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Does hyperhomocysteinaemia contribute to gastric carcinogenesis in Helicobacter pylori infected patients?
  1. L Peyrin-Biroulet1,
  2. Jean-Louis Guéant1
  1. 1Department of Hepato-Gastroenterology, University Hospital of Nancy, Vandoeuvre-les-Nancy, France
  1. Correspondence to:
    Dr Laurent Peyrin-Biroulet
    INSERM U724, Department of Hepato-Gastroenterology, University Hospital of Nancy, Allée du Morvan, 54 511 Vandoeuvre-les-Nancy, France; peyrin-biroulet{at}netcourrier.com

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In a recent issue of Gut, Marino et al showed that eradication of Helicobacter pylori resulted in increased levels of vitamin B-12 (cobalamin) and decreased levels of plasma homocysteine in elderly patients (Gut 2007;56:469–74), confirming preliminary reports.1 The authors recall that cobalamin deficiency is associated with Hpylori infection and is a major cause of hyperhomocysteinaemia in the general population.

Global DNA hypomethylation, which is associated with hyperhomocysteinaemia,2 is an epigenetic event often found in tumour cells.3 The homocysteine raising effect of Hpylori may thus promote gastric carcinogenesis. Consistently, a recent study showed that hyperhomocysteinaemia may increase the risk of developing gastric cancer in a Chinese population.4 Along with Marino’s results, these findings may provide new insights in our understanding of Hpylori related gastric carcinogenesis.

One question remains open: Is eradication of Hpylori the best way to prevent gastric cancer? The conclusion of the Maastricht III consensus report was that “Eradication of Hpylori infection has the potential to reduce the risk …

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