Post-COVID-19 Pulmonary Fibrosis

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected millions worldwide with a high mortality rate due to a lack of definitive treatment. Despite having a wide range of clinical features, acute respiratory distress syndrome (ARDS) has emerged as the primary cause of mortality in these patients. Risk factors and comorbidities like advanced age with limited lung function, pre-existing diabetes, hypertension, cardiovascular diseases, and obesity have increased the risk for severe COVID-19 infection. Rise in inflammatory markers like transforming growth factor β (TGF-β), interleukin-6 (IL-6), and expression of matrix metalloproteinase 1 and 7 (MMP-1, MMP-7), along with collagen deposition at the site of lung injury, results in extensive lung scarring and fibrosis. Anti-fibrotic drugs, such as Pirfenidone and Nintedanib, have emerged as potential treatment options for post-COVID-19 pulmonary fibrosis. A lung transplant might be the only life-saving treatment. Despite the current advances in the management of COVID-19, there is still a considerable knowledge gap in the management of long-term sequelae in such patients, especially concerning pulmonary fibrosis. Follow up on the current clinical trials and research to test the efficacy of various anti-inflammatory drugs is needed to prevent long-term sequelae early mortality in these patients.

The Effect of Nintedanib in Post-COVID-19 Lung Fibrosis: An Observational Study

“…When medication was initiated may be another important factor. Fibrosis in COVID-19 is partly caused by cytokines such as interleukin-1 and interleukin-6 during the inflammatory phase of the disease or caused by injury from mechanical ventilation that stimulates fibroblast malfunction, causing the excessive accumulation of collagen, all of which results in fibrosis [ 5 , 7 ]. In our study, some patients were in acute inflammatory phase or received mechanical ventilation for treatment of severe pneumonia or acute respiratory distress syndrome, and antifibrotic drug therapy at this stage may not have been as effective as expected.…”

“…Pulmonary brosis is a consequence of COVID-19 infection and the basis for poor prognosis in COVID-19 patients [5,6]. e mechanism of pulmonary brosis occurs after lung injury caused by stimuli such as viral in ammation or ventilator-induced lung injury, stimulating the function of broblasts via in ammatory markers such as transforming growth factor β and interleukin-6, leading to the accumulation of collagen and pulmonary brosis [5,[7][8][9]. e prevalence of post-COVID-19 brosis varies from 2% to 45%, depending on the severity of the virus [10][11][12].…”

Lenfopenik Olan Hafif COVID-19 Vakalarında İmmun Plazma Tedavisi Ne Kadar Güvenliydi?

“…[28] Due to the negative impacts of uncontrolled diabetes on vascular structure and immune response, COVID-19 has been quite mortal in diabetic patients. [29] Although there are determinations regarding the pathogenesis focused on microvascular immunothrombolysis, [30,31] unclear parts remain in the etiology. In line with the literature, fibrosis was detected in all the diabetics in our study.…”

COVID-19 disease and autoimmune disorders: A mutual pathway

“…IL-6 is a pro-inflammatory cytokine with a pro-fibrotic activity that activates the neutrophils and their accumulation at the injury site. Neutrophil accumulation causes proteases and oxygen-free radical release causing pulmonary interstitial edema and acute inflammation[ 131 ]. Annexin A2 is crucial to protect against pulmonary fibrosis as it is essential to activate endogenous tissue plasminogen activator to lyse clots and promote fibrin clearance and pulmonary fibrinolysis[ 132 ].…”