Abstract

Helicobacter pylori is a human pathogen that causes chronic gastritis and peptic ulcers. Epidemiological studies demonstrated that individuals who are blood group 0 positive or represent non-secretors of their blood group antigens are more likely to develop peptic ulcers. The Lewis(b) blood group antigen has been reported to mediate the attachment of H. pylori to human gastric mucosa. The aim of this study was to examine the interrelation between Le(a-b+) phenotype, blood group 0, H. pylori infection, and peptic ulcer occurrence. The study population consisted of 330 consecutive patients (185 men, 145 women) referred to endoscopy of the upper gastrointestinal tract for various reasons. AB0(H) blood groups and Lewis(a,b) phenotype were carried out by standard haemagglutination assays. Antibodies (IgG) against H. pylori were determined by a quantitative enzyme-linked immunosorbent assay (ELISA). 49 of the 330 patients (14.8 %) showed duodenal or gastric ulcers with a H. pylori seroprevalence of 87.8 %. The IgG immune response to H. pylori was not dependent on ABH blood group phenotype. There was also no significant association between the secretor status and the presence of H. pylori infection. Secretors, 35/238 (14.7 %), were no more likely to have gastroduodenal ulcer compared with non-secretors, 9/65 (13.8 %). Our data show no association between secretor status or specific ABH blood group on the one hand, and H. pylori infection or occurrence of gastroduodenal ulcers on the other. Determination of ABH blood groups or secretor status is, therefore, not a useful tool to characterize the individual risk for gastroduodenal ulcer or to guide any diagnostic procedures.

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