Published online Dec 21, 2013. doi: 10.3748/wjg.v19.i47.8986
Revised: October 30, 2013
Accepted: November 18, 2013
Published online: December 21, 2013
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.
Core tip: Gastric cancer is a multi-factorial and multi-step disease associated with various risk factors including environmental and pathogenic microbial chronic inflammation. Pharmaceutical intervention and the eradication strategy can provide rapid relief of acute inflammation but fails to correct the underlying cause of chronic inflammation. A non-microbial approach for modulating Helicobacter pylori associated gastric inflammation may be an attractive and rapid alternative to optimize cancer prevention strategies and minimize adverse side effects associated with therapeutic regimens.