Gastritis

Definition of gastritis has its basis in histological features of the gastric mucosa. It is not erythema observed during gastroscopy, and there are no specific clinical presentations or symptoms defining it. The current classification of gastritis centers on time course (acute versus chronic), histological features, anatomic distribution, and underlying pathological mechanisms. Acute gastritis will evolve to chronic, if not treated. Helicobacter pylori (H. pylori) is the most common cause of gastritis worldwide. However, 60 to 70% of H. pylori-negative subjects with functional dyspepsia or non-erosive gastroesophageal reflux were also found to have gastritis. H. pylori-negative gastritis is a consideration when an individual fulfill all four of these criteria (i) A negative triple staining of gastric mucosal biopsies (hematoxylin and eosin, Alcian blue stain and a modified silver stain), (ii) A negative H pylori culture, (iii) A negative IgG H. pylori serology, and (iv) No self-reported history of H. pylori treatment. In these patients, the cause of gastritis may relate to tobacco smoking, consumption of alcohol, and/or the use of non-steroidal anti-inflammatory drugs (NSAIDs) or steroids. Other causes of gastritis include: 1. Autoimmune gastritis associated with serum anti-parietal and anti-intrinsic factor antibodies; characterized by chronic atrophic gastritis limited to the corpus and fundus of the stomach that is causing marked diffuse atrophy of parietal and chief cells. 2. Gastritis causes include organisms other than H. pylori such as Mycobacterium avium intracellulare, Herpes simplex, and Cytomegalovirus. 3. Gastritis caused by acid reflux. Rare causes of gastritis include collagenous gastritis, sarcoidosis, eosinophilic gastritis, and lymphocytic gastritis. Clinical presentation, laboratory investigations, gastroscopy, as well as the histological and microbiological examination of tissue biopsies are essential for the diagnosis of gastritis and its causes. Treatment of H. pylori-associated gastritis results in the rapid disappearance of polymorphonuclear infiltration and a reduction of chronic inflammatory infiltrate with the gradual normalization of the mucosa. Mucosal atrophy and metaplastic changes may resolve shortly, but it is not necessarily the outcome of treatment of H. pylori in all treated patients. Other types of gastritis should be treated based on their causative etiology.