Campylobacter pylori in a sample of Finnish population: relations to morphology and functions of the gastric mucosa.

Abstract

The occurrence of Campylobacter pylori (CP) was examined in 179 subjects representing a sample collected from the population of South Finland. In a normal antral and body mucosa CP was present in 5% and 11% and in superficial gastritis (SG) in 71% and 91% of subjects, respectively. In atrophic gastritis (AG) of antrum and body the prevalence of CP decreased significantly with an increasing degree of atrophy, so that CP was not found in severe body AG. Different combinations of antral and body gastritis revealed a characteristic pattern. Campylobacter pylori was lacking when antral and body mucosa were normal, but was present in 41% when normal mucosa was associated with gastritis in the opposite area. In SG affecting diffusely antrum and body, the bacterium was present in every case, but when SG was associated with AG in the opposite area it was lacking in 29% of the subjects. When SG affecting both areas was compared with SG accompanied by different degrees of AG in the body, there was a highly significant decrease of the prevalence of CP in antrum and body along with an increasing degree of AG in the body. This decrease showed a highly significant positive correlation with the acid output. On the whole, acid output correlated well with the occurrence of CP in both antrum and body. Thus the prevalence of CP was 10% in achlorhydria and rose up to 100% in cases with acid output above 30 mmol/h. The presence of CP did not correlate with signs of acute inflammation, but correlated significantly with those of chronic inflammation. No correlation was found in the antrum and a significant negative one in the body, between CP infestation and the extension of intestinal metaplasia. It is concluded that increased pH of gastric contents and mucus secreted by intestinalised glands may create unfavourable conditions for survival of the bacteria and might explain the decrease in the prevalence of CP in the more severe degrees of AG. The present results, however, give no definite answer to the question of the pathogenic significance of CP in the development of chronic gastritis.