Pulmonary fibrosis associated with COVID-19
DOI: 10.32364/2587-6821-2021-5-7-492-496
N.A. Kuzubova1, O.N. Titova1, E.S. Lebedeva1, E.V. Volchkova2
1I.P. Pavlov First St. Petersburg State Medical University, Saint-Petersburg, Russian Federation
2Saint-Petersburg State Pediatric Medical University, Saint Petersburg, Russian Federation
An analysis of scientific publications based on the study results conducted during the COVID-19 pandemic indicates a possible risk of pulmonary fibrosis or progression of existing interstitial lung disease with the pulmonary fibrosis development in patients with the SARS-CoV-2 virus. A fibrous histological pattern was detected in about 22% of COVID-19 cases, starting from the third week of the disease. The molecular basis of the pulmonary fibrosis progression after infection with the SARS-CoV-2 virus remains unclear, but it is considered multifactorial, including direct viral effects, immune dysregulation, cytokine storm and increased oxidative stress. The question needs to be answered why a certain part of patients undergo a transition to uncontrolled cell proliferation with the accumulation of fibroblasts and myofibroblasts, excessive deposition of collagen and extracellular matrix, which leads to progressive pulmonary fibrosis, a more severe disease course and increases the risk of severe complications and mortality. There is no regulated therapeutic approach to the treatment of pulmonary fibrosis associated with a new coronavirus infection. Along with the approved antifibrotics for the treatment of idiopathic pulmonary fibrosis, nintedanib and pirfenidone, new means of preventing the fibrosis process are being investigated. An important research area is a search for biomarkers for early identification of patients with a high risk of severe COVID-19, burdened by the development of interstitial fibrotic lung lesions.
Keywords: pulmonary fibrosis, COVID-19, SARS-CoV-2, pneumonia, angiotensin-converting enzyme 2, immune dysregulation, antif ibrotics.
For citation: Kuzubova N.A., Titova O.N., Lebedeva E.S., Volchkova E.V. Pulmonary fibrosis associated with COVID-19. Russian Medical Inquiry. 2021;5(7):492–496 (in Russ.). DOI: 10.32364/2587-6821-2021-5-7-492-496.
2. Lechowicz K., Drożdżal S., Machaj F. et al. COVID-19: The potential treatment of pulmonary fibrosis associated with SARS-CoV-2 infection. J Clin Med. 2020;9(6):1917. DOI: 10.3390/jcm9061917.
3. George P.M., Wells A.U., Jenkins R.G. Pulmonary fibrosis and COVID-19: The potential role for antifibrotic therapy. Lancet Respir Med. 2020;8(8):807–815. DOI: 10.1016/S2213-2600 (20) 30225-3.
4. Bösmüller H., Matter M., Fend F., Tzankov A. The pulmonary pathology of COVID-19. Virchows Arch. 2021;478(1):137–150. DOI: 10.1007/s00428-021-03053-1.
5. Li Y., Wu J., Wang S. et al. Progression to fibrosing diffuse alveolar damage in a series of 30 minimally invasive autopsies with COVID-19 pneumonia in Wuhan, China Histopathology. 2021;78(4):542–555. DOI: 10.1111/his.14249.
6. Mauad T., Duarte-Neto A.N., da Silva L.F.F. et al. Tracking the time course of pathological patterns of lung injury in severe COVID-19. Respir Res. 2021;22(1):32. DOI: 10.1186/s12931-021-01628-9.
7. Polak S.B., van Gool I.C., Cohen D. et al. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol. 2020;33(11):2128–2138. DOI: 10.1038/s41379-020-0603-3.
8. Udwadia Z.F., Koul P.A., Richeldi L. et al. Post-COVID lung fibrosis: The tsunami that will follow the earthquake. Lung India. 2021;38(Suppl.): S41–S47. DOI: 10.4103/lungindia.lungindia_818_20.
9. Wu C., Chen X., Cai Y. et al. Risk factors associated with acute respiratory distress syndrome and death in patients with coronavirus disease 2019 pneumonia in Wuhan, China. JAMA Intern Med. 2020;180(7):934–943. DOI:10.1001/jamainternmed.2020.0994.
10. Xu J., Xu X., Jiang L. et al. SARS-CoV-2 induces transcriptional signatures in human lung epithelial cells that promote lung fibrosis. Respir Res. 2020;21(1):182. DOI: 10.1186/s12931-020-01445-6.
