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Review
. 2013 Dec 21;19(47):8986-95.
doi: 10.3748/wjg.v19.i47.8986.

Non-microbial Approach for Helicobacter Pylori as Faster Track to Prevent Gastric Cancer Than Simple Eradication

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Free PMC article
Review

Non-microbial Approach for Helicobacter Pylori as Faster Track to Prevent Gastric Cancer Than Simple Eradication

Sang-Ho Park et al. World J Gastroenterol. .
Free PMC article

Abstract

Although the International Agency for Research on Cancer declared Helicobacter pylori (H. pylori) as a definite human carcinogen in 1994, the Japanese Society for Helicobacter Research only recently (February 2013) adopted the position that H. pylori infection should be considered as an indication for either amelioration of chronic gastritis or for decreasing gastric cancer mortality. Japanese researchers have found that H. pylori eradication halts progressive mucosal damage and that successful eradication in patients with non-atrophic gastritis most likely prevents subsequent development of gastric cancer. However, those who have already developed atrophic gastritis/gastric atrophy retain potential risk factors for gastric cancer. Because chronic perpetuated progression of H. pylori-associated gastric inflammation is associated with increased morbidity culminating in gastric carcinogenesis, a non-microbial approach to treatment that provides long-term control of gastric inflammation through nutrients and other interventions may be an effective way to decrease this morbidity. This non-microbial approach might represent a new form of prerequisite "rescue" therapy that provides a quicker path to the prevention of gastric cancer as compared to simple eradication.

Keywords: Atrophic gastritis; Gastric cancer; Helicobacter pylori; Non-microbial approach; Prevention.

Figures

Figure 1
Figure 1
Point of no return in Helicobacter pylori infection. Helicobacter pylori (H. pylori) infection is responsible for acute and chronic gastritis, chronic atrophic gastritis, and intestinal metaplasia. The results of a few studies have shown that the eradication of H. pylori significantly reverted these gastric pathologies and promoted restoration of gastric function. H. pylori is also implicated in several extragastric manifestations including idiopathic thrombocytopenic purpura, iron deficiency anemia, atherosclerosis, and chronic urticaria. Because there are no biomarkers suggestive of a point of no return, the results of several large scale cohort studies continue to provide support for the strategy of H. pylori eradication in gastric cancer prevention.
Figure 2
Figure 2
Host adoptive response through a non-microbial approach as the core defensive mechanism against Helicobacter pylori infection, especially gastric cancer prevention. Even though host genotype, environmental risk, and bacterial virulence factor are all implicated in Helicobacter pylori (H. pylori) infection, a non-microbial approach may provide the fastest means of cancer prevention as well as amelioration of H. pylori-associated gastric pathologies.
Figure 3
Figure 3
A non-microbial approach for Helicobacter pylori-associated gastritis as well as gastric cancer. Simply removing Helicobacter pylori (H. pylori) can contribute to gastric cancer prevention in some patients. For example, H. pylori eradication suppressed the metachronous occurrence of gastric cancer in patients who underwent endoscopic submucosal dissection, whereas insignificant outcomes were noted in general eradication. Supplementation or treatment with long-term phytoceuticals or other agents were proven to be very efficacious in the prevention of H. pylori-associated gastric carcinogenesis. These treatment strategies are supported by the clear mechanisms of anti-inflammation, anti-oxidation, and anti-mutagenesis associated with their use.

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