AN INFLUENCE OF ACUTE CORONAVIRUS DISEASE ON HEPATIC TISSUE (LITERATURE REVIEW)

Nowadays we have a great number of patients who have suffered from acute coronavirus disease. More than 687 million people at least once had the positive COVID-test. Moreover, more than 27 thousand people are suffering from this disease in Ukraine now. SARS-CoV-2 virus can damage various organs and systems, primarily the respiratory system that will manifest in a dry cough, shortness of breath, general weakness, up to the development of acute respiratory distress syndrome, shock and acute heart failure. The damage of lover by SARS-CoV-2 virus can be both direct and indirect. The presence of liver damage often leads to a more severe course of acute coronavirus disease. In order to treat new cases more effectively and deal with complications of old ones it is necessary to study better the mechanisms of the viral effect on various organs, in particular the liver. The best way to find out this mechanism is to examine main laboratory and instrumental indicators, learn about the changes in histological sections. Aim. The aim of the research was to investigate the results of up-to-date researches of the main changes in laboratory and instrumental indicators because of acute coronavirus disease, as well as possible mechanisms of liver damage. Materials and methods. Analysis of open publications of Scopus, Web of Science, PubMed for the last 10 years. The results. In patients with acute coronavirus disease an increase in the levels of transaminases (in most cases due to alanine aminotransferase), lactate dehydrogenase, bilirubin, prolongation of prothrombin time, an increase in the level of D-dimer, and a decrease in the number of platelets and albumins were often observed. Histological examination of biopsies revealed diffuse lung damage, significant desquamation of pneumocytes and hyaline membranes, extensive interstitial fibrosis with areas of fibrinous exudation and inflammation in the alveolar space. Hepatocyte apoptosis, moderate microvascular and minor macrovascular steatosis were observed in the hepatic tissue. Thus, we can suppose that the possible mechanisms of liver damage are direct virus damage, immunomodulated inflammation, hypercoagulative processes, hepatic hypoxia, drug-induced damage. Virus SARS-CoV-2 can get into the cell using angiotensin-converting enzyme 2 receptors. Direct virus influence can be possible because of high quantity of ACE2 receptors in bile-ducts and hepatocytes. Great amount of them is also present in vascular endothelium. As a result of apoptosis of COVID- infected cells a great amount of cytokines is released. This can lead to immunomodulated damage of different organs including liver. Moreover, inflammation leads to hypercoagulable state that in future can cause hypoxia of hepatic tissue because of thrombosis of liver vessels. Cytokine storm that developed in patients with severe COVID-19 pneumonia can lead to the destruction of tissues in the center of inflammation. The large number of cytokines that are released can increase vascular permeability that leads to dyspnea and respiratory failure because of blood and fluid migration. Researches showed us that some of the drugs that are uses as a treatment for COVID-19 may cause drug-induced damage of liver. Remdesivir is known to increase hepatic enzymes, reducing the level of albumin and increasing the level of bilirubin. LPV/r caused side effects more often than other drugs. Conclusions. As a result of the research the main symptoms, clinical and instrumental changes typical for acute coronavirus infection, possible mechanisms of liver damage because of this disease were revealed. However, we don’t have enough information to prescribe a pathogenetically justified treatment so the further investigation is needed.