Influence of the Immunocorrection on the State of Nonspecific Cellular and Humoral Immunological Reactivity Patients with Chronic Heart Failure

Pavlova Ye. A.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

The problem of chronic heart failure (CHF) continues to be relevant and currently holds a lead-ing position in the structure of morbidity and mortality from cardiovascular disease. CHF – complex circulatory and metabolic reactions arise owing to cardiac dysfunction. Pathogenesis of heart failure is a complex multi-factorial process, resulting impact on the cardiovascular system of etiological factors and mobilizing complex compensatory mechanisms involving the violation of various parts of the immunological reactivity of the or-ganism, which further defines the course and prognosis of CHF. The aim of this work was to study regularities of changes nonspecific cellular and humoral immunological reactivity in patients with chronic heart failure, before and after standard therapy compared to similar patients where, in addition to standard therapy, was carried immunotherapy. We observed two groups of patients with chronic heart failure, which accompanied by moderate hemodynamic disorders. Cause of heart failure was coronary heart disease. For treatment of one group of the patients we used the standard therapy, and the other carried immunocorection in addition to standard therapy. As an immunomodulator, we used immunofan. The study of immunological reactivity was performed twice – before and 10 days after of treatment. Determination of hemolytic complement activity, phagocytic activity of neutrophils in peripheral blood was determined by standardized method. Phagocytic number, phagocytic index and neutrophil bactericidal index was also determined by standardized. Quantitative content of cytokines (TNF-α, IL-1β, IL-4, IL-6) and C-reactive protein examined by ELISA using sets of reagents firm “Protein contour” (St. -Petersburg). Analysis of the results of research which characterize the state nonspecific cellular immunological reactiv-ity in patients with chronic heart failure of moderate severity showed a decrease in the initial protective function of polymorphonuclear leukocytes (рhagocytic number, phagocytic index and neutrophil bactericidal index). Use of immunocorrection in addition to standard therapy, accompanied by an increase functional activity of polymorphonuclear leukocytes, the activity of the complement system. Activation nonspecific cellular and humoral reactivity is adaptive in nature and is aimed at restoring the functional state of the immune system in patients of the study group. At the same time reduction of proinflammatory cytokines TNF-ά, IL-1, IL-6 necessary condition for the realiza-tion the reparative effects of cytokines in the focus their reasonable concentration, which is possible only after the utilization of antigenic material by neutrophils and macrophages. Increased levels in the blood of IL-4 (antiinflam-matory, multifunctional cytokine) actively influences on cell-mediated reactions of late-phase and processes to repair damaged, decrease in the activity of the process during CHF and a whole – reducing the risk of possible com-plications. To restore altered nonspecific cellular and humoral immunological reactivity, which is associated with the severity of chronic heart failure, there is a necessity of using immunomodulators in addition to standard therapy.

chronic cardiac insufficiency, ischemic heart disease, preventive immunocorrection, nonspe-cific cellular and humoral reactivity

• 1. Барна О. М. Маркери запалення в стратифікації ризику серцево-судинних захворювань / О. М. Барна // Ліки України.– 2007. – №115-116. – С. 6-11.
• 2. Гмурман В. Е. Теория вероятностей и математическая статистика / В. Е. Гмурман. – М.: Высшая школа, 2001. – 479 с. 3. Медицинские лабораторные технологии / под ред. А. И. Карпищенко. – СПб.: Интермедика, 1999. – Т. 2. – 656 с.
• 4. Олиферук Н. С. Оценка фагоцитарной и бактерицидной активности нейтрофилов, макрофагов и незрелых дендрид-ных клеток / Н. С. Олиферук, А. Н. Ильинская, Б. В. Пинегин // Иммунология. – 2005. – №1. – С. 10–12.
• 5. Писарева В. Г. Динамика цитокинов при хронической сердечной недостаточности под влиянием комбинированной терапии /ВГ.Псарева, Н. В.Демихова, О. А.Власенко // Проблеми сучасної медичної науки та освіти. – 2009. – №2.– С. 19–21.
• 6. Прилуцкий А. С. Иммунодефицитные состояния в клинической практике. Варианты, клинико-лабораторные призна-ки, методы оценки / А. С. Прилуцкий // Лікування та діагностика. – 2004. – №2. – С. 25-32.
• 7. Скуинь Л. М. Иммунная система и вторичные иммунодефицитные состояния / Л. М. Скуинь // Медицинская помощь.– 2004. – №3. – С. 25-27.
• 8. Тодоріко Л. Д. Цитокіни – нова система регуляції захисних реакцій організму, їх роль у формуванні запалення / Л. Д. Тодоріко, К. В. Рихлецька // Клінічна та експериментальна патологія. – 2004. – Т. 3, №1. – С. 91-96.
• 9. Халафян А. А. STATISTICA 6. Статистический анализ данных / А. А. Халафян. – 3-е изд. – М.: ООО Бином-Пресс, 2007.– 512 с.
• 10. Hudzik B. Serum interleukin-6 concentration reflects the extent of asymptomatic left ventricular dysfunction and predicts pro-gression to heart failure in patients with stable coronary artery disease / B. Hudzik, J. Szkodzinski, W. Romanowski [et al.] // Cytokine. – 2011. – Vol. 54, №3. – P. 266–271.
• 11. Kalogeropoulos A. Inflammatory markers and incident heart failure risk in older adults: the Health ABC (Health, Aging, and Body Composition) study / A. Kalogeropoulos, V. Georgiopoulou, B. M. Psaty [et al.] // J. Am. Coll. Cardiol. – 2010. – Vol. 55, №19. – P. 2129–2137.
• 12. Martins T. B. Risk factor analysis of plasma cytokines in patient with coronary artery disease by a multiplexed fluorescent immunoassay / T. B. Martins, J. L. Anderson, J. B. Muhlestein [et al.] // Am. J. Clin. Pathol. – 2006. – Vol. 125. -P. 906-913.
• 13. Memon L. Association of C – reactive protein with the рresence and еxtent of аngiographically verified coronary artery dis-ease / L. Memon, V. Spasojevic – Kalimanovska // Tohoku J. Exp. Med. – 2006. – Vol. 209. – P. 197-206.
• 14. Nakagomi A. Upregulation of monocyte proinflammatory cytokine production by C-reactive protein is significantly related to ongoing myocardial damage and future cardiac events in patients with chronic heart failure / A. Nakagomi, y. Seino, y. Endoh [et al.] // J. Card. Fail. – 2010. – Vol. 16, №7. – P. 562–571.
• 15. Richter B. Differences in the predictive value of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in advanced ischemic and non-ischemic heart failure /B.Richter, K.Rychli, P.J.Hohensinner, [et al.] //Atherosclerosis. – 2010. – Vol.213, №2. – P. 545–548.
• 16. Zhang H. F. Tumor necrosis factor-alpha G-308A gene polymorphism and coronary heart disease susceptibility: an updated meta-analysis / H. F. Zhang, S. L. Xie, J. F. Wang [et al.] // Thromb. Res. – 2011. – Vol. 127, №5. – P. 400–405.
• 17. Zourdidaks E., Avanzas P. Marcers of inflammation and rapid coronary artery disease progression in patients with stable an-gina pectoris// Circulation. – 2004. – Vol. 110. – P. 1747-1753.

«Bulletin of problems biology and medicine» Issue 2 part 3 (109), 2014 year, 175-178 pages, index UDK 616. 12-008. 46-036. 12-085. 37:612. 017. 1