Aim To evaluate the prevalence of autoimmune gastritis in children with celiac disease, according to enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescence reaction (IIFR).
Methods 155 children of both sexes at the age of 3 to 17 years were examined. The study involved 78 children with different clinical forms of celiac disease (CD). The diagnosis was confirmed according to ESPGHAN criteria: was biopsy-proven, was based on clinical manifestation, positive serological and genetic data. 72 children with chronic gastritis and excluded celiac disease were a control group.
All patients underwent a same examination: histological examination of gastric biopsies, histological verification of H. pylori infection and biopsy urease test. The biopsies were evaluated by a single pathologist who was blinded to all clinical data. Identification of anti-parietal cell antibodies (APCA), anti-Intrinsic Factor (ELISA) was carried out in 76 patient and anti- H+/K+ ATPase (ELISA) in 66. APCA, using indirect immunofluorescence reaction, were determined in 62 children.
Results In both groups of children chronic gastritis was diagnosed. Helicobacter pylori infection was verified in the majority of patients in both groups (53,7% and 55,9% p>0,05).
Anti- H+/K+ ATPase antibodies were common in both groups with no statistically significant difference (8.8% and 6.25%, p>0.05), but only in the group with celiac antibodies combined with gastric atrophy (2.9% and 0%, p<0.01). Anti-Intrinsic Factor antibodies were presented only in the control group (0% and 6.8%, p<0.01) and weren’t combined with atrophy. APCA identified with IIFR were detected only in patients with celiac disease (4.54% and 0%, p<0.01) and were associated with gastric atrophy.
Conclusion Thus, the ELISA detected APCA with no evidence of gastric atrophy in both groups. This requires additional examination to confirm or to exclude the diagnosis of autoimmune gastritis. IIFR displayed complete concurrence of immunological and histological criteria of autoimmune atrophic gastritis, including the lack of association with H. pylori infection. This may indicate a systemic autoimmune process in celiac disease.
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