SEROEPIDEMIOLOGY OF GASTRITIS IN JAPANESE AND DUTCH WORKING POPULATIONS - EVIDENCE FOR THE DEVELOPMENT OF ATROPHIC GASTRITIS THAT IS NOT RELATED TO HELICOBACTER-PYLORI

Serological markers of gastritis, like pepsinogen A, pepsinogen C, gas trin, and Helicobacter pylori antibodies, can be used to explore the s tate of the gastric mucosa in populations with contrasting cancer risk s. A decreasing pepsinogen A:C ratio and an increasing serum gastrin a re known to reflect an increasing severity of atrophic corpus gastriti s, which is a precursor of gastric cancer. In 723 subjects (without ga stroduodenal surgery) from Japanese (n = 225) and Dutch (n = 498) work ing populations, which had a similar composition of age (mean 48 years ), sex (male to female ratio 6:1), and type of occupation, fasting ser um samples were analysed for IgG antibodies to H pylori, pepsinogen A, pepsinogen C, and gastrin in the same laboratory. H pylori infection was significantly more prevalent in the Japanese than in the Dutch (74 .7% and 31.3%); as was a very low pepsinogen A, indicative of severe m ucosal atrophy (4.4% and 1.6%). Among subjects with and without severe mucosal atrophy the H pylori seropositivity rate was similar. Between the Japanese and the Dutch there were significant differences in mean gastrin (31.8 and 13.4 pmol/l) and pepsinogen A:C ratio (1.7 and 2.9) . These intercountry differences were as great for H pylori negative s ubjects (gastrin: 23.7 and 10.3 pmol/l, pepsinogen A:C ratio: 2.4 and 3.2) as for H pylori positive subjects (gastrin: 34.6 and 20.1 pmol/l, pepsinogen A:C ratio: 1.5 and 2.5). The intercountry difference in ga strin nearly disappeared after stratification into categories of pepsi nogen A:C ratio. In conclusion, the intercountry differences in pepsin ogen A:C ratio and gastrin reflect a higher prevalence of mild and sev ere mucosal atrophy of the corpus in the Japanese than in the Dutch, b oth among H pylori positive and negative subjects. Thus, these finding s suggest that in the Japanese the development of atrophic gastritis i s in part unrelated to H pylori.