AMINO ACIDS IN THE PATHOGENESIS OF PERINATAL HYPOXIC-ISCHEMIC ENCEPHALOPATHY

The share of hypoxic-ischemic encephalopathy (HIE) accounts for about half of all perinatal brain lesions, which are a major cause of disability and maladjustment of children. The role and interaction of metabolic pathways in the pathogenesis of HIE still not fully clear; revealed significant changes in amino acid (AA) metabolism. The aim of the study – to investigate changes in the metabolism of amino acids (AA) in HIE. Materials and Methods. The study involved 117 infants with HIE, including 60 in the acute period (under the age of 1 month), and 57 in the early recovery period of hypoxic-ischemic encephalopathy (ages 1–4 months). All patients surveyed free blood amino acids by high performance liquid chromatography. Results and Discussion. In the acute period of HIE, an increase in the level of neuroamic acids – glutamate (р = 0.001), glycine (р = 0.038), methionine (р = 0.015) and AA, involved in energy metabolism and maintenance of a constant level of blood glucose: alanine (р = 0.001), threonine (р = 0.028), branched-chain amino acids – valine (p = 0.01), leucine (p = 0.021); decreased levels of tryptophan (р = 0.000) and tyrosine (р = 0.015), which are precursors of neurotransmitters. In the early recovery period, HIE was diagnosed with frequent changes in the AA of the urea cycle, aspartate; decrease in the level of valine. Conclusions. Identified data suggest that the metabolism of amino acids is one of the leading places in the pathogenesis of HIE; the most commonly identified amino acid changes that are involved in neurotransmission processes and energy metabolism is detoxification of ammonia. This gives grounds for metabolic correction and prevention of complications