PEPTIC ULCER DISEASE

Worldwide, duodenal ulcers are more common than gastric ulcers and there is a significantly higher incidence of duodenal ulceration in males of all age groups. Dietary factors, drug ingestion (NSAIDs) and smoking are important in the aetiology. The most common causes are environmental ulcerogens (chemical or infective) acting in consort with factors that impair gastric mucosal resistance to injury and healing of mucosal lesions thereby leading to chronicity. The most important infective agent responsible for peptic ulceration (duodenal and gastric) is H. pylori. Not all patients who are infected with this organism develop ulcers. The risk of peptic ulceration is determined by the severity of the H. pylori-associated gastritis. The organism impairs the mucus-bicarbonate protective layer and is responsible for the chronicity and the tendency to relapse, as evidenced by the permanent healing when infection is eradicated by appropriate antibiotic therapy. Strains of H. pylori with vacA signal-sequence type S1A are associated with severe gastritis and duodenal ulcers, whereas vacA S2 strains cause mild gastric mucosal inflammation without ulceration. The most important group of chemical ulcerogens is constituted by aspirin and other NSAIDs. These are the most common cause of peptic ulceration in H. pylorinegative individuals. However, these drugs are not specific gastroduodenal ulcerogens as they also induce damage and ulceration of the small and large intestine. There are a number of differences between ulcers caused by H. pylori and those caused by NSAIDs.

•      NSAID-associated ulcers are more likely to cause gastrointestinal haemorrhage. Thus, overall 75% of patients with upper gastrointestinal bleeding from peptic ulcers are on NSAID medication.

•      Gastric ulcers caused by H. pylori are rarely encountered on the greater curve (5%), being most commonly situated on the lesser curve (85%). In contrast, NSAIDassociated ulcers (in the absence of H. pylori infection) occur along the lesser and greater curvatures in 35 and 45% respectively.

Infection with H. pylori and use of NSAIDs is encountered in 20% of patients. Eradication of the infection does not influence the healing and recurrence of gastric and duodenal ulcers associated with chronic NSAID medication.

Although some 30-40% of duodenal ulcer patients exhibit acid hypersecretion, the overlap between the acid secretory status of these patients and controls is considerable. Gastric acid is an important factor in the chronicity of the disease and suppression of acid secretion by medical or surgical treatment undoubtedly permits healing in the majority of patients. The secretory characteristics of the usual duodenal ulcer patient include increased acid secretory capacity, increased gastrin response to food and insulin, increased sensitivity to gastrin and defective inhibition of acid secretion. There is an increased concentration of pepsins in the gastric juice of patients with duodenal ulceration, especially pepsin I (the most mucolytic). The disruption of the mucus-bicarbonate layer by pepsin I exposes the underlying mucosa to injury by ulcerogens and impairs healing by removal of the protective mucus cap (blister effect). Stress induces gastric hypersecretion and can lead to acute (stress) ulceration in seriously ill patients.

Upper gastrointestinal endoscopy showing duodenal ulcer.