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Conference Paper: Eradication of H. pylori: is it necessary for gastric cancer prevention?
Title | Eradication of H. pylori: is it necessary for gastric cancer prevention? |
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Authors | |
Issue Date | 2007 |
Publisher | John Wiley & Sons, Inc. |
Citation | Asian Pacific Digestive Week, Kobe, Japan, 15-18 October 2007. In Journal of Gastroenterology and Hepatology, 2007, v. 22 n. S2, p. A64 Abstract no.SY-G3-5 How to Cite? |
Abstract | Gastric cancer remains one of the top cancer killers in the World. Strategies to prevent cancer in high risk areas are important. Chronic Helicobacter pylori infection increases the risk of gastric cancer, by stepwise progression from chronic active gastritis to gastric atrophy, intestinal metaplasia, dysplasia and cancer. These stepwise progressions may take many years, and at present there is no proven effective treatment for the presence of premalignant lesions including intestinal metaplasia or dysplasia. Hence the two prevailing questions in gastric cancer prevention are (a) whether treatment of H. pylori-related gastritis can reduce the risk of gastric cancer, and (b) whether treatment of H. pylori-related IM or dysplasia can both reverse the premalignant lesions and reduce the risk of gastric cancer. Our randomized placebo controlled trial in China started in year 1994 included both patients with H. pylori related gastritis and patients with H pylori related premalignant lesions (1). After 7.5 years of follow up, patients receiving H pylori treatment showed a non-signifi cant trend of having less gastric cancer than those patients that received placebo. The sub-group analysis showed that patients with H pylori related gastritis benefi ted most from treatment, with no cancer developing in 7.5 years. However, in patients with H pylori related premalignant lesions, there was no difference in the risk of gastric cancer in both treatment and placebo groups. Hence our study suggests that the benefi t of treating H pylori in cancer prevention may be restricted to patients with gastritis only. Correa et al performed another randomized placebo controlled trial in Columbia which included mainly patients with H pylori related premalignant lesions (2). Their 12-year follow up result suggested that subjects who were H pylori negative after treatment had 14.8% more regression and 13.7% less progression than patients who were positive at 12 years (p = 0.001). Hence he concludes that it is benefi cial to treat H pylori in patients with premalignant lesions. However the magnitude of benefi t may be in the range of 15% only. Based on these and other studies, the recommendation is that treatment of H pylori is benefi cial in prevention of gastric cancer. The benefi t is greater in patients without premalignant lesions. Hence treatment earlier in life may give better results. This recommendation is however based on studies carried out in areas with high risk of gastric cancer. Areas with low to moderate risk of gastric cancer may need to consider the pros and cons and cost-effectiveness of screen and treat for H pylori. It remains to be emphasized that the cause of gastric cancer is multi-factorial. Dietary factor is certainly one of the most important causes. High salt content and various unhealthy dietary habits are frequently seen in high risk areas, together with high prevalence of H pylori infection. Hence public education in healthy diet is essential. References: 1. Wong BCY, Lam SK, Wong WM, et al. Helicobacter pylori eradication to prevent gastric cancer in a high-risk region in China: A randomized controlled trial. JAMA 2004; 291(2): 187-194. 2. Mera R, Fontham ET, Bravo LE et al. Long term follow up of patients treated for Helicobacter pylori infection. Gut 2006;54 :1536 |
Persistent Identifier | http://hdl.handle.net/10722/102657 |
ISSN | 2023 Impact Factor: 3.7 2023 SCImago Journal Rankings: 1.179 |
DC Field | Value | Language |
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dc.contributor.author | Wong, BCY | en_HK |
dc.date.accessioned | 2010-09-25T20:39:31Z | - |
dc.date.available | 2010-09-25T20:39:31Z | - |
dc.date.issued | 2007 | en_HK |
dc.identifier.citation | Asian Pacific Digestive Week, Kobe, Japan, 15-18 October 2007. In Journal of Gastroenterology and Hepatology, 2007, v. 22 n. S2, p. A64 Abstract no.SY-G3-5 | - |
dc.identifier.issn | 0815-9319 | - |
dc.identifier.uri | http://hdl.handle.net/10722/102657 | - |
dc.description.abstract | Gastric cancer remains one of the top cancer killers in the World. Strategies to prevent cancer in high risk areas are important. Chronic Helicobacter pylori infection increases the risk of gastric cancer, by stepwise progression from chronic active gastritis to gastric atrophy, intestinal metaplasia, dysplasia and cancer. These stepwise progressions may take many years, and at present there is no proven effective treatment for the presence of premalignant lesions including intestinal metaplasia or dysplasia. Hence the two prevailing questions in gastric cancer prevention are (a) whether treatment of H. pylori-related gastritis can reduce the risk of gastric cancer, and (b) whether treatment of H. pylori-related IM or dysplasia can both reverse the premalignant lesions and reduce the risk of gastric cancer. Our randomized placebo controlled trial in China started in year 1994 included both patients with H. pylori related gastritis and patients with H pylori related premalignant lesions (1). After 7.5 years of follow up, patients receiving H pylori treatment showed a non-signifi cant trend of having less gastric cancer than those patients that received placebo. The sub-group analysis showed that patients with H pylori related gastritis benefi ted most from treatment, with no cancer developing in 7.5 years. However, in patients with H pylori related premalignant lesions, there was no difference in the risk of gastric cancer in both treatment and placebo groups. Hence our study suggests that the benefi t of treating H pylori in cancer prevention may be restricted to patients with gastritis only. Correa et al performed another randomized placebo controlled trial in Columbia which included mainly patients with H pylori related premalignant lesions (2). Their 12-year follow up result suggested that subjects who were H pylori negative after treatment had 14.8% more regression and 13.7% less progression than patients who were positive at 12 years (p = 0.001). Hence he concludes that it is benefi cial to treat H pylori in patients with premalignant lesions. However the magnitude of benefi t may be in the range of 15% only. Based on these and other studies, the recommendation is that treatment of H pylori is benefi cial in prevention of gastric cancer. The benefi t is greater in patients without premalignant lesions. Hence treatment earlier in life may give better results. This recommendation is however based on studies carried out in areas with high risk of gastric cancer. Areas with low to moderate risk of gastric cancer may need to consider the pros and cons and cost-effectiveness of screen and treat for H pylori. It remains to be emphasized that the cause of gastric cancer is multi-factorial. Dietary factor is certainly one of the most important causes. High salt content and various unhealthy dietary habits are frequently seen in high risk areas, together with high prevalence of H pylori infection. Hence public education in healthy diet is essential. References: 1. Wong BCY, Lam SK, Wong WM, et al. Helicobacter pylori eradication to prevent gastric cancer in a high-risk region in China: A randomized controlled trial. JAMA 2004; 291(2): 187-194. 2. Mera R, Fontham ET, Bravo LE et al. Long term follow up of patients treated for Helicobacter pylori infection. Gut 2006;54 :1536 | - |
dc.language | eng | en_HK |
dc.publisher | John Wiley & Sons, Inc. | - |
dc.relation.ispartof | Journal of Gastroenterology and Hepatology | en_HK |
dc.title | Eradication of H. pylori: is it necessary for gastric cancer prevention? | en_HK |
dc.type | Conference_Paper | en_HK |
dc.identifier.email | Wong, BCY: bcywong@hku.hk | en_HK |
dc.identifier.authority | Wong, BCY=rp00429 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1111/j.1440-1746.2007.05187.x | - |
dc.identifier.hkuros | 150308 | en_HK |
dc.identifier.issnl | 0815-9319 | - |