Pathology of non‐infective gastritis

Abstract

The discovery of Helicobacter pylori and its intimate role in the development of the most common form of chronic gastritis has elicited a much-needed interest in non-neoplastic gastric pathology. This has been paralleled by an increase in upper endoscopic examinations, which allow recognition of novel patterns and distribution of mucosal injury. Numerous attempts at classification have been made, most based on the acuteness or chronicity of gastric mucosal injury. In this review, we will not offer a new classification but present a detailed description of the major clinicopathological entities, based either on the salient morphological features or the underlying aetiologies, i.e. iatrogenic, autoimmune, vascular or idiopathic.

Haemorrhagic gastritis following Gastrografin administration for adhesive small bowel obstruction: A case report of a rare outcome

“…Acute causes include infection (especially Helicobacter pylori), caustic ingestion and ulcero-haemorrhagic. The latter occurs typically in the presence of ischaemia secondary to shock [16]. Other aetiologies include reactive (bile reflux), iatrogenic (e.g.…”

Rare Gastric Lesions Associated with Helicobacter pylori Infection: A Histopathological Review

“…LG and GG are not distinct clinicopathological entities, but rather morphologic patterns of injury that can be secondary to a variety of underlying etiologies [2-4,6]. The histological identification of intraepithelial lymphocytosis and granuloma formation are key diagnostic features of LG and GG, respectively [1-7].…”

“…However, a morphological diagnosis of LG and GG should elicit clinical and laboratory workups to identify the underlying etiology. In Western countries, LG and GG are generally classified as special forms of H. pylori –negative gastritis [3,4]. However, there is convincing evidence that H. pylori infection contributes to the pathogenesis of both LG [1,5] and GG [6,7,22], and that H. pylori eradication therapy may be an effective treatment [7,13-15,17,23,24].…”

“…H. pylori infection has been linked to a number of rare gastric mucosal lesions with distinctive histological features, including rare forms of gastritis, such as lymphocytic gastritis (LG) [1-5] or granulomatous gastritis (GG) [3,4,6,7], and abnormal immunoglobulin deposits, such as Russell body gastritis (RBG) [8,9] or crystal-storing histiocytosis (CSH) [10,11]. These lesions are easily diagnosed based on their distinctive histological features; however, their development can be attributed to various factors besides H. pylori infection.…”

“…These lesions are easily diagnosed based on their distinctive histological features; however, their development can be attributed to various factors besides H. pylori infection. Therefore, the role of H. pylori as a causative organism remains debatable, and it has been suggested that H. pylori may be an “innocent bystander [2,4,12]. ” Nevertheless, H. pylori eradication therapy has been linked to clinical and histological improvements in a subset of these lesions [7,13-21], which supports the role of H. pylori infection in their development and implies that H. pylori eradication therapy could be an effective treatment.…”