Abstract B49: Multiplex serology for Helicobacter pylori and severity of precancerous gastric lesions in a high risk population

Helicobacter (H.) pylori infection has been shown to be associated with markedly increased risks for chronic atrophic gastritis and noncardia gastric cancer (GC). DNA evidence of H. pylori infection and its associated cagA and vacA bacterial virulence genotypes decreases with disease progression, and risk appears greatest 10 years prior to diagnosis. Bead-based multiplex ELISA assays are now available to detect past infection through quantification of serum antibodies against several H. pylori proteins. If established as a marker of gastric histology, multiplex serology would be useful as a noninvasive screen for chemoprevention studies in high risk populations. In combination with cagA DNA status, serology might also improve currently available GC risk estimates.

This investigation was designed to estimate the association of multiplex serology for 12 H. pylori antigens with levels of severity of pre-cancerous gastric lesions in a high risk population. Baseline sera from 900 subjects enrolled in a chemoprevention trial for gastric pre-cancerous lesions in Tachira State, Venezuela were analyzed. Logistic regression was used to estimate the association between seropositivity and H. pylori or cagA DNA status, and alone or combined with cagA DNA status, between seropositivity and levels of gastric histology.

Multiplex serology showed weak associations with H. pylori DNA status, with AUC values ranging from 0.53 to 0.66. A significant, positive gradient in risk was seen with CagA seropositivity and histologic grade (p<0.001 for linear trend). Among those who were cagA DNA negative, a significantly increased risk was seen for those with chronic atrophic gastritis/IM type I and IM types II-III/dysplasia compared with those who had chronic gastritis (OR = 3.00, 95% CI: 2.05-4.37; OR=2.72, 95% CI: 1.43-5.16, respectively). With regard to risk associations of H. pylori seropositivity and histologic severity, a significant positive gradient was also observed (p<0.001 for linear trend). For those with the most severe histologic grades, CagA seropositivity and cagA DNA status combined led to higher estimates of risk compared to cagA DNA status alone.

CagA seropositivity or a combination of other H. pylori antigens was positively associated with severity of pre-cancerous gastric lesions. This trend appeared stronger in those without evidence of current H. pylori infection. Further consideration should be given to the use of serologic markers of H. pylori infection in epidemiologic and chemoprevention studies.

Citation Information: Cancer Prev Res 2008;1(7 Suppl):B49.