Asante M A, Mendall M A, Ballam L, Morris J, Northfield T C
Division of Gastroenterology, Endocrinology and Metabolism, St George's Hospital Medical School, London, UK.
Eur J Gastroenterol Hepatol. 1999 Dec;11(12):1365-70. doi: 10.1097/00042737-199912000-00005.
The relationship between Helicobacter pylori and autoimmune (type A) gastritis is unclear. Infections may trigger autoimmune phenomena but the underlying mechanisms are unknown.
To determine the relationships between H. pylori infection and gastric parietal cell antibodies (PCA), and PCA and heat shock protein (HSP) antibody.
Fifty-five serum samples positive for PCA, 22 males and 33 females (median age 61 years, range 29-108 years) were compared with 60 control samples negative for PCA, 24 males and 36 females (median age, 48 years, range 11-91 years). H. pylori infection and HSP65K antibodies were determined by enzyme-linked immunosorbent assay. CagA and VacA status were determined by Western blotting.
The prevalence of H. pylori was higher in PCA-positives than controls, 29/55 [53%, 95% confidence interval (CI) 39-66%] versus 13/60 (22%, 95% CI 12-34); P= 0.0009. Age was not a confounding factor. Odds ratio for PCA seropositivity if H. pylori-positive was 4.0 (1.79-9.07), P= 0.003. There was an interaction between age and H. pylori, particularly in younger patients. CagA strains were less common in PCA-positives than controls, 10/29 (35%, 95% CI 19-54) versus 9/13 (69%, 39-91), P< 0.05. HSP65K antibodies were elevated in H. pylori infection but to a similar degree for both PCA-positives and controls.
H. pylori, particularly CagA-negative strains, are associated with autoimmune gastritis and may be implicated in the pathogenesis of autoimmune (type A) gastritis, particularly in younger persons.
