LAUSR

We thank Prof Ferraccioli for his positive comments on our open-label trials with sarilumab, tocilizumab, anakinra and mavrilimumab in patients with severe hyperinflamed COVID-191–4 and for remarking the unprecedented opportunity offered by our studies to better understand the relative contribution of different targetable inflammatory pathways to the pathogenesis of severe COVID-19.5 The study designs we adopted should be definitely interpreted in light of the scientific data that progressively became available and of the course of the pandemic wave that struck Northern Italy and our Institution. Between 24 February and 22 May 2020, San Raffaele Hospital (Milan, Italy) admitted more than 1000 patients with COVID-19.6–8 Intriguingly, the clinical phenotype of admitted patients changed over time and the severity of the disease progressively varied in parallel with outbreak exhaustion.6 When our hospital was first hit by the pandemic, accumulating evidence from China was pointing at interleukin (IL)-6 as a master regulator of the cytokine storm occurring in severe COVID-19.9 Tocilizumab was, therefore, first used as a potential treatment2 and subsequently replaced by intravenous sarilumab due to sudden shortage of the drug.1 As described in …