Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/25513
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dc.contributor.authorRobinson, Philip C-
dc.contributor.authorLiew, David F L-
dc.contributor.authorLiew, Jean W-
dc.contributor.authorMonaco, Claudia-
dc.contributor.authorRichards, Duncan-
dc.contributor.authorShivakumar, Senthuran-
dc.contributor.authorTanner, Helen L-
dc.contributor.authorFeldmann, Marc-
dc.date2020-12-18-
dc.date.accessioned2020-12-15T04:27:55Z-
dc.date.available2020-12-15T04:27:55Z-
dc.date.issued2020-12-03-
dc.identifier.citationMed 2020; 1(1): 90-102en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/25513-
dc.description.abstractCoronavirus disease 2019 (COVID-19) currently has few effective treatments. Given the uncertainty surrounding the effectiveness and uptake of a vaccine, it is important that the search for treatments continue. An exaggerated inflammatory state is likely responsible for much of the morbidity and mortality in COVID-19. Elevated levels of tumor necrosis factor (TNF), a key pro-inflammatory cytokine, have been shown to be associated with increased COVID-19 mortality. In patients with rheumatoid arthritis, TNF blockade reduces not only biologically active TNF but other pro-inflammatory cytokines important in COVID-19 hyperinflammation. Observational data from patients already on anti-TNF therapy show a reduced rate of COVID-19 poor outcomes and death compared with other immune-suppressing therapies. Anti-TNF has a long history of safe use, including in special at-risk populations, and is widely available. The case to adequately assess anti-TNF as a treatment for COVID-19 is compelling.en
dc.language.isoeng
dc.subjectSARS-CoV-2en
dc.subjectcoronavirus disease-2019en
dc.subjectglucocorticoidsen
dc.subjectpandemicen
dc.subjecttumor necrosis factoren
dc.subjectCOVID-19en
dc.titleThe Potential for Repurposing Anti-TNF as a Therapy for the Treatment of COVID-19.en
dc.typeJournal Articleen
dc.identifier.journaltitleMeden
dc.identifier.affiliationDepartment of Clinical Pharmacology and Therapeutics, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSection of Rheumatology, Department of Medicine, Boston University School of Medicine, Boston, MA, USAen
dc.identifier.affiliationKennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UKen
dc.identifier.affiliationOxford Clinical Trials Research Unit, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UKen
dc.identifier.affiliationUniversity of Queensland Faculty of Medicine, Herston, Queensland, Australiaen
dc.identifier.affiliationDepartment of Medicine, Royal Brisbane and Women's Hospital, Metro North Hospital and Health Service, Herston, Queensland, Australiaen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationKennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UKen
dc.identifier.doi10.1016/j.medj.2020.11.005en
dc.type.contentTexten
dc.identifier.pubmedid33294881
local.name.researcherLiew, David F L
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptRheumatology-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptClinical Pharmacology and Therapeutics-
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