Вісник проблем біології і медицини (Sep 2020)

CORRELATION BETWEEN CHRONIC SYSTEMIC INFLAMMATION, LIPID SPECTRUM, LIVER FUNCTION AND ANTIOXIDANT SYSTEM IN PATIENTS WITH COMORBID PATHOLOGY OF STABLE CORONARY HEART DISEASE WITH NONALCOHOLIC FATTY LIVER DISEASE

  • Manusha Yu. I.,
  • Goncharova O. O.,
  • Sakevich V. D.,
  • Chekalina N. I.,
  • Kazakov Yu. M.

DOI
https://doi.org/10.29254/2077-4214-2020-3-157-118-121
Journal volume & issue
no. 3
pp. 118 – 121

Abstract

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The aim of the study was to examine the correlations between markers of chronic systemic inflammation (CHD), inflammatory endothelial activation, blood lipid spectrum, antioxidant system, liver and heart function in patients with stable coronary heart disease in combination with non-alcoholic fatty liver disease. The study involved 110 people with coronary heart disease: stable angina pectoris, II FC, CH 0-I in combination with non-alcoholic fatty liver disease aged 40-69 years. The analysis of indicators of a lipid spectrum of blood is made, studied the level of ceruloplasmin, cytokines (IL-6, TNFα, IL-10), circulating endothelial microparticles (CEM) CD32+ CD40+ in the blood, the expression of kappa B inhibitor mRNA gene α (IkBα) of nuclear kappa B transcription factor in peripheral blood mononuclear cells was studied and echocardiography, liver ultrasound with color and pulse Doppler imaging were performed (blood flow velocity in portal and hepatic veins was established). The relationship between the variables was then studied by correlation analysis. Conclusion. The correlation analysis established the relationship between the expression of mRNA IkBα nuclear transcription factor Kappa B with chronic systemic inflammation of low intensity, lipid metabolism with dysfunctional changes in blood flow in the liver (blood flow velocity in the portal vein), we can conclude that chronic systemic inflammation at the molecular genetic level plays an important role in the development of both coronary heart disease and nonalcoholic fatty liver disease and confirms the common pathogenetic mechanism of this comorbid pathology.

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