Роль неинвазивных маркеров повреждения энтероцитов и повышенной проницаемости в патогенезе целиакии

Abstract

Celiac disease (CD) is an immune-mediated enteropathy characterized by atrophy/damage to the mucous membrane of the small intestine in genetically susceptible individuals in response to gluten administration. In CD morphology, atrophy is the result of increased enterocyte apoptosis due to autoimmune inflammation. Since the enterocyte is an anatomical and functional unit of the mucous membrane of the small intestine, responsible for the barrier function and for the absorption of nutrients, to understand the pathogenesis of CD, the study of the processes of restoration of the mucosa is of paramount importance. Antibodies to tissue transglutaminase, antibodies to deamidated gliadin peptides, antibodies to endomysium, which are used to monitor disease activity and represent the body's immune response, can only indirectly indicate the degree of damage/recovery of enterocytes. During histological examination it is not always possible to assess the degree of damage at the cellular level, taking into account the complexity of the interpretation of morphological changes and patchiness of mucosa damage. In recent years, researchers have paid much attention to new markers of mucosa permeability, which include: I-FABP − a marker reflecting damage to enterocytes, citrulline − a marker of the functional mass of enterocytes, zonulin − a marker of increased mucosa permeability and alpha-1-antitrypsin − a marker reflecting the failure of the barrier function of the small intestine and protein loss. Using of these markers will help optimize the algorithm for non-invasive diagnostics of CD, improve monitoring of disease activity, and will also usefull for understanding the processes of mucosa recovery.