Komarytsia O. Y., Radchenko O. M., Pylypiv L. I.

COVID-19 AND ASSOCIATED WITH METABOLIC DYSFUNCTION HEPATOSTEATOSIS: LITERATURE REVIEW

---

Show/Download

About the author:

Komarytsia O. Y., Radchenko O. M., Pylypiv L. I.

Heading:

LITERATURE REVIEWS

Type of article:

Scientific article

Annotation:

The combination of metabolic-associated liver disease starting with liver steatosis (MASLD) and coronavirus disease (COVID-19) in the clinic has not been sufficiently studied. We reviewed the literature on the combination of COVID-19 and liver steatosis in the Pubmed database and assessed the frequency of its manifestations in patients with COVID-19-associated community-acquired pneumonia of clinical group III by examining 22 inpatients aged 54.7±2.1 years. It was found that liver steatosis can either be a background condition or occur as a result of COVID-19 due to hepatocyte damage by the virus, excessive activation of the systemic inflammatory response, hypoxia, coagulopathy, endotheliitis, cardiac right ventricular failure, and drug-induced liver damage. Adverse effects on hepatocytes of high doses of glucocorticosteroids, azithromycin and several antiviral drugs have been described, which may be aggravated by taking them in combination with NSAIDs. Background liver disease is also important, as COVID-19 has been described to activate the persistence of hepatitis B and C viruses, and treatment of COVID-19 with massive doses of corticosteroids may affect viral replication. According to their own observations, 68% of inpatients with COVID-19-associated community-acquired pneumonia of clinical group III of mature age were diagnosed with MASLD, which was manifested by a heterogeneous structure with increased echogenicity (100%) with clear, even liver contours and non-expanded bile ducts and normal choledochus; moderate increase in liver size (92%), loss of liver vascular pattern (23%). At the same time, normal liver function tests and lipid metabolism were observed, moderate hyperglycaemia and a more pronounced inflammatory syndrome were noted. However, the course of pneumonia was more severe with lower oxygen saturation.

Tags:

Bibliography:

