophy after HP eradication, whilst the remaining 80% retained gastric atrophic change or IM that was initially observed.44 Of note, patients with CAG may progress to intestinal metaplasia (IM).