Abstract

Helicobacter pylori is a gram negative organism involved in peptic ulcer disease and has been linked to a number of extra-intestinal diseases. There is a large body of evidence describing the link between blood group O/non-secretor phenotypes with H. pylori infection and the risk of peptic ulcer disease. Blood group O individuals also have a higher risk of bleeding disorders due to low levels of the circulating plasma protein von Willebrand factor (vWf). vWf is one of the main proteins that binds platelets during platelet activation and aggregation. The mechanisms of how ulcers develop during H. pylori infection are not fully understood. There is however recent evidence of vWf involvement in platelet aggregation in H. pylori infection. Our new hypothesis states that H. pylori bacteria present in blood group O/non-secretor individuals are binding the available vWf to promote adhesion and subsequent platelet aggregation within the microvasculature. This in turn may deplete any available vWf for wound repair to take place leading to an increased risk of peptic ulceration and bleeding and eventually leading to an ulcer.

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