11. Delpino M.V., Quarleri J. SARS-CoV-2 Pathogenesis: Imbalance in the renin-angiotensin system favors lung fibrosis. Front Cell Infect Microbiol. 2020;10:340. DOI: 10.3389/fcimb.2020.00340.
12. Nile S.H., Nile A., Qiu J. et al. COVID-19: Pathogenesis, cytokine storm and therapeutic potential of interferons. Cytokine Growth Factor Rev. 2020;53:66–70. DOI: 10.1016/j.cytogfr.2020.05.002.
13. Yuki K., Fujiogi M., Koutsogiannaki S. COVID-19 pathophysiology: A review. Clin Immunol. 2020;215:108427. DOI: 10.1016/j.clim.2020.108427.
14. Xiong Y., Liu Y., Cao L. et al. Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients. Emerg. Microbes Infect. 2020;9(1):761–770. DOI: 10.1080/22221751.2020.1747363.
15. Sahin M., Akkus E. Fibroblast function in COVID-19. Pathol Res Pract. 2021;219:153353. DOI: 10.1016/j.prp.2021.153353.
16. Albert R.K., Smith B., Perlman C.E., Schwartz D.A. Is progression of pulmonary fibrosis due to ventilation-induced lung injury? Am J Respir. Crit. Care Med. 2019;200(2):140–151. DOI: 10.1164/rccm.201903-0497PP.
17. Spagnolo P., Distler O., Ryerson C.J. et al. Mechanisms of progressive fibrosis in connective tissue disease (CTD) — associated interstitial lung diseases (ILDs). Ann Rheum Dis. 2021;80(2):143–150. DOI: 10.1136/annrheumdis-2020-217230.
18. Chaudhary S., Natt B., Bime C. et al. Antifibrotics in COID-19 lung disease: Let us stay focused. Front Med (Lausanne). 2020;7:539. DOI: 10.3389/fmed.2020.00539.
19. Yavas G., Yavas C., Celik E. et al. The impact of spironolactone on the lung injury induced by concomitant trastuzumab and thoracic radiotherapy. J Thorac Oncol. 2018;13(10): S638. DOI: 10.1016/j.jtho.2018.08.997.
20. Kobayashi T., Tanaka K., Fujita T. Bidirectional role of IL-6 signal in pathogenesis of lung fibrosis. Respir Res. 2015;16(1):99. DOI: 10.1186/s12931-015-0261-z.
21. Henry B.M., de Oliveira M.H.S., Benoit S. et al. Hematologic, biochemical and immune biomarker abnormalities associated with severe illness and mortality in coronavirus disease (COVID-19): a meta-analysis. Clin Chem Lab Med. 2020;58(7):1021–1028. DOI: 10.1515/cclm-2020-0369.
22. Qin C., Zhou L., Hu Z. et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, Chine Clin Infect Dis. 2020:71(15):762–768. DOI: 10.1093/cid/ciaa248.
23. Vasarmidi E., Tsitoura E., Spandidos D.A. et al. Pulmonary fibrosis in the aftermath of thr COVID-19 era (Review). Exp Ther Med. 2020;20(3):2557–2560. DOI: 10.3892/etm.2020.8980.
24. Giamarellos-Bourboulis E.J., Netea M.G., Rovina N. et al. Complex immune dysregulation in COVID-19 patients with severe respiratory failure. Cell Host Microbe. 2020;27(6):992–1000.e3. DOI: 10.1016/j.chom.2020.04.009.
25. Yan L., Zhang H-T., Goncalves J. et al. An interpretable mortality prediction model for COVID-19 patients. Nat Mach Intell. 2020;2:283–288. DOI: 10.1038/s42256-020-0180-7.
26. Frater J.L., Zini G., d’Onofrio G., Rogers H.J. COVID-19 and the clinical hematology laboratory. Int J Lab Hematol. 2020;42 Suppl 1:11–18. DOI: 10.1111/ijlh.13229.
27. Wang Y., Wang H., Zhang C. et al. Lung fluid biomarkers for acute respiratory distress syndrome: A systematic review and meta-analysis. Crit Care. 2019;23(43) DOI: 10.1186/s13054-019-2336-6.
28. Ponti G., Maccaferri M., Ruini C. et al. Biomarkers associated with COVID-19 disease progression. Crit Rev Cli Lab. Sci. 2020;57(6):389–399. DOI: 10.1080/10408363.2020.1770685.
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