The link between Helicobacter. pylori and peptic ulcer disease in 1997 is an irrefutable one. The association between infection and ulcerogenesis has been shown to be biologically plausible with induction of epithelial inflammation and cell damage and its effect on gastrin/acid homeostasis. The association of H. pylori infection and peptic ulcer disease is a close and consistent one. There is ample evidence indicating that H. pylori eradication results in virtual abolition of ulcer relapse. Several studies have demonstrated that eradication of H. pylori results in ulcer healing and there is evidence showing a temporal relationship between infection and development of peptic ulcer disease.
The results of 2449 investigations of the upper gastrointestinal tract were analysed to determine the incidence of disease. Abnormalities were detected in 53% of patients who had endoscopy, but were found in only 24% of patients who had barium studies (p <= 0.001). Altogether 916 patients had abnormal findings. Duodenal ulcer accounted for 42% of cases, gastric ulcer 16% and gastric cancer 9%. The prevalence of perforated ulcer was 13%. The annual incidence/1000 in males and females (>14 years) were respectively, for duodenal ulcer 1.66 and 0.42, for gastric ulcer 0.57 and 0.25, for perforated ulcer 0.36 and 0.05, and for gastric cancer 0.29 and 0.14. Most types of gastro-duodenal disease were less common in Malays than expected (p = <0.001). However oesophageal cancer and varices were more common in Indians compared to Malays and Chinese (p = <0.001). This study showed that the pallern of perforating ulcers was not the same as that of non-peforating ulcers, suggesting a differing pathogenesis. Identification of the factors causing a different prevalence of disease between the three ethnic groups would help in the understanding of the causes of upper gastrointestinal disease.
Basal and pentagastrin stimulated acid output was measured in 80 normal and 179 duodenal ulcer subjects of Chinese, Indian and Malay origin. Basal and maximally stimulated acid output was significantly higher in duodenal ulcer patients compared with normal subjects. There was however considerable overlap and less than one in four duodenal ulcer patients were hypersecretors. The acid output (and hence the parietal cell mass) was lower than in Caucasian subjects and this was possibly related to weight differences. The acid output did not differ significantly in the Chinese, Indian and Malay subjects, suggesting that parietal cell mass in the three racial groups is closely similar. The difference in frequency of duodenal ulcer disease in the three racial groups is thus not related to gastric secretory capacity.
A consecutive series of 2,277 patients presenting for upper gastrointestinal endoscopy was analysed. The following groups of patients were studied with reference to sex, race and dialect groups: those presenting with dyspepsia but no haemorrhage, those presenting with upper gastrointestinal haemorrhage, those with non-ulcer dyspepsia, gastric ulcer and duodenal ulcer. Males out-numbered females in all diagnostic groups. Male and female Malays were under-represented in all diagnostic groups when compared to the Singapore population. Amongst female Chinese, there was an excess of Cantonese patients and an under-representation of Teochew patients in most diagnostic groups. These dialect differences were not remarkable amongst male Chinese. The possible reasons for these differences and their significance are discussed.