Autoimune component in the development of celebrovascular insufficiency in children with bronchial asthma

Abstract

Bronchial asthma (BA) remains one of the most serious diseases of our time. A number of studies have shown that this disease in a number of cases, especially with the threat of termination of pregnancy, acute and chronic diseases of mothers, accompanied by fetal hypoxia, originates in the ante- and postnatal period. In general, taking into account the peculiarities of the cellular tissue organization of the brain and cerebrovascular blood supply, prolonged hypoxic lesions increase the activity of the hypothalamic-diencephalic structures and the cerebral cortex. The existing respiratory disorders lead to hemodynamic and metabolic disorders of cerebral structures, emotional sphere and autonomic regulation. However, this issue in childhood requires further study. The aim is to study autoimmune processes in the pathogenesis of cerebrovascular insufficiency in children with BA. Materials and methods. We examined 121 patients with asthma aged 5 to 15 years in the period of exacerbation. To study the role of the autoimmune component in the development of cerebrovascular insufficiency and its relationship with the autoimmune process in the bronchopulmonary system in AD in children, we used a method for the quantitative determination of autoantibodies to lipopolysaccharide antigens (LA) of cerebral vessels and topographic structures of the brain, as well as to homologous LA bronchi and lung tissue. The results of the studies have shown that the first signs of cerebral hemodynamic disturbance are recorded already in patients with mild disease and are aggravated depending on the severity of BA. Conclusions. The most characteristic changes are an increase in the tone of small and medium vessels and impaired cerebral venous circulation. It was also found that the levels of autoantibodies to lipopolysaccharide antigens of cerebral vessels and cellular tissue structures of the brain correlate with an increase in the level of autoantibodies to lipopolysaccharide antigens of the trachea, bronchi and lung tissue and reflect the severity of AD in children.