1. Vos DY, van de Sluis B. Function of the endolysosomal network in cholesterol homeostasis and metabolic-associated fatty liver disease (MAFLD). Mol Metab. 2021;50:101146. DOI: 10.1016/j.molmet.2020. 101146.
2. Fougerat A, Montagner А, Loiseau N, Guillou H, Wahli W. Peroxisome Proliferator Activated Receptors and Their Novel Ligands as Candidates for the Treatment of Non-Alcoholic Fatty Liver Disease. Cells. 2020;9(7):1638. DOI: 10.3390/cells90716.
3. Lopez-Mendez І, Aquino-Matus J, Murua-Beltrán GS, Prieto-Nava JD, Juarez-Hernandez E, Uribe M, et al. Association of liver steatosis and fibrosis with clinical outcomes in patients with SARS-CoV-2 infection (COVID-19). Annals of Hepatology. 2021;20:100271.
4. Portincasa P, Krawczyk M, Smyk W, Lammert F, Di Ciaula A. COVID-19 and non-alcoholic fatty liver disease: Two intersecting pandemics. Eur. J Clin. Invest. 2020;50(10):e13338. DOI: 10.1111/eci.13338.
5. Steenblock C, Schwarz PEH, Ludwig B, Linkermann A, Zimmet P, Kulebyakin K, et al. COVID-19 and metabolic disease: mechanisms and clinical management. Lancet Diabetes Endocrinol. 2021;9(11):786-798. DOI: 10.1016/S2213-8587(21)00244-8.
6. Herta T, Berg T. COVID-19 and the liver - Lessons learned. Liver Int. 2021;41(1):1-8. DOI: 10.1111/liv.14854.
7. Nardo AD, Schneeweiss-Gleixner M, Bakail M, Dixon ED, Lax SF, Trauner M. Pathophysiological mechanisms of liver injury in COVID-19. Liver Int. 2021;41(1):20-32. DOI: 10.1111/liv.14730.
8. Sharma A, Jaiswal P, Kerakhan Y, Saravanan L, Murtaza Z, Zergham A, et al. Liver disease and outcomes among COVID-19 hospitalized patients - A systematic review and meta-analysis. Ann Hepatol. 2021;21:100273. DOI: 10.1016/j.aohep.2020.10.001.
9. Dong Z-Y, Xiang B-J, Jiang М, Sun M-J, Dai С. The Prevalence of Gastrointestinal Symptoms, Abnormal Liver Function, Digestive System Disease and Liver Disease in COVID-19 Infection: A Systematic Review and Meta-Analysis. Journal of Clinical Gastroenterology. 2021;55(1):67-76.
10. Merola E, Pravadelli C, de Pretis G. Prevalence of liver injury in patients with coronavirus disease 2019 (COVID-19): a systematic review and meta-analysis. Acta Gastro-Enterologica Belgica. 2020;83(3):454-460.
11. Amin M. COVID-19 and the liver: overview. Eur J Gastroenterol Hepatol. 2021;33(3):309-311. DOI: 10.1097/MEG.0000000000001808.
12. Ji D, Qin E, Xu J, Zhang D, Cheng G, Wang Y, et al. Non-alcoholic fatty liver diseases in patients with COVID-19: A retrospective study. J Hepatol. 2020;73(2):451-453. DOI: 10.1016/j.jhep.2020.03.044.
13. Lei HY, Ding YH, Nie K, Dong YM, Xu JH, Yang ML, et al. Potential effects of SARS-CoV-2 on the gastrointestinal tract and liver Biomed Pharmacother. 2021;133:111064. DOI: 10.1016/j.biopha.2020.111064.
14. Taylor-Robinson SD, Morgan MY. COVID-19 and the Liver: A Complex and Evolving Picture. Hepat Med. 2023;15:209-220. DOI: 10.2147/ HMER. S384172.
15. Martinez MA, Franco S. Impact of COVID-19 in Liver Disease Progression. Hepatol Commun. 2021;5(7):1138-1150. DOI: 10.1002/ hep4.1745.
16. Ekpanyapong S, Bunchorntavakul C, Reddy KR. COVID-19 and the Liver: Lessons Learnt from the EAST and the WEST, а Year Later. J. Viral Hepat. 2022;29(1):4-20. DOI: 10.1111/jvh.13590.
17. Russo FP, Burra P, Zanetto A. COVID-19 and liver disease: where are we now? Nat Rev Gastroenterol Hepatol. 2022;19(5):277-278. DOI: 10.1038/s41575-022-00607-9.
18. Sonzogni A, Previtali G, Seghezzi M, Grazia Alessio M, Gianatti A, Licini L, et al. Liver histopathology in severe COVID 19 respiratory failure is suggestive of vascular alterations. Liver Int. 2020;40(9):2110-2116. DOI: 10.1111/liv.14601.
19. Wang Y, Liu S, Liu H, Li W, Lin F, Jiang L, et al. SARS-CoV-2 infection of the liver directly contributes to hepatic impairment in patients with COVID-19. J Hepatol. 2020;73(4):807-816. DOI: 10.1016/j.jhep.2020.05.002.
20. Paizis G, Tikellis C, Cooper ME, Schembri JM, Lew RA, Smith AI, et al. Chronic liver injury in rats and humans upregulates the novel enzyme angiotensin converting enzyme 2. Gut. 2005;54(12):1790-6. DOI: 10.1136/gut.2004.062398.
21. Miller B, Silverstein A, Flores M, Xiang W, Cao K, Kumagai H, et al. SARS-CoV-2 induces a unique mitochondrial transcriptome signature. Research Square. 2020. DOI: 10.21203/RS.3.RS-36568/V1.
22. Rutkowski DT, Wu J, Back SH, Callaghan MU, Ferris SP, Iqbal J, et al. UPR pathways combine to prevent hepatic steatosis caused by ER stress-mediated suppression of transcriptional master regulators. Dev Cell. 2008;15(6):829-40. DOI: 10.1016/j.devcel.2008.10.015.
23. Yang RX, Zheng RD, Fan JG. Etiology and management of liver injury in patients with COVID-19. World. J. Gastroenterol. 2020;26(32):4753- 4762. DOI: 10.3748/wjg.v26.i32.4753.
24. Li J, Tian A, Zhu H, Chen L, Wen J, Liu W, et al. Mendelian Randomization Analysis Reveals No Causal Relationship Between Nonalcoholic Fatty Liver Disease and Severe COVID-19. Clin Gastroenterol Hepatol. 2022;20(7):1553-1560.e78. DOI: 10.1016/j.cgh.2022.01.045.
25. Lin HXJ, Aravamudan VM. Metabolic associated fatty liver disease and COVID-19: a double whammy? Singapore Medical J. 2022;63(9):542- 544.

Publication of the article:

«Bulletin of problems biology and medicine», 2024 Issue 2, 173, 45-51 pages, index UDC 616.36-003.826-06-008.9:616.98:578.834.1

DOI:

10.29254/2077-4214-2024-2-173-45-51