[Effect of Helicobacter pylori infection on the apoptotic and cell proliferative processes of the gastric mucosa].
The role of the Helicobacter pylori in the induction of gastric carcinogenesis seems to be certain. The exact pathomechanism is not yet known, although the special genetic conditions both of the microbe and the host just as the imbalance of the apoptotic and proliferative processes caused by the chronic inflammation are assumed to be involved. The latter one can be proved by the use of different cell proliferative and apoptotic markers. The results are inconsistent whether the eradication therapy causes the regression of premalignant atrophic gastritis. The regression of the MALT-associated lymphoma after the eradication therapy seems to be more convincing. The need of the eradication to prevent gastric cancer can be judged by the follow-up of some biomarkers (e.g. HLA II genotype, PCNA index, anti HP-IgA titer and the serum pepsinogen level), although their diagnostical application could be hardly introduced in the everyday practise so far.
Törgyekes
E
E
II. sz. Belgyógyászati Klinika, Semmelweis Orvostudományi Egyetem, Budapest.
Molnár
B
B
D017209:Apoptosis; D004378:Duodenal Diseases / Q000382:microbiology / Q000473:pathology; D004379:Duodenal Neoplasms / Q000382:microbiology / Q000473:pathology; D005753:Gastric Mucosa / Q000166:cytology / Q000382:microbiology*; D005757:Gastritis, Atrophic / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000382:microbiology / Q000473:pathology; D013274:Stomach Neoplasms / Q000382:microbiology / Q000473:pathology