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Canadian Journal of Gastroenterology
Volume 22, Issue 3, Pages 255-258
Original Article

CagA and VacA Helicobacter Pylori Antibodies in Gastric Cancer

Renzo Suriani,1 Maurilio Colozza,2 Enrico Cardesi,3 Dario Mazzucco,1 Maria Marino,4 Silvia Grosso,1 Sabina Sanseverinati,4 Ivo Venturini,4 Athos Borghi,4 and Maria Luisa Zeneroli4

1Gastroenterology Clinical Unit, Gastroenterologia ed Endoscopia Digestiva, Italy
2Laboratorio analisi, Ospedale Nuovo, Rivoli, Italy
3Dipartimento di Anatomia Patologica, Ospedale Martini, Torino, Italy
4Medicina Interna II, Università di Modena e Reggio Emilia, Modena, Italy

Received 19 August 2006; Accepted 30 October 2007

Copyright © 2008 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


BACKGROUND: Infection with different genotypes of virulent Helicobacter pylori strains (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 and H pylori-negative histological staining had previously been infected with H pylori CagA- and/or VacA-positive virulent strains.

METHODS: Twenty-three GC patients with a mean (± SD) age of 68.14±9.8 years who tested H pylori-negative on histological staining took part in the study. Three control groups were included. The first group comprised 19 patients with past H pylori infection 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 with H pylori-negative fecal tests; the final group contained 30 patients without clinical symptoms of H pylori infection, with a mean age of 68±11.6 years, who tested H 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% in H pylori-negative DU patients; 25% and 5% in H 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 the H 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 when H pylori-negative at the time of the present study, may have been infected by H pylori before the onset of the disease, as confirmed by CagA and VacA seropositivity. These data reinforce the hypothesis that H pylori may be a direct carcinogenic agent of GC.