Prodanchuk G. Clinical and experimental study of the hematotoxic mechanisms caused by hydroxylaminsulfate poisoning and optimization of approaches for diagnosis and treatment for such poisoning.

Dissertation is devoted to clinical and experimental study of the basic laws and characteristics of the formation of hematotoxic effects of hydroxylamine (LRA) in acute poisoning and the justification of new methods of diagnosis and treatment. Clinical study of examination and treatment results for 158 patients with acute poisoning by hydroxylaminsulfate and experimental evaluation of the hematotoxic effects in rats in vivo and in vitro on thymocytes and erythrocytes showed that hydroxylaminsulfate causes oxidative stress due to release of NO and other reactive oxygen compounds with formation of toxic methemoglobinemia (TM), methemoglobin (MetHb), sulfgemoglobin (S-Hb), poikilocytosis, Heinz bodies and persistent hemnirosile complexes in red blood cells during depletion of thiol compounds and activation of LPO, inhibition of antioxidant system and increase of the free ferric iron (Fe3+) level in the blood. It is established that all these processes contribute to disruption of the structure and of the oxygen transporting function of red blood cells, causing them to premature disposal in the spleen and hemolysis with the development of hemolytic anemia with compensatory reticulocytosis, hyperbilirubinemia and urobilinemia. The administration of antioxidants such as tocopherol and ?-lipoic (thioctic acid) on the background of nonspecific detoxification therapy and correction of metabolic acidosis increases the effectiveness of treatment due to significantly reducing of recovery time of MetHb (p <0,05), S-Hb (p <0.05) and hemoglobin (p <0.05) and reduces the severity of violations.