Gastritis

Acute non-erosive gastritis is most commonly due to Helicobacter pylori infection.[3][4] Chronic H pylori infection predisposes to atrophic gastritis and autoimmune gastritis.

Acute erosive gastritis may be caused by chronic non-steroidal anti-inflammatory drug (NSAID) or alcohol use/misuse.[3][21] Factors that have been identified as placing patients at increased risk for NSAID-related gastrointestinal (GI) complications include prior history of a GI event (peptic ulcer, haemorrhage), age >60 years, high dosage of NSAIDs, and concurrent use of corticosteroids or anticoagulants.[22][23]

Erosive gastritis may also be due to reflux of bile salts into the stomach as a result of compromised pyloric function (e.g., following gastric surgery).[5][6][7][8]

Critically ill patients are at risk of developing stress-induced GI bleeding.[9] The main risk factors associated with clinically important haemorrhage are mechanical ventilation for >48 hours and coagulopathy.[9]

Autoimmune-mediated atrophic gastritis is associated with the development of antibodies to the gastric parietal cells (present in about 90% of patients).[3][10][24] Autoimmune disorders associated with increased risk of autoimmune gastritis include thyroid disease, idiopathic adrenocortical insufficiency, vitiligo, type 1 diabetes mellitus, and hypoparathyroidism. North European or Scandinavian ancestry is a recognised risk factor for autoimmune gastritis.[10]

Phlegmonous gastritis is an uncommon form of acute gastritis caused by Staphylococcus aureus, streptococci, Escherichia coli, Enterobacter, other gram-negative bacteria, and Clostridium welchii.[11][12][13][14]

There are a variety of processes that are characterised by acute and chronic inflammation and disruption of the gastric mucosal protective layer:

Helicobacter pylori infection induces a severe inflammatory response with gastric mucin degradation and increased mucosal permeability, followed by gastric epithelial cytotoxicity.[3][4]
Non-steroidal anti-inflammatory drugs (NSAIDs) and alcohol decrease gastric mucosal blood flow with loss of the mucosal protective barrier.[3] NSAIDs inhibit prostaglandin production, whereas alcohol promotes depletion of sulfhydryl compounds in gastric mucosa.[21]
In autoimmune atrophic gastritis, antiparietal cell antibodies stimulate a chronic inflammatory, mononuclear, and lymphocytic infiltrate involving the oxyntic mucosa, leading to the loss of parietal and chief cells in the gastric corpus.[3][24][25][26]
The high concentration of hydrochloric acid normally present in gastric fluid prevents the growth of bacteria in the stomach and small intestine. Gastric atrophy and acid blocking medications raise gastric pH and disrupt the acid barrier to bacterial overgrowth. Under rare circumstances, damage to the gastric mucosa (e.g., gastric ulcer or carcinoma, ingestion of caustic materials, ingestion of foreign bodies) may allow ingested bacteria to become invasive, resulting in phlegmonous gastritis.[27] In phlegmonous gastritis, the suppurative process primarily involves the submucosa and muscularis layers of the gastric wall.[27]

Aetiological classification

A variety of classification systems describe the causes of gastritis and their associated histological features. Classifications that are in use include the updated Sydney system and the operative link on gastritis assessment (OLGA).[15][16] In clinical practice, an aetiological classification often provides a basis for therapy. Aetiologies responsible for the development of gastritis include:

Helicobacter pylori infection
Chemical substances
- Non-steroidal anti-inflammatory drugs (NSAIDs) or alcohol
- Bile reflux
Autoimmune-related
Mucosal ischaemia
Bacterial invasion of the gastric wall.

Aetiology

Pathophysiology

Classification

Aetiological classification