ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 31 of 60
JMBS 2019, 4(6): 217–222
Clinical Medicine

The State of Fibrinolysis and Proteolysis System, Homeostasis of Nitrogen Monoxide, Plasma and Platelet Hemostasis in Patients with Nonalcoholic Steatohepatitis and Comorbid Coronary Heart Disease

Khukhlina O., Kuzminska O., Antofiichuk T., Kotsiubiichuk Z., Hryniuk O., Kropyva V.

Non-alcoholic fatty liver disease is now recognized worldwide as a common chronic liver disease. Due to metabolic risk factors common to non-alcoholic fatty liver disease and cardiovascular disease, patients with non-alcoholic steatohepatitis are at increased risk of developing hepatic encephalopathy and cardiovascular death. The purpose of the study was to investigate the state of fibrinolysis and proteolysis system, homeostasis of nitrogen monoxide, plasma and platelet hemostasis in patients with non-alcoholic steatohepatitis, depending on the presence of comorbid coronary heart disease. Material and research methods. We examined 120 patients with non-alcoholic steatohepatitis: 30 patients with non-alcoholic steatohepatitis and obesity of I-II degree (group 1), 90 patients with non-alcoholic steatohepatitis and comorbid obesity of I-II degree and coronary heart disease (stable angina pectoris I-II) (group 2). The average age of the examined patients was 56.81±8.38 years. There were 16 (53,37 %) men and 14 (46,63 %) women in group 1. In the group 2 there were 48 (53,35 %) men and 42 (46,65 %) women. The control group consisted of 30 practically healthy persons aged from 40 to 60 years. Results and discussion. The vast majority of patients with non-alcoholic steatohepatitis and comorbid coronary heart disease showed a decrease in fibrinolytic potential of blood plasma (total (p <0.05) and enzymatic fibrinolytic activity (p <0.05), increased blood coagulation (a significant decrease of prothrombin time) (p<0.05) and increased fibrinogen content (p <0.05) in the blood, NO deficiency (p <0.05), platelet aggregation capacity (significant increase of spontaneous (p <0.05) and induced platelet aggregation (p <0.05)). Conclusions. The cause of revealed disorders of rheology and blood clotting at non-alcoholic steatohepatitis is accumulation in the systemic circulation of toxic substances, which create a high level of endotoxicosis, contribute to the release of biologically active substances, cytokines, activation of kallikrein-kinin system, the formation of plasmin and thrombin with subsequent disturbance of equilibrium between them, development of stasis, erythrocyte aggregates in an extended portal system with low blood flow velocity. The slowing of blood circulation in the liver due to the formation of microthrombuses in the microcirculatory system contributes to the deepening of organ hypoxia, processes of lipid peroxidation with subsequent damage of cell membranes and closure of the vicious circle of pathogenesis of non-alcoholic steatohepatitis and coronary heart disease progression.

Keywords: nonalcoholic steatohepatitis, coronary heart disease, fibrinolysis, proteolysis, platelet aggregation

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  1. Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, et al. Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. Am J Gastroenterol. 2012; 55(6): 2005-23.
  2. Musso G, Gambino R, Cassader M, Pagano G. Meta-analysis: natural history of non-alcoholic fatty liver disease (NAFLD) and diagnostic accuracy of non-invasive tests for liver disease severity. Ann Med. 2011; 43(8): 617-49.
  3. Kowdley KV. Advances in the diagnosis and treatment of nonalcoholic steatohepatitis. Gastroenterol Hepatol (NY). 2014; 10(3): 184-6.
  4. Lam B, Younossi ZM. Treatment options for nonalcoholic fatty liver disease. Therap Adv Gastroenterol. 2010; 3(2): 121-37.
  5. Latea L, Negrea S, Bolboaca S. Primary non-alcoholic fatty liver disease in hypertensive patients. Australas Med J. 2013; 6(6): 325-30.
  6. Anstee QM, Targher G, Day CP. Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis. Nat Rev Gastroenterol Hepatol. 2013; 10: 330-44.
  7. Brea A, Puzo J. Non-alcoholic fatty liver disease and cardiovascular risk. Int J Cardiol. 2013; 167(4): 1109-17.
  8. Nascimbeni F, Pais R, Bellentani S, Day CP, Ratziu V, Loria P, et al. From NAFLD in clinical practice to answers from guidelines. J Hepatol. 2013; 59(4): 859-71.
  9. Babak OIa. Hlutatyon v norme y pry patolohyy: byolohycheskaia rol y vozmozhnosty klynycheskoho prymenenye [Glutathione in health and disease: the biological role and possibilities of clinical use]. Zdorovia Ukrainy. Tem nomer Hastroenterolohiia. Hepatolohiia. Koloproktolohiia. 2015; 1: 1-3. [Russian]
  10. Khukhlina OS, Drozd VYu. Optymizatsiia likuvannia nealkoholnoho steatohepatytu u khvorykh na ozhyrinnia ta ishemichnu khvorobu sertsia [Optimization of treatment of NASH in patients with obesity and coronary heart desease]. Liky Ukrainy. 2016; 9: 46-52. [Ukrainian]
  11. Polyanskaya OS. Proteoliticheskaya aktivnost u bolnyih so stenokardiey. [The proteolytic activity in patians with angina pectoris]. Kardiologiya: teoriya i praktika. Sbornik materialov mezhdunarodnogo nauchnogo e-simpoziuma. Rossiya, Moskva, 27-30 iyunya 2013. 2013: 31-6. [Russian]
  12. Khukhlina OS, Antoniv AA, Kanovska LV, Matushchak MV, Vivsyannuk VV. The intensity of the antioxidant protection system and oxidative stress factors in patiencts with non-alcoholic steatohepatitis depending on the form of chronic kidney disease. Georgian Medical News. 2018; 3(276): 71-6.
  13. Khukhlina OS, Antoniv AA, Mandryk OIe, Smanduch VS. The role of endothelial dysfunction in the progression mechanisms of non-alcoholic steatohepatitis in patients with obesity and chronic kidney disease. Wiadomosci Lekarskie. 2019; 4: 523-7.