Beyond Helicobacter: dealing with other variants of gastritis-an algorithmic approach

Abstract

In daily practice, the presence of inflammation in gastric biopsies prompts a mental algorithm, an early question being whether the lesion present is Helicobacter-associated. If Helicobacter organisms are not found, then there is a further algorithm, governed by the predominant type of inflammatory cells present, and the presence of other features such as intraepithelial lymphocytosis, a subepithelial collagen band, granulomas, coexisting chronic inflammation, focality, and superimposed reactive changes including erosions and ulcers. Each of these generates its own differential diagnosis. If no inflammation is present, then the two major changes specifically looked for are the changes associated with hypergastrinaemia, by far the most common cause of which is treatment with proton pump inhibitors, and reactive changes. These may be present with and without accompanying inflammation, and, when the epithelial changes dominate, the term gastropathy is preferred. In this article, we present an approach to non-Helicobacter inflammation and gastropathies.

Keywords: Helicobacter; Gastritis; IBD; atrophic; autoimmune; gastropathy; lymphocytic; medication; metaplasia.