Post–Coronavirus Disease 2019 Pulmonary Fibrosis: Wait or Needs Intervention

Abstract

Coronavirus disease 2019 (COVID-19) has become a major health burden worldwide, with over 450 million confirmed cases and 6 million deaths. Although the acute phase of COVID-19 management has been established, there is still a long way to go to evaluate the long-term clinical course or manage complications due to the relatively short outbreak of the virus. Pulmonary fibrosis is one of the most common respiratory complications associated with COVID-19. Scarring throughout the lungs after viral or bacterial pulmonary infection have been commonly observed, but the prevalence of post-COVID-19 pulmonary fibrosis is rapidly increasing. However, there is limited information available about post-COVID-19 pulmonary fibrosis, and there is also a lack of consensus on what condition should be defined as post-COVID-19 pulmonary fibrosis. During a relatively short follow-up period of approximately 1 year, lesions considered related to pulmonary fibrosis often showed gradual improvement; therefore, it is questionable at what time point fibrosis should be evaluated. In this review, we investigated the epidemiology, risk factors, pathogenesis, and management of post-COVID-19 pulmonary fibrosis.

Pulmonary fibrosis in critically ill patients with COVID-19: A multi-center retrospective cohort study in South Korea

“…The complex and multifactorial nature of pulmonary brosis development in COVID-19 may also explain these inconsistencies. 23 A retrospective study conducted, 24 involving 227 patients with COVID-19, Li et al demonstrated a negative correlation between hemoglobin and pulmonary brosis (r = − 0.368, P < 0.001). In another study involving 159 patients, Zhang et al 25 reported that hemoglobin level can distinguish between patients with severe and non-severe COVID-19 infections, with an area under the curve of 0.79 in the receiver operating characteristic analysis, suggesting its utility in assessing disease severity.…”

Integrative single‐cell transcriptome analysis provides new insights into post‐COVID‐19 pulmonary fibrosis and potential therapeutic targets

“…IPF and PCPF share similar clinicopathological features, such as reduced DLCO, disrupted alveolar‐capillary barriers, renin‐angiotensin‐aldosterone system imbalance, increased oxidative stress, and chronic inflammation. Hence, they both may respond to similar therapeutic strategies 5,15 . In the present study, we profiled single‐cell gene expression in the lung tissues of COVID‐19 and IPF patients.…”

“…Hence, they both may respond to similar therapeutic strategies. 5,15 In the present study, we profiled single-cell gene expression in the lung tissues of COVID-19 and IPF patients. Comparative single-cell transcriptome analyses revealed altered abundance and activity of individual cell types, prioritizing certain key cell types, cellular processes, signaling pathways, and genes may be common to both IPF and PCPF pathophysiology.…”

“…COVID‐19 pneumonia may induce fibrotic lung damage known as post‐COVID pulmonary fibrosis (PCPF), which is a frequent complication in patients with long COVID‐19 5 . Between 45% and 54% of all hospitalized COVID‐19 survivors experience lung fibrosis 6 .…”

“…4 COVID-19 pneumonia may induce fibrotic lung damage known as post-COVID pulmonary fibrosis (PCPF), which is a frequent complication in patients with long COVID-19. 5 Between 45% and 54% of all hospitalized COVID-19 survivors experience lung fibrosis. 6 Even after 1 year, one-third of all patients with moderate COVID-19 present with fibrotic changes and severe impairment of the diffusing capacity for carbon monoxide in the lungs (DLCO).…”