Helicobacter pylori is the major causal factor in chronic gastritis. Its 
acquisition leads to a chronic, usually lifelong, inflammation of the gastric 
mucosa, which may gradually progress to atrophy (with intestinal metaplasia) in 
a significant proportion of infected individuals. This progression is probably 
multifactorial, being influenced by genetic or environmental factors in addition 
to H. pylori infection. The pathogenesis of peptic ulcer and gastric cancer is 
closely associated with H. pylori gastritis and its subsequent atrophic sequelae 
(atrophic gastritis). H. pylori-induced gastritis is an important risk factor in 
the multifactorial aetiology of these diseases. It causes a cascade of reactions 
that damage the gastric mucosa and epithelium in various ways. The specific 
mechanisms involved are largely unknown. Some are probably bacterium-related 
reactions, which are influenced by various virulence factors, and others are 
consequences of the mucosal inflammation and atrophy. The risk of peptic ulcer 
and gastric cancer in patients with H. pylori gastritis can be summarized as 
follows: i) the risk of both peptic ulcer and gastric cancer is low in 
individuals with a normal stomach; ii) the risk of peptic ulcer is approximately 
ten times higher and the risk of gastric cancer approximately twice as high in 
patients with non-atrophic H. pylori-positive gastritis as in those with a 
normal stomach; iii) these risks are further increased (twofold to threefold) 
when there is antral atrophy; whereas iv) in the presence of corpus atrophy the 
risk of gastric cancer remains high, but that of peptic ulcer decreases 
gradually to zero with increasing severity of corpus atrophy.