Helicobacter pylori and gastric cancer

Gastric cancer despite a declining incidence remains a significant cause of morbidity and mortality world wide. There is strong epidemiological and hi stological evidence to associate Helicobacter pylori infection with the sub sequent development of gastric cancer. The exact pathophysiological mechani sms involved remain to be elucidated. There is evidence to relate Helicobac ter pylori infection and subsequent inflammation with an increase in gastri c epithelial cell proliferation and with the induction of apoptosis. Such a lterations in cellular dynamics may promote the development of mitogenic ce ll lines by inducing DNA damage. Studies have that following successful tre atment, proliferation rates return to normal. At what histological stage, e radication is of benefit is less clear Ir is likely that following the deve lopment of atrophy or intestinal metaplasia eradication will only slow prog ression. It would, therefore, seem logical, that to establish any benefit f or a population, treatment should be employed at an earlier stage. As yet, an at risk group has not been identified, and as such population screening cannot be advised, mainly as a result of financial implications and the ris k of promoting the development of resistant strains. Recent studies have ex plored the rules of bacterial factors,, CagA and VacA status, host factors, HLA type, and environmental factors as determinants of outcome. Results ha ve been variable. The establishment of an at risk group would enable select ive screening and treatment, and thus prevent the development of gastric ca rcinoma as a result of Helicobacter pylori infection in the long-term.