Autoimmune gastritis is characterised by severe atrophy of fundic and body gastric mucosa as well as by the presence of auto-antibodies against parietal cells (PCA) and intrinsic factor (IFA). The prevalence of H. pylori infection tends to be lower in patients with autoimmune gastritis in comparison with controls, due to gastric atrophy. However, the presence of anti-H. pylori antibodies may suggest a past infection, which could trigger an autoimmune reaction leading, over time, to mucosal atrophy. This hypothesis is strenghtened by recent immunoistochemical and immunoenzimatic studies showing the presence of antibodies against the gastric mucosa, also in H. pylori-positive chronic gastritis. We carried out a sierological study on IFA in healthy blood donors and in consecutive dyspetic patients who underwent oesophagogastroduodenoscopy, with the aim of evaluating their prevalence and association with H. pylori infection. We evaluated in 600 blood donors and 180 patients IgG against purified IF from gastric pig (ELISA). Gastric IgG autoantibodies were also determinated in patients by mean of an immunoenzimatic test. The frequency of IFA were in 0.9% and 6.8% in blood donors and dyspeptic patients respectively. Antibodies against epithelial mucins and PCA were also found in 72% and 22% of patients. Presence of IFA was associated with gastric atrophy at histology in 40% of cases. Presence of autoantibodies was associated with precence of H. pylori infection in most subjects. These findings suggest that H. pylori infection has a major role in the development of autoantibodies against parietal cells and IFA.
Anti-intrinsic factor antibodies, antiepithelial mucins and Helicobacter pylori infection / Negrini, R.; Barbarini, M.; Moretti, G.; Bertalot, G.; Annibale, B.. - In: ARGOMENTI DI GASTROENTEROLOGIA CLINICA. - ISSN 1120-8651. - 15:1(2002), pp. 82-84.
Anti-intrinsic factor antibodies, antiepithelial mucins and Helicobacter pylori infection
Bertalot G.;
2002-01-01
Abstract
Autoimmune gastritis is characterised by severe atrophy of fundic and body gastric mucosa as well as by the presence of auto-antibodies against parietal cells (PCA) and intrinsic factor (IFA). The prevalence of H. pylori infection tends to be lower in patients with autoimmune gastritis in comparison with controls, due to gastric atrophy. However, the presence of anti-H. pylori antibodies may suggest a past infection, which could trigger an autoimmune reaction leading, over time, to mucosal atrophy. This hypothesis is strenghtened by recent immunoistochemical and immunoenzimatic studies showing the presence of antibodies against the gastric mucosa, also in H. pylori-positive chronic gastritis. We carried out a sierological study on IFA in healthy blood donors and in consecutive dyspetic patients who underwent oesophagogastroduodenoscopy, with the aim of evaluating their prevalence and association with H. pylori infection. We evaluated in 600 blood donors and 180 patients IgG against purified IF from gastric pig (ELISA). Gastric IgG autoantibodies were also determinated in patients by mean of an immunoenzimatic test. The frequency of IFA were in 0.9% and 6.8% in blood donors and dyspeptic patients respectively. Antibodies against epithelial mucins and PCA were also found in 72% and 22% of patients. Presence of IFA was associated with gastric atrophy at histology in 40% of cases. Presence of autoantibodies was associated with precence of H. pylori infection in most subjects. These findings suggest that H. pylori infection has a major role in the development of autoantibodies against parietal cells and IFA.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione