The clinical course or natural history of the infection is quite variable and is likely to be dependent on host, environmental and bacterial factors. The majority of children and adults infected with this bacterium are asymptomatic. Most infected patients with H. pylori develop gastritis, particularly nodular gastritis in children [17, 18]. Those with antral predominant gastritis are more likely to develop duodenal ulcers and have a reduced risk of gastric cancer compare to those with corpus predominant atrophic gastritis who have an increase risk of gastric cancer (Fig. 1) . As an example of a host factor that determine disease outcome, polymorphism in the HLA-DQA1 gene results in resistance to atrophic gastritis and thus lower the risk of gastric cancer in Japanese but not in Italian individuals [20, 21], whereas polymorphisms of IL-1|3 gene give rise to corpus gastritis and thus increase the risk of gastric cancer [22, 23].
The lifetime risk of peptic ulcer disease is approximately 3-25%, depending on the population [19, 24]. In children, the risk for peptic ulcer is low; in one Japanese study, the prevalence of H. pylori in duodenal ulcer, and gastric ulcer was 83.0%, and 44.2%, respectively [18, 25]. In those with H. pylori infection and peptic ulcer disease, there is now little doubt that eradication of H. pylori is superior to ulcer-healing drugs for duodenal ulcers; for gastric ulcers, eradication achieves similar result to ulcer-healing drugs. In terms of preventing recurrence of peptic ulcer disease, eradication is superior to placebo .
The lifetime risk of gastric cancer though is approximately 1% based on large epi-immunological case-controlled studies. The association between
gastric cancer and H. pylori infection has been confirmed further in animal studies using the Mongolian gerbil . In a prospective cohort study of Japanese patients, gastric cancer was shown to develop in 2.9% of 1246 adult patients infected with H. pylori. Mean follow-up was 7.8 years. No gastric cancer was found in those not infected or in a subgroup of patients who received eradication therapy for H. pylori . However, in another prospective randomized placebo-controlled population-based primary study of 1630 healthy Chinese patients, carriers of H. pylori infection in a region of China with a high prevalence of gastric cancer, 817 received eradication therapy and 813 a placebo. No difference was found in terms of the incidence of gastric cancer development between the two groups over a period of 7.5 years. In a subgroup analysis of patients without precancerous lesions, such as atrophic gastritis and intestinal metaplasia, eradication seemed to decrease the development of gastric cancer . A recent trial suggests that eradication of H. pylori may reduce the incidence of precancerous lesions
. Eradication of H. pylori in the older individuals with precancerous lesions appeared not to be effective in preventing gastric cancer. Since these precancerous lesions are rarely seen in children , perhaps eradication should take place in childhood to prevent the development of these precancerous lesions later in life. Currently, the effect of H. pylori eradication on the incidence of gastric cancer is unknown and conclusive trials will take many years. Most experts favor eradication in first-degree relatives of gastric cancer patients [32-34]. Mucosal associated lymphoid tissue (MALT) lymphoma is rare in those infected with H. pylori, with a lifetime risk of less than 1%.
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