PMC:7102591 / 19693-21221 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7102591","sourcedb":"PMC","sourceid":"7102591","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7102591","text":"Beyond the use of specific anti-viral products, many drugs commonly used in the treatment of RA have been proposed as possible therapies for COVID-19 as a consequence of the increased knowledge about the pathophysiology of the infection (Table 1 ).\nTable 1 Potential role of anti-rheumatic drugs in COVID-19 infection.\nPROS CONS\nChloroquine Anti-viral effect (increase of endosomal pH required for virus/cell fusion, inhibition of toll-like receptor activity, interference with terminal glycosylation of the cellular receptor ACE 2) –\nHydroxychloroquine\nIL-6 inhibitors Treatment of cytokine storm manifestations during ARDS Lack of definite criteria to identify patients to be treated\nPotential community-acquired pneumonia due to immunosuppression\nBaricitinib Interference with viral penetration into the cell by blocking NAK-mediated endocytosis Impairment of IFN anti-viral response\nTreatment of cytokine storm manifestations during ARDS Increased risk of secondary HZV infections\nTNF-inhibitors Interference with viral penetration into the cell Slight increase in viral infection risk\nNSAIDs – Facilitation of viral penetration by overexpression of ACE2\nDelay in diagnosis due to fever masking\nCorticosteroids – Increased risk of viral infection\nIncreased mortality and risk of secondary bacterial or fungal infection\nACE2 = angiotensin converting enzyme 2, ARDS = acute respiratory distress syndrome, NAK = numb-associated kinase; HZV = Herpes Zoster virus,\nIFN = interferon, NSAIDs = nonsteroidal anti-inflammatory 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