Kibar V. Clinical and pathogenetic aspects of community-acquired pneumonia depending on the iodine supply of the body in children

The dissertation is devoted to increase an efficiency of early diagnosis and prognosis of a severe course of community-acquired pneumonia (CAP) with various iodine maintenance of an organism at children. The indicators of oxidative stress, apoptosis in interrelation with intracellular distribution of iodine and features of thyroid system function were studying. The iodine supply to the body of children with pneumonia was analyzed on the basis of studying the content of total iodine in the serum and the processes of its further intracellular division into organized and inorganic fractions. It is proved that the course of CAP in children with ID is accompanied by a marked decrease in the concentration of total and organic iodine with a significant increase in inorganic iodine in the serum, indicating a violation of subcellular distribution of iodine in the inflammatory process caused by pneumonia. The thyroid status of children with pneumonia in iodine deficiency was assessed. Functional changes in thyroid status which are manifested in the form of an isolated decrease in the level of free triiodothyronine (fT3) in children with severe community-acquired pneumonia with insufficient iodine supply leads to the development of "euthyroid pathology syndrome". The role of apoptosis processes, oxidative stress and features of leukocyte DNA damage as pathogenetic links of PP in children with optimal and insufficient iodine supply of the organism are analyzed and confirmed. The influence of the severity of the inflammatory process in pneumonia on the indicators of gene and cytotoxicity in the conditions of ID has been established. The relationships between the concentration of inorganic iodine, the intensity of the formation of oxyradicals, the processes of peroxidation of proteins and lipids were determined. The influence of iodine deficiency on the state of activity of free radical oxidation and antioxidant system in children with community-acquired pneumonia has been established. An inverse correlation was found between the level of inorganic iodine and the apoptosis system, the level of damage to DNA chains under oxidative stress, the effect of iodine deficiency on apoptotic activity and gene and cytotoxicity in children with CAP with insufficient iodine supply. It has been proven that oxidative stress and impaired intracellular distribution of iodine, which leads to an increase in its inorganic fraction in the blood, are among the leading factors in the induction of apoptosis. The complex clinical and pathogenetic characteristics of community-acquired pneumonia are presented, the systemic relationship between the main clinical indicators of the functioning of the respiratory system in children and ID is established. The diagnostic value of the study of apoptotic activity, oxidative stress and iodine status as predictors of the severity of the disease and the development of complications of PP in children living in iodine-deficient regions has been proved.