Helicobacter pyloriIgA and IgG antibodies, serum pepsinogen I and the risk of gastric cancer: Changes in the risk with extended follow-up period

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The prediction ofHelicobacter pyloriantibodies immunoglobulin A (IgA) and immunoglobulin G (IgG) and serum pepsinogen I (PG I) on gastric cancer occurrence was studied in a nested case-control study, based on 225 incident cancer cases and 435 matched controls from a Finnish cohort followed from 1966–1991. The odds ratio of noncardia gastric cancer between infected and noninfected persons was 3.12 (95% confidence interval (CI) = 1.97–4.95) for elevated IgA and 2.88 (CI: 1.63–5.07) for elevated IgG antibodies. The odds ratio between low and high PG I was 2.24 (CI: 1.43–3.49). The strength of association was significant for IgA antibodies during the total follow-up, but for IgG antibodies this was only true for follow-up periods of 15 years or more. IgA antibodies were significantly associated with all registered histological subtypes apart from intestinal type adenocarcinoma. The highest gastric cancer risk was found among individuals with simultaneously elevated IgA and IgG antibodies and low PG I with an odds ratio of 10.9 (CI: 4.31–27.7) in comparison with those who were negative for both antibodies and had normal PG I. Elevated IgA and IgG antibodies and low PG I were not associated with cancers of the gastric cardia. The findings support the hypothesis thatH. pyloriinfection is a cause of noncardia gastric cancer. Although elevatedH. pyloriIgA and IgG antibodies and low PG I independently could predict the occurrence of noncardia gastric cancer, their power to do so varied with the stage and length of the follow-up period and it increased when they were applied in combination.

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