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Abstract
The prevalence and density of Helicobacter pylori (HP) colonisation was assessed twice, with an interval of six years from antral and corpus biopsies from a randomly collected Estonian urban population sample. Positive HP colonisation was found in either at 1st or 2nd or in both examinations in 85 out of 86 subjects in whom gastritis without atrophy (chronic inflammation without atrophic changes, SG) either developed or remained during the follow-up at the SG level. There was a clear intraindividual tendency to keep the grade of HP colonisation at an unchanged level during the follow-up: the hypothesis of random variation of HP colonisation during follow-up could be statistically rejected. Close to half of the subjects had at both examinations an identical grade of HP colonisation in the antral or corpus mucosa. Distinct changes in HP colonisation were observed in three instances: (1) the appearance of HP colonisation occurred concomitantly with appearance of gastritis; (2) the development of antrum atrophic gastritis (AG) occurred with concomitant diminution and eventual disappearance of HP in the antral side, and (3) normalization of antral mucosa occurred with persistence of corpus AG with concomitant disappearance of HP colonisation at both sites of the stomach mucosa. The grade of HP colonisation increased with increase in severity of SG and decreased with the progression of AG changes. In the antrum at the SG level a distinct increase was seen both in the grade of HP colonisation and in the severity of SG up to middle age, but in the corpus mucosa only HP colonisation but no SG progression was seen in the younger age-groups. In the antrum, a life-long correlation was found between HP colonisation and inflammatory reaction. The efficiency of immune response against HP colonisation was calculated by using the ratio of SG score to grade of HP colonisation (IRR). The youngest age group (15–19 years at 1st examination) had a significantly higher immune response ratio (IRR) than other age groups. With regard to antral gastritis, those subjects whose SG regressed during the follow-up had a higher IRR than the other subjects. Parietal cell antibodies (PCA) developed in 2 subjects. Both the two subjects had positive HP colonisation at the 1st examination. In addition, one of them preserved HP positivity at the 2nd examination. These findings suggest that autoimmune mechanisms may start in subjects previously exposed to HP-related gastritis.
