Publié le 11 mai 2020

Extrait de l’ar­ti­cle :

Résumé :

“On human lung parenchy­mal explants, chloro­quine con­cen­tra­tion clin­i­cal­ly achiev­able in the lung (100 microM) inhib­it­ed the lipopolysac­cha­ride-induced release of TNF-alpha (by 76%), IL‑6 (by 68%), CCL2 (by 72%) and CCL3 (by 67%). Beside its antivi­ral activ­i­ty, chloro­quine might also mit­i­gate the cytokine storm asso­ci­at­ed with severe pneu­mo­nia caused by coro­n­avirus­es.”

Fin de dis­cus­sion et con­clu­sion :“Chloro­quine treat­ment would prefer­ably be ini­ti­at­ed in the first days of lung symp­toms caused by SARS-CoVs; first to reduce viral repli­ca­tion and then to mit­i­gate the cytokine storm that typ­i­cal­ly occurs a few days lat­er in last-stage dis­ease. Giv­en that chloro­quine and hydrox­y­chloro­quine both appear to affect cytokine pro­duc­tion by human mono­cytes and to accu­mu­late in the lung in a sim­i­lar way, they might exert the same effect on the cytokine storm [9,12]. Although the in vit­ro effects on viral repli­ca­tion have yet to be con­firmed in patients and trans­lat­ed into clin­i­cal ben­e­fits, a recent ran­dom­ized clin­i­cal study sug­gest­ed that hydrox­y­chloro­quine has the poten­tial to con­trol acute inflam­ma­tion and pre­vent dis­ease pro­gres­sion in patients infect­ed with SARS-CoV­‑2 [15].”

Source : Clin­i­cal Infec­tious Dis­eases

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