Post Covid-19 pulmonary fibrosis: A review article

Dhwani Patel 1, *, Prutha Patel 1, Neel Raval 1 and Jagdish Kakadiya 2

1 Parul Institute of Pharmacy and Research, Parul University, Vadodara, Gujarat, India.
2 Department of Pharmacy Practice, Parul Institute of Pharmacy and Research, Parul University, Vadodara, Gujarat, India.
 
Review
International Journal of Biological and Pharmaceutical Sciences Archive, 2022, 04(01), 040–045.
Article DOI: 10.53771/ijbpsa.2022.4.1.0048
Publication history: 
Received on 22 June 2022; revised on 09 August 2022; accepted on 11 August 2022
 
Abstract: 
COVID-19 also known as Coronavirus disease 2019 is an infectious disease caused by the highly contagious pathogen SARS-CoV-2.Various studies have found that 70–80% of patients who recovered from COVID-19 continue to have at least one or more symptoms even after being pronounced COVID-free. Pulmonary fibrosis is a severe respiratory illness consequence. It is defined by the lungs' failure to repair the injured alveolar epithelium, the persistence of fibroblasts, and the excessive deposition of collagen and other extracellular matrix components. An initial phase of lung injury is followed by acute inflammation and an effort at healing. Oxygen toxicity and ventilator-induced lung injury are two iatrogenic variables that may contribute to the fibrosis seen in survivors of severe COVID19 pneumonia. Based on scientific evidence and demographic findings, Pirfenidone and Nintedanib, used alone or in combination with anti-inflammatory agents and this combination is effective in preventing serious complications during COVID-19 infection. Pirfenidone inhibits TGF-β stimulated collagen synthesis and the synthesis of tumor necrosis factor, interferon-gamma, interleukin- 1beta, and interleukin-6 resulting in anti-inflammatory action. Depending on the concentration, pirfenidone has been demonstrated to have antioxidant capabilities. Nintedanib saw inhibitory action on pro-fibrotic mediators like platelet-derived growth factor and fibroblast growth factor, transforming growth factor-beta, and vascular endothelial growth factor. Who were already taking antifibrotic therapy saw a reduction in the number of acute exacerbations of IPF. Thus, Nintedanib and Pirfenidone both drugs slowed down the progression of Lung Fibrosis in patients over 18yr of age. However, more studies are required for usage of antifibrotics in Non- IPF patients.
 
Keywords: 
COVID-19; Post covid-19 pulmonary fibrosis; Pirfenidone; Nintedanib
 
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