The role of cytokines and their genetic polymorphism in the development of hypoxic-ischemic encephalopathy among full-term newborn children

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The problem of ischemic brain damage among newborns is still relevant in the modern world. The frequency of occurrence of this pathology among full-term newborns remains at a fairly high level, both in Russia and abroad. Moreover, it has a high mortality rate and the percentage of early childhood disability is 60-70%, participating in the development of such diseases as minimal brain dysfunction, infantile cerebral palsy, epilepsy. According to the World Health Organization, about 20% of children suffer from neuropsychic disorders, whose causes in 65-80% of cases are perinatal brain lesions of hypoxic origin. The article deals with modern concepts of molecular genetic mechanisms of development of hypoxic-ischemic encephalopathy among newborns, as well as issues of classification and conditions under which this pathology develops. The author studied the latest domestic and foreign literature data on the properties and role of pro and anti-inflammatory cytokines, such as IL-1, IL-4, IL-6, IL-8, IL-10, IL-13, TNF-α, which are, according to modern concepts, one of the main links in the pathogenesis of ischemic brain injury. Also, special attention is paid to their genetic polymorphism, since qualitatively or quantitatively the genetically altered molecules of cytokines affect the immune response. Investigation of the level of cytokines and their genetic polymorphism before the onset of clinical symptoms will allow prediction the onset of the disease and preventing the adverse effects of the damage of the central nervous system.

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Marina Panova

Chita State Medical Academy

编辑信件的主要联系方式.
Email: merik2002@mail.ru

Assistant Professor, Department of Propaedeutics of Children's Diseases

俄罗斯联邦, Chita

Alexandra Panchenko

Chita State Medical Academy

Email: sashawomen@mail.ru

MD, PhD, Dr Med Sci, Associate Professor, Head, Department of Propaedeutics of Children's Diseases

俄罗斯联邦, Chita

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