Abstract
Objective. Analysis of clinical significance of auto-antibodies level as screening method for the diagnostics of cardiovascular and central
nervous systems damage in infants with intrauterine growth retardation.
Introduction. Intrauterine fetus development determines the state of health during subsequent life. Risk factors for the development
of cardiovascular pathology in infants with intrauterine growth retardation (1C1GR) are understudied.
Material and methods. Seventy-six "mother-neonate" pairs were studied in the Children's Infectious Diseases Clinical Hospital #6.
Among them, there were 18 neonates with intrauterine growth retardation (1UGR). The control group comprised 58 neonates without
1UGR. Besides general clinical examinations, the levels of the auto-antibodies (auto-Abs) to DNA fragments, P2-glycoprotein,
rheumatoid factor; serum auto-Abs to myocardial antigens (membrane antigen of СоМ-015-15 cardiomyocytes, cytoplasmic protein
GoS-05-40, NO-synthetase, P1-adrenoreceptors); the level of the main neurotropic auto-Abs directed at nervous system cells
proteins and neuromediators (S100, GFAP, MP-65, NF-200) were determined for all pairs.
Results. The analysis revealed that the infants with 1UCR more often had an increased level of neurospecific auto-Abs. 1n 11% of
cases the infants with 1UCR had a decreased level of auto-antibodies to cardiomyocytes protein GoS-05-40, P1-adrenereceptors and
membrane protein СоМ-015-15. Herewith, a decreased level of the studied antibodies in the comparison group was revealed in no
more than 3% of cases. The revealed decrease of antibodies to the structures of cardiovascular system in infants with intrauterine
growth retardation can be conditioned by an "enhancement" of apoptosis and elimination processes.
Conclusion. The revealed new diagnostic markers of the damage of cardiovascular and central nervous systems can contribute to
early diagnostics of pathological deviations for timely protection and the choice of the rehabilitation tactics.
References
- Barker D.J.P. A new model for the origins of chronic disease.
Med. Health CarePhilos. 2001; 4 (1): 31-5.
- Gortner L. 1ntrauterine growth restriction and risk for arterial
hypertension: a causal relationship? J. Perinat. Med. 2007; 35
(5): 361-5.
- Охапкин М.Б., Хитров М.В. Внутриутробная задержка
роста плода. АГ-инфо. 2008; 3: 29-33.
- Barker D.J.P., WinterP.D., Osmond C. et al. Weight in infancy
and death from ischaemic heart disease. Lancet. 1989; 2:
577-80.
- Osmond C., Barker D.J.P., Winter P.D. et al. Early growth and
death from cardiovascular disease in women. BMJ. 1993; 307:
1519-24.
- Кельмансон И.А. Отсроченный риск кардиоваскулярной
патологии, ассоциированный с малой массой тела при
рождении. Российский вестник перинатологии и педиатрии. 1999; 2: 12-8.
- Muhammad Т., Khattak A.A., Shafiq-ur-Rehman et al.
Maternal factors associated with intrauterine growwth restriction. J. Ayub. Med. Coll. Abbottabad. 2010; 22 (4): 64-9.
- Lau C., Rogers J.M. Embryonic and fetal programming of
physiological disorders in adulthood. Birth Defects Res. C.
Embryo. Today. 2004; 72 (4): 300-12.
- Barker D.J.P., Martyn C.N., Osmond C. et al. Growth in utero
and serum cholesterol concentrations in adult life. BMJ. 1993;
307: 1524-7.
- Gluckman P.D., Hanson M.A. Living with the past: evolution,
development, and patterns of disease. Science. 2004; 305
(5691): 1733-6.
- Полетаев А.Б., Алиева Ф., Мальцева Л.И. Иммунопатология
беременности и здоровье ребенка. РМЖ. 2010; 18 (4):
162-7.
- Shoenfeld Y. Etiology and pathogenetic mechanisms of the
antiphosphlipid syndrome unraveled. Trends Immunol. 2003;
24 (1): 5-7.
- Полетаев А.Б. Физиологическая иммунология (естественные аутоантитела и проблемы наномедицины). М.: Миклош; 2010.
- Notkins A.L. New predictors of disease. Sci. Amer. 2007; 3:
72-9.
- Shoenfeld Y. Etiology and pathogenetic mechanisms of the
antiphosphlipid syndrome unraveled. Trends Immunol. 2003;
24 (1): 5-7.
- Finkenzeller D., Fischer B., McLaughlin J., Schrewe H. et al.
Trophoblast cell-specific carcinoembryonic antigen cell adhesion molecule 9 is not required for placental development or a
positive putcome of allotypic pregnancies. Mol. Cell. Biol.
2000; 20 (19): 7140-5.
- TongZ.B., Gold L . , De Pol A., Vanevski K. et al. Developmental
expression and subcellular localization of mouse MATER, an
oocyte-specifi c protein essential for early development.
Endocrinology. 2004; 145: 1427-34.
- LemkeH., Lange H. 1s there a maternally induced immunological
imprinting phase a la Konrad Lorenz? Scand. J. Immunol.
1999; 50: 348-54.
- Полетаев А.Б. Иммунофизиология и иммунопатология. М.:
МИА; 2008.
- Макаров О.В., Богатырев Ю.А., Осипова Н.А. Значение
аутоантител в патогенезе преэклампсии. Акушерство и гинекология. 2012; 4 (1): 16-21.
- Мальцев С.В., Полетаев А.Б., Мансурова Г.Ш. Диагностическое и прогностическое определение естественных аутоантител к почечным антигенам в развитии пиелонефрита
у детей. Педиатрия. 2007; 6: 60-4.
- De Laat B., de Groot P.G. Autoantibodies directed against
domain 1 of p2-glycoprotein. J. Curr. Rheumatol. 2011; 13:
70-6.
- Школьникова М.А., Полякова Е.Б. Значение аутоиммунных механизмов в патофизиологии синдрома слабости синусового узла. Российский вестник перинатологии и педиатрии. 2006; 5: 46-8.
- Бекбосынова М.С. Показатели иммуновоспалительных
процессов и состояние симпатической иннервации миокарда у пациентов с предсердными и желудочковыми нарушениями ритма сердца: Автореф. ... д-ра мед. наук. М.;
2007.
- Кантемирова М.Г., Луценко Я.В., Абросимова А.А., Кузьменко Л.Г., Полетаев А.Б., Дегтярева Е.А. Особенности
спектра кардиоспецифических аутоантител у детей с аритмиями. Российский вестник перинатологии и педиатрии. 2010; 55 (2): 68-72.
