Helicobacter pylori antibodies (CagA and VacA) detection. The link between cancer and infection

Infection with different genotypes of virulent Helicobacter pylori (Hp) strain, CagA and/or VacA positive, can play a role in the development of atrophic gastritis, duodenal ulcer (DU), and gastric carcinomas (GC). This study was undertaken to investigate if patients with GC with Hp negative histological Giemsa staining had a past infection by virulent strains of Hp CagA and/or VacA positive.

Twenty GC, (average age +/- SD) 68.14+/-9.8 years old, Hp negative to histological take part to the study. Two-control group were included: 19 Hp infected patients with DU eradicated 10 years before, 58+/-18.2 yrs. Hp negative status was determined every year with histology and follow-up after therapy was 120+/-32 months; range 96-144 months. Twenty asymptomatic children, 7+/-4.47 yrs, with Hp negative faecal test. The immunoblot assay was used to detect serum antibodies against CagA and VacA.

Prevalence of CagA and VacA seropositivity was 90 and 95% in GC, 84 and 84% in DU Hp negative, 25 and 5% in children Hp negative, respectively. CagA and VacA antibody positivity was not significantly different between GC and patients with DU eradicated 10 years before. A true significant positivity was found against children (''t''-Student test; p<0.0001). Statistical difference was found in age between groups p<0.03.

Patients with GC, although Hp negative at present, could be infected by Hp before the appearance of the disease as confirmed by CagA and VacA seropositivity. These data may reinforce the idea to consider Hp as a direct carcinogenetic agent of GC.