Pulmonary fibrosis in the aftermath of the Covid-19 era (Review)

Abstract

The year 2020 is characterized by the COVID-19 pandemic that has resulted in more than half a million deaths in recent months. The high mortality is associated with acute severe respiratory failure that results in ICU admission and intubation. While facing this fatal disease, research and clinical observations need to be carried out in order to evaluate the long-term effects of the COVID-19 acute respiratory distress syndrome (ARDS). Potent clinical and laboratory biomarkers should be studied to be able to predict the subgroup of patients that are going to deteriorate or develop lung fibrosis. The opportunity of personalized medicine is a good way to consider for these patients. Contents 1. Introduction 2. Post-ARDS lung fibrosis 3. Possible biomarkers of disease progression 4. Is there a role for antifibrotic therapy? 5. Conclusion

The potential indicators for pulmonary fibrosis in survivors of severe COVID-19

“…It remains unclear why certain individuals are able to recover from lung injury, whereas others develop into fibrotic damage [7] . Several markers associated with mortality risk, including age, illness severity, length of ICU stay, mechanical ventilation and hyper-inflammatory markers, might be the potential predictors for pulmonary fibrosis [8] .…”

“…7 Several markers associated with mortality risk, including age, illness severity, length of ICU stay, mechanical ventilation and hyper-inflammatory markers, might be the potential predictors for pulmonary fibrosis. 8 The highlight here reported a series of early indicators after tracing backwards to the features of disease progression between fibrosis and non-fibrosis group. Other than common factors of advancing age, male and underlying diseases, that had been well described, 9 it should be noted that the dynamic evolution of inflammatory markers within two weeks of hospitalization might point to fibrosis.…”

Correcting the imbalanced protective RAS in COVID-19 with angiotensin AT2-receptor agonists

“…As indicated in Figure 2, the excessive immune response in patients with severe COVID-19 may lead to various pathological outcomes: coagulopathy with associated venous and arterial thrombosis, subsequent stroke and possible death or disability [57,58]; multi-organ failure, partly due to coagulopathy, and possible death [59][60][61][62]; deleterious effects on vital organs, including acute kidney injury [63,64], myocarditis [65] and pulmonary fibrosis [66][67][68][69].…”

“…It is established that pulmonary inflammation is a major causative factor in the development of pulmonary fibrosis [142,143]. As indicated in Figure 2 one of the major long-term outcomes in COVID-19 is the development of pulmonary fibrosis [66][67][68][69], likely due to the hyperinflammatory state. In fact, pulmonary fibrosis is one of the pathological situations in which AT 2 R agonists may have beneficial effects for COVID-19 patients.…”

Pulmonary fibrosis in critically ill patients with novel coronavirus pneumonia during the convalescent stage and a proposal for early intervention

“…Although there is no reliable evidence on the efficacy of corticosteroids in treating pulmonary fibrosis following SARS-CoV-2 infection, they are commonly used as an empirical therapy for postinflammatory pulmonary fibrosis on the basis of the patient's clinical condition, High-Resolution Computed tomography manifestation and disease behavior. It could be suggested that pirfenidone, which shows effective against inflammation, fibrosis and oxidation [13], can attenuate lung injury because pirfenidone reduces LPSinduced acute lung injury and subsequent fibrosis [14]. Nintedanib can slow the progression of pulmonary fibrotic disease regardless of the pathological pattern by inhibiting the release of proinflammatory and profibrotic mediators, the migration and differentiation of fibrocytes and fibroblasts, and deposition of the extracellular matrix [15].…”