Peptic ulcer: from epidemiology to cause.

Any postulate that attempts to explain the aetiology of peptic ulcer must take into consideration a number of established facts. (i) At the beginning of the 20th century there was a steep rise in the incidence of peptic ulcers. Over the past 2 decades, trends have shown a significant decline in some Western countries, such as the United Kingdom, and a significant rise in certain Asian countries, such as Hong Kong and Singapore. (ii) There are marked geographical variations in incidence (for example, it is five times more common in Hong Kong than in Sydney), male: female ratio (for example, 1:1 in USA and 17:1 in India), duodenal ulcer (DU): gastric ulcer (GU) ratio (for example, 0.8:1 in Japan and 32:1 in India), and placebo healing rates. (iii) There is genetic heterogeneity. (iv) A proportion of patients has gastric hyperacidity. (v) Ulcer healing is speeded up by the reduction of gastric acidity, but usually only when the stomach is made relatively hypochlorhydric. (vi) Chronic antral gastritic occurs in 90% of DU and 70% of GU cases. (vii) Ulcer occurs most commonly at the duodenal bulb for DU and at the incisura for GU. No single causative factor can explain these facts, and the aetiology must, therefore, be heterogeneous. Cigarette smoking, ingestion of aspirin and other non-steroidal anti-inflammatory agents and environmental stress are reasonably well-established factors. Current evidence indicates that Campylobacter pylori is causally related to antral gastritis but not to peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)