Comment on "Colchicine may not be effective in COVID-19 infection; it may even be harmful?"

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dc.authoridŞenol Kobak / 0000-0001-8270-640Xen_US
dc.authorscopusidŞenol Kobak / 12782228700
dc.authorwosidŞenol Kobak / AAO-2482-2020
dc.contributor.authorKobak, Şenol
dc.date.accessioned2020-08-30T20:06:08Z
dc.date.available2020-08-30T20:06:08Z
dc.date.issued2020
dc.departmentİstinye Üniversitesi, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümüen_US
dc.description.abstractWe read with great interest the report by Cure et al. which speculated that colchicine may not be effective in COVID-19 infection [1]. The main argument of the authors is that colchicine may have not increased the intracellular pH enough and cannot prevent the binding of the virus to the target angiotensin converting enzyme 2(ACE2) receptors. Also, they suggest that colchicine may increase the risk of acute respiratory distress syndrome(ARDS) and disseminated intravascular coagulation(DIC) which may occur during COVID-19 infection. We have not agreed with the authors at these points. Fırst, the colchicine and anti-malarial drugs both may increase the intracellular pH by different mechanisms. There are no studies investigating the intracellular concentration of colchicine in corona infection, while such data exist regarding chloroquine [2]. So, this view is only an author’s hypothesis that is not based on scientific data. Second, there is no any data supporting Cure et al. that colchicine increases the risk of ARDS and DIC in COVID-19 patients. On the contrary, we hypothesize that colchicine may protect rheumatic patients from COVID-19 or perhaps cause them to pass in a milder form of disease. COVID-19 is not only a viral infection, it is an autoinflammatory/autoimmune process that develops as a result of immune system dysfunction, cytokine release syndrome, and hemophagocytic lymphohistiocytosis [3]. It acts by binding toACE2 receptors in target organs such as lung alveolar type 2 cells [4].When COVID-19 is passed into the cell via ACE2, activation of NLRP3 inflammasome is triggered by immunological mechanisms. The presence of high NLRP3- induced pro-inflammatory cytokines (IL-1, IL-1beta) in the sera of COVID-19 patients supports this hypothesis [5]. Colchicine is an anti-inflammatory agent that inhibit the microtubuleen_US
dc.identifier.citationSenol, K. Comment on" Colchicine May Not Be Effective in COVID-19 Infection; It May Even Be Harmful?". Clinical rheumatology.en_US
dc.identifier.doi10.1007/s10067-020-05233-xen_US
dc.identifier.endpage2488en_US
dc.identifier.issn0770-3198en_US
dc.identifier.issn1434-9949en_US
dc.identifier.issue8en_US
dc.identifier.pmid32564212en_US
dc.identifier.scopus2-s2.0-85086784639en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage2487en_US
dc.identifier.urihttps://doi.org/10.1007/s10067-020-05233-x
dc.identifier.urihttps://hdl.handle.net/20.500.12713/385
dc.identifier.volume39en_US
dc.identifier.wosWOS:000542842000001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorKobak, Şenolen_US
dc.language.isoenen_US
dc.publisherSpringer London Ltden_US
dc.relation.ispartofClinical Rheumatologyen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleComment on "Colchicine may not be effective in COVID-19 infection; it may even be harmful?"en_US
dc.typeLetteren_US

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