Autoimmune gastritis in children

Abstract

Etiology of autoimmune gastritis, particularly in children, is still unknown. However, the role of Helicobacter pylori and Epstein–Barr virus in the development of autoimmune gastritis is being considered. The formation of autoimmune gastritis is based on an autoimmune reaction mediated by CD4+ T-lymphocytes and the formation of antibodies to gastric parietal cells, the target of which is gastric Н+/К+-АТPase, with subsequent destruction of parietal cells and the development of mucosal atrophy. Autoimmune gastritis is considered a precancerous condition. The clinical picture of autoimmune gastritis in children is not associated with any specific symptoms of the digestive organs. Abdominal pain is uncommon. Specific manifestations of a dyspeptic nature are rare. Often there is a syndrome of chronic nonspecific intoxication. Red blood counts in most children with autoimmune gastritis are within the age norm. Iron deficiency anemia occurs in 13.8% of patients. Vitamin B12 deficiency anemia does not occur in children. Autoantibodies to the parietal cells of the stomach are considered to be a serum marker and diagnostic criterion for autoimmune gastritis in children. Treatment of autoimmune gastritis is aimed at preventing iron and/or vitamin B12 deficiency. No specific methods of treatment have been developed so far. Conclusion. The incidence of autoimmune gastritis in children is underestimated. The role of Helicobacter pylori in autoimmune gastritis has not been confirmed. There is a close correlation of antibodies to gastric parietal cells with Epstein–Barr viral DNA. Due to adverse outcomes and the risk of malignancy, early diagnosis of the disease is important. Atrophic gastritis and intestinal metaplasia are precancerous conditions, although extremely rare in childhood, they should not be neglected.