Review
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World J Gastroenterol. Sep 14, 2006; 12(34): 5458-5464
Published online Sep 14, 2006. doi: 10.3748/wjg.v12.i34.5458
H pylori and gastric cancer: Shifting the global burden
Christian Prinz, Susanne Schwendy, Petra Voland
Christian Prinz, Susanne Schwendy, Petra Voland, II. Medical Department, Technical University of Munich, D-81675 Munich, Germany
Supported by Deutsche Forschungsgemeinschaft (DFG Graduiertenkolleg 333: Biology of Human Diseases) and by a grant from the DFG to C.P. (Pr 411/9-1) and the Dr. Else Kröner Fresenius Stiftung
Correspondence to: Dr. Christian Prinz, Professo, Klinikum rechts der Isar, Technischen Universität München, II. Medizinische Klinik und Poliklinik, Ismaninger Str. 22, D-81675 München, Germany. christian.prinz@lrz.tum.de
Telephone: +49-89-41404073 Fax: +49-89-41407366
Received: January 4, 2006
Revised: January 8, 2006
Accepted: January 24, 2006
Published online: September 14, 2006
Abstract

Infection with H pylori leads to a persistent chronic inflammation of the gastric mucosa, thereby increasing the risk of distal gastric adenocarcinoma. Numerous studies have determined a clear correlation between H pylori infection and the risk of gastric cancer; however, general eradication is not recommended as cancer prophylaxis and time points for treatment remain controversial in different areas of the world. Prevalence rates in Western countries are decreasing, especially in younger people (< 10%); and a decline in distal gastric adenocarcinoma has been observed. Risk groups in Western countries still show considerably higher risk of developing cancer, especially in patients infected with cagA+ strains and in persons harboring genetic polymorphism of the IL-1B promoter (-511T/T) and the corresponding IL-1 receptor antagonist (IL-1RN*2). Thus, general eradication of all infected persons in Western countries not recommended and is limited to risk groups in order to achieve a risk reduction. In contrast, infection rates and cancer prevalence are still high in East Asian countries. A prevention strategy to treat infected persons may avoid the development of gastric cancer to a large extent and with enormous clinical importance. However, studies in China and Japan indicate that prevention of gastric cancer is effective only in those patients that do not display severe histological changes such as atrophy and intestinal metaplasia. Thus, prophylactic strategies to prevent gastric cancer in high risk populations such as China should therefore especially aim at individuals now at younger age when the histological alterations caused by the bacterial infection was still reversible. In countries with a low prevalence of gastric cancer, risk groups carrying cagA+ strains and IL-1 genetic polymorphisms should be identified and treated.

Keywords: H pylori; Gastric cancer