| pubmed-article:8924488 | pubmed:abstractText | Helicobacter Pylori (HP) has been noticed in about 80% of cases of superficial chronic gastritis. In about 75% of HP positive biopsies degenerative lesions of superficial gastric epithelium, represented by irregularities of the superficial profile, micropapillar-transformation and erosions have been observed. Furthermore, it is possible the observation, in areas of high bacterial colonization, of vacuoles which are the result of a direct action of HP strains producing vacuolating cythotoxin. In correspondence with the glandular necks active inflammation is present in about 90% of cases. Hp is responsible, by means of direct cytotoxicity and inflammatory cell aggression, of most superficial gastritis, it may help the evolution towards atrophic gastritis and may superimpose on an already noted gastritis situation, promoting their inflammatory exacerbation. The presence of HP infection decreases with the increase histological damage: superficial gastritis (SG) 89%, atrophic gastritis (AG) 58%, intestinal metaplasia (IM) 51% and dysplasia (D) 47%. The founding of the bacterium in conditions such as AG or in surrounding zones IM or D is the demonstration of a possible role of the bacterium in the development of the phases subsequent to AG or of phenomena like IM and D, and not confined to the already verified passage SG/AG. The continuous rearrangement in correspondence with the glandular necks induced by active inflammation HP induced and the subsequent hyperproliferation may help mytotic error, giving rise to metaplastic or dysplastic cellular lines. Therefore, HP in the progression towards IM and D should act as promoter by means of the increase of cellular kinetics. | lld:pubmed |
