key: cord-0056816-jz0nkxek authors: Blasco Patiño, Felipe; Guillamón Sanchez, Ana Elena title: Indication of glucocorticoid pulses for patients with SARS-CoV-2 infection() date: 2021-03-03 journal: Med Clin (Engl Ed) DOI: 10.1016/j.medcle.2020.06.035 sha: 2d8ae183e6f6640318e6f993908a943b0abc58f4 doc_id: 56816 cord_uid: jz0nkxek nan This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Letter to the Editor Treating this inflammatory response on the assumptions used in autoimmune processes in the case of macrophage activation syndrome with uncontrolled proliferation of T cells is a conceptual error. What happens in coronavirus infection, with significant lymphopenia in the most severe cases, has little to do with this syndrome. The study authors use ferritin and IL-6 levels as parameters to predict cytokine storm, without taking into account that both molecules, and especially IL-6, are high in most viral infections (influenza , hemorrhagic fevers, HIV, HCV, HBV, coronavirus) 3 . It has been observed that an increase in the production of IL-6 can be detrimental to the cellular immune response during viral infections, and this is taken advantage of by some viral strains that use the stimulation of IL-6 secretion as an evasion strategy that slows down the humoral response and as a result there is an increase in viral loads 4 . The higher the IL-6 level, the higher the viral load. Liu et al. 5 found that the viral load is up to 60 times higher in people with a more severe course of COVID-19 infection. The established concept of viral and inflammatory phase is also erroneous, as these patients maintain high viral loads for weeks. The response to viral infections is a humoral immune response mediated by the activation of T░cells. The inflammatory effect of GCs is linked to the inhibition of IL-2, which causes T░cell apoptosis. We should not slow down lymphocyte activity in patients with severe lymphopenia. All of the above would explain why a high percentage of patients treated with GC required tocilizumab. An increase in viral load is to be expected in all of them. It would have been interesting if the authors had reported the viral load and IL-6 levels after the steroid pulses. In such a short follow-up, it remains to be clarified if any patient has had a recurrence, a reactivation of TB, or how many of these patients had septic shock. Based on the above assumptions, we are against the systematic use (most of them meet the criteria set out by the authors) of GC pulses in patients with COVID-19 pneumonia, as not only do they not show a clear benefit on