CagA and VacAHelicobacter PyloriAntibodies in Gastric Cancer

BACKGROUND: Infection with different genotypes of virulentHelicobacter pyloristrains (cytotoxin-associated gene A [CagA]-and/or vacuolating cytotoxin A [VacA]-positive) can play a role in the development of atrophic gastritis, duodenal ulcer (DU) and gastric cancer (GC).OBJECTIVE: To determine whether patients with GC andH pylori-negative histological staining had previously been infected withH pyloriCagA- and/or VacA-positive virulent strains.METHODS: Twenty-three GC patients with a mean (± SD) age of 68.14±9.8 years who testedH pylori-negative on histological staining took part in the study. Three control groups were included. The first group comprised 19 patients with pastH pyloriinfection and DUs eradicated 10 years earlier, with a mean age of 58±18.2 years.H pylori-negative status for this group was determined every year with Giemsa staining, and follow-up testing occured 120±32 months (mean ± SD) after therapy. The subsequent control groups included 20 asymptomatic children, with a mean age of 7±4.47 years, and withH pylori-negative fecal tests; the final group contained 30 patients without clinical symptoms ofH pyloriinfection, with a mean age of 68±11.6 years, who testedH pylori-negative by histological staining.RESULTS: Prevalence of CagA and VacA seropositivity, respectively was 82.6% and 73.91% in GC patients; 84.2% and 84.2% inH pylori-negative DU patients; 25% and 5% inH pylori-negative children; and 36.6% and 16.6% in the patients without clinical symptoms on histological staining. CagA and VacA antibody positivity was not significantly different between GC patients and patients with DUs that had been eradicated 10 years earlier. Significant positivity was found between the children’s group and theH pylori-negative (with past DUs) group (P<0.001). A statistically significant difference was found in age between groups (P<0.03).CONCLUSIONS: Patients with GC, even whenH pylori-negative at the time of the present study, may have been infected byH pyloribefore the onset of the disease, as confirmed by CagA and VacA seropositivity. These data reinforce the hypothesis thatH pylorimay be a direct carcinogenic agent of GC.