PropertyValue
?:abstract
  • [Image: see text] The COVID-19 pandemic rapidly became a worldwide healthcare emergency affecting millions of people, with poor outcomes for patients with chronic conditions and enormous pressure on healthcare systems. Pulmonary fibrosis (PF) has been cited as a risk factor for a more severe evolution of COVID-19, primarily because its acute exacerbations are already associated with high mortality. We reviewed the available literature on biochemical, pathophysiological, and pharmacological mechanisms of PF and COVID-19 in an attempt to foresee the particular risk of infection and possible evolution of PF patients if infected with SARS-COV-2. We also analyzed the possible role of medication and risk factors (such as smoking) in the disease’s evolution and clinical course. We found out that there is a complexity of interactions between coexisting idiopathic pulmonary fibrosis/interstitial lung disease (ILD) and COVID-19 disease. Also, patients recovering from severe COVID-19 disease are at serious risk of developing PF. Smokers seem to have, in theory, a chance for a better outcome if they develop a severe form of COVID-19 but statistically are at much higher risk of dying if they become critically ill.
?:creator
?:doi
  • 10.1021/acs.jproteome.0c00387
?:doi
?:journal
  • J_Proteome_Res
?:license
  • no-cc
?:pdf_json_files
  • document_parses/pdf_json/278afad358d03ed223e49ba5baf311da49f6519b.json
?:pmc_json_files
  • document_parses/pmc_json/PMC7640958.xml.json
?:pmcid
?:pmid
?:pmid
  • 32883081.0
?:publication_isRelatedTo_Disease
?:sha_id
?:source
  • Medline; PMC
?:title
  • “A Chain Only as Strong as Its Weakest Link”: An Up-to-Date Literature Review on the Bidirectional Interaction of Pulmonary Fibrosis and COVID-19
?:type
?:year
  • 2020-09-04

Metadata

Anon_0  
expand all