The review analyzes up-to-date knowledge on structure and biological functions of a-acid glycoprotein. A special attention is given to alterations in fucosylation, sialylation and branching of orosomucoid at the acute, chronic inflammation and oncotrans formations.

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Introduction. The critical state of extremely premature newborns is accompanied by significant oxidative stress, which leads to an increase in anaerobic metabolism; impaired oxygen utilization in mitochondrial oxidation may occur due to thiamine deficiency. The aim of the study – to learn the thiamine status of extremely premature new-borns in the neonatal period follow-up. Research Methods. The study involved 55 of premature newborns with birth weight less than 1000 g and 35 healthy full-term newborns. The indicated children’s blood tests were made in the first day of life and at the end of the neonatal period. The lactate and magnesium were determined by colorimetric method; the pyruvate content was determined enzymatically; the concentration of vitamin B1 was studied using a fluorimeter. Results and Discussion. In the first days of life, all premature infants have a significantly lower level of thiamine in the blood than the normal one, with the low limit of the norm of mature infants, due to the greatest intensity of adaptive reactions and the redistribution of nutrients in fasting. The deficiency of thiamine of extremely premature infants is accompanied by hypomagnesemia. The defining factor of thiamine deficiency of premature infants is morphofunctional immaturity. Deficiency of thiamine of premature infants is correlated with hyperlactatemia throughout the neonatal period. The metabolic features of an organism of a newborn with an extremely low birth weight reflect hypoxic disturbances (increased lactate and pyruvate level, changes in their ratio), which indicates the activation of glycolysis. The highest level of pyruvate was observed in premature infants in the first day of life and significantly exceeded the reference values with subsequent decrease during the first month of life, but remained beyond the norm, resulting in the development of secondary acidosis and persistent decrease in aerobic metabolism. Thiamine deficiency contributes to the pathogenesis of suppression of the pyruvate-dehydrogenase complex, bypassing pyruvate towards lactate overproduction and the development of metabolic acidosis. Conclusion. Deficiency of thiamine in premature newborns may lead to a deeper critical condition.