Gastritis may be an acute or chronic condition. The acute form may be precipitated by the ingestion of chemicals such as salicylates, non-steroidal anti-inflammatory agents, acid, and alkali. Other possible causes include thermal injury, ionizing radiation, uraemia, generalized stress, and shock following infection by Gram-negative bacteria. Damage to the gastric mucosal barrier results in acute inflammation, with oedema and polymorphonuclear infiltration of the mucosa, submucosa, and lamina propria. In severe cases this process can lead to ischaemia, followed by sloughing of necrotic mucosa and by erosive gastritis or frank ulcer formation. For the most part, acute gastritis is self-limiting and is amenable to medical therapy alone; operative intervention is required in only a small percentage of cases. Appropriate surgical treatment of the complications of acute gastritis may involve simple oversewing of ulcerations, vagotomy and pyloroplasty, or even total gastric resection, as dictated by the nature of the specific case.

The common forms of chronic gastritis—chronic superficial gastritis, atrophic gastritis, and gastric atrophy—exist as a spectrum of disease with respect to both mucosal inflammation and glandular atrophy. The inflammatory infiltrate typically seen in chronic gastritis is composed predominantly of lymphocytes and plasma cells, and may be limited to the mucosa or extend into the muscularis. The degree of glandular cell atrophy is not related to the intensity of the infiltrate in a simple fashion, little inflammation typically being seen in patients with complete gastric atrophy. Chronic superficial gastritis is characterized by limitation of the inflammatory infiltrate to the foveolar region of gastric mucosa without appreciable glandular atrophy. In chronic atrophic gastritis a variable degree of parietal loss of chief cells is seen. In true gastric atrophy glandular elements are entirely lost, although mucus-secreting cells are retained in the gastric pits. The gross pathological and endoscopic appearance of atrophic gastritis is that of a friable, grey mucosa with reduced or absent folds. Chronic superficial gastritis may be difficult to recognize grossly, endoscopic biopsy being required for diagnosis.

Functional alterations associated with atrophic gastritis include reduction in both basal acid output and maximal acid response, which may exceed that predicted on the basis of the degree of glandular cell loss observed histologically. Decreased secretion of pepsinogen and intrinsic factor are also observed. Because most of these abnormalities are asymptomatic, chronic gastritis is often diagnosed as an incidental finding during evaluation of an acute episode. Frank pernicious anaemia occurs only with the development of autoantibodies to intrinsic factor, as well as to parietal cell components. Only a fraction of patients producing such antibodies suffer inadequate cobalamin absorption, however, and functional assessment is required to establish the diagnosis.

Two forms of chronic atrophic gastritis have been defined on serological, morphological, and functional grounds. Type A is characterized by the presence of antibody to parietal cells. Mucosal abnormalities typically affect the corpus of the stomach diffusely, resulting in severe impairment of acid secretion. The antrum is spared and gastrin secretion is frequently elevated. It is this form that may progress to pernicious anaemia. Parietal cell antibody is not detectable in patients with type B gastritis. Patchy mucosal changes of the corpus with only moderate secretory impairment and extensive antral involvement are characteristic; serum gastrin levels are often low. This is the more common form and has been referred to as antral gastritis.

The pathogenesis of chronic gastritis remains unclear. Ageing is a factor; the condition appears to be quite common among the elderly, which is associated with Hashimoto's thyroiditis, hyperthyroidism, hypothyroidism, insulin-dependent diabetes mellitus, hypoparathyroidism, and addisonian hypoadrenalism. An increased incidence of pernicious anaemia among first-degree relatives of those with the condition further suggests that autoimmune response genes may be involved. The development of type B gastritis may be related to repeated episodes of acute gastritis or to chronic irritation due to duodenal reflux. Infection with the spiral Gram-negative bacterium Helicobacter pylori has been associated with gastric and duodenal ulcer, dyspepsia, and gastritis of the antral form. There is mounting evidence that H. pylori infection the cause, not the consequence, of chronic gastritis. Chronic superficial gastritis resulted after an investigator intentionally ingested the organism, and improvement in symptoms has been observed following treatment for such infection. Unfortunately, effective antimicrobial therapy is hindered by the acid environment of the stomach. It is likely that antral gastritis. shares aetiological factors with gastric ulcer. Alternatively it may be a precursor lesion: such ulcers are often associated with type B gastritis.

The sequelae of chronic gastritis include haemorrhage and carcinoma, and both are apparently more common in patients with type B gastritis than in those with type A disease. The incidence of both approaches 10 per cent, but the true risk of carcinoma in patients with atrophic gastritis is difficult to estimate, as rates of gastric cancer vary greatly between populations, and the prevalence of chronic gastritis is uncertain. Since atrophic gastritis is common, routine surveillance endoscopy is not generally recommended for patients with chronic gastritis among populations in which the incidence of gastric malignancy is low.

Metaplasia is often seen in atrophic gastritis and may be intestinal or pseudopyloric in type, the latter being more commonly associated with antral gastritis. Although metaplasia is not necessarily premalignant, atrophic gastritis with intestinal metaplasia is often found in patients with adenocarcinoma. Experimental models of gastric carcinoma in rats using N-methyl- N′-nitro- N-nitrosoguanidine demonstrate both cancer and intestinal metaplasia, suggesting an association with similar causative factors, if not progression from one to the other.

Multiple carcinoids and endocrine cell micronests can occur in the fundal mucosa of patients with Type A atrophic gastritis. This phenomenon may be related to the trophic action of gastrin, which is present in high levels in patients with this form of atrophic gastritis. Because such tumours can metastasize, excision is recommended for isolated carcinoid tumours. Multifocal disease requires either total gastrectomy or careful endoscopic surveillance.

There may be an increased risk of carcinoma following gastric resection. Experimentally, an increased risk of malignancy has been demonstrated, possibly resulting from the development of atrophic gastritis and intestinal metaplasia secondary to chronic bile reflux. There is increased cell turnover and development of carcinoma following a gastrectomy and Polya reconstruction (which is associated with bile reflux) in experimental animals fed N-methyl- N′-nitro- N-nitrosoguanidine.

In a recent comparison of patients who underwent Billroth I, Billroth II, or Roux-en-Y reconstructions following gastric resection, atrophic gastritis and intestinal metaplasia seemed more common following the Billroth operations. Metaplasia was generally moderate, and no evidence of carcinoma occurred in this series. Because patients were usually symptomatic following Roux-en-Y reconstructions, however, there was no clear mandate against the Billroth operation.

The less common forms of chronic gastritis include chronic cystic gastritis, in which flattened epithelial cells line dilated gastric glands deep in the lamina propria. Granulomatous gastritis related to tuberculous infection, sarcoid, or Crohn's disease is characterized by antral and duodenal involvement with mucosal inflammation and ulceration that may lead to gastric outlet obstruction. Eosinophilic gastritis is a rare condition in which eosinophils infiltrate the distal stomach and the proximal small bowel to a variable extent, resulting in enlargement of antral folds and simulating the giant hypertrophic gastritis characteristic of Ménétrier's disease. Although this condition may lead to obstruction, it is generally amenable to medical therapy alone.

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