Introduction

Normal gastric mucosa contains few, if any, inflammatory cells. Gastritis represents the inflammatory response within the gastric mucosa resulting from injury, whatsoever the nature. The diagnosis is essentially histological since naked eye appearances are known to be unreliable. The advent of fibre-optic endoscopy and biopsy has considerably increased our knowledge about this condition and its natural history (Heatley & Wyatt, 1994). On a worldwide basis, gastritis is extremely common. Various classifications of gastric inflammation have developed based upon current knowledge at the time but, more recently, existing systems have been swept aside by the current terminology based upon known pathogenic mechanisms (Misiewicz, 1991). Most cases of gastritis are now known to be caused by infection with Helicobacter pylori. Other causes, including auto-immune gastritis, probably represent less than 10% of all cases of gastritis in most populations (Heatley & Wyatt, 1994).

Acute gastritis

The histological changes observed are usually simply those associated with acute inflammation, namely hyperaemia, infiltration with polymorphonuclear cells and oedema, together with a variable loss of surface epithelium. Macroscopically, oedema, small superficial haemorrhages and erosions or small ulcers may be visible (Heatley & Wyatt, 1994). A range of external influences have been shown to produce these changes but amongst the most important are alcohol excess, some spices, non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin and metabolic disturbances associated with acute illnesses, in particular uraemia. Salicylate ingestion is one of the most studied models of acute injury.