The pathogenesis, epidemiology and biomarkers of susceptibility of pulmonary fibrosis in COVID-19 survivors

Abstract

Pulmonary fibrosis (PF), a pathological outcome of chronic and acute interstitial lung diseases associated to compromised wound healing, is a key component of the “post-acute COVID-19 syndrome” that may severely complicate patients’ clinical course. Although inconclusive, available data suggest that more than a third of hospitalized COVID-19 patients develop lung fibrotic abnormalities after their discharge from hospital. The pathogenesis of PF in patients recovering from a severe acute case of COVID-19 is complex, and several hypotheses have been formulated to explain its development. An analysis of the data that is presently available suggests that biomarkers of susceptibility could help to identify subjects with increased probability of developing PF and may represent a means to personalize the management of COVID-19’s long-term effects. Our review highlights the importance of both patient-related and disease-related contributing risk factors for PF in COVID-19 survivors and makes it definitely clear the possible use of acute phase and follow-up biomarkers for identifying the patients at greatest risk of developing this disease.

One-year evolution of DLCO changes and respiratory symptoms in patients with post COVID-19 respiratory syndrome

“…A notable result of our study is that no patients showed further deterioration in respiratory function from 3 to 6 months to 1 year after admission. These data seem to suggest that changes in the pulmonary interstitium, frequently detected in the first months after the acute phase of COVID-19 [9], do not tend to worsen over time. The possible evolution into pulmonary fibrosis secondary to COVID-19 is a matter of concern [10].…”

Laboratory Biomarkers for Diagnosis and Prognosis in COVID-19

“…The pathogenesis of COVID-19 in the lung includes an initial phase of local inflammation, endothelial cell damage, and antifibrinolytic activation in the upper and lower respiratory tracts, followed by repair mechanisms that can elicit the restoration of normal pulmonary architecture. Inflammation is followed by platelet recruitment with degranulation, clot formation, altered vessel permeability, and accumulation of leukocytes in the injury site, leading to the recruitment of other inflammatory cells with the involvement of specific cytokines (i.e., IL-4, IL-13, transforming growth factor-β) that are also responsible for pro-fibrotic activity ( 12 ).…”

“…Although not specific to pulmonary disease, several biomarkers of different stages of lung involvement in COVID-19 have been identified and have been associated with pulmonary and systemic hyperinflammation and fibrotic damage ( 12 ). In the early disease course, neuron-specific enolase (NSE) can be used to differentiate patients who are going to develop dyspnea ( 21 ).…”

Pulmonary Fibrosis in the Time of COVID-19

“…In sharp contrast, COVID-19 pneumonia has affected millions of people worldwide, and even a very small proportion of patients with pulmonary fibrosis may represent a considerable clinical and health system problem. 5 Finally, viral infections have been associated (indirectly) with pulmonary fibrosis. 6 …”

“…Special attention will be required in individuals with some putative risk factors such as male gender, aging, active smoking, 5 accelerated biological age, and abnormal telomere shortening. 7 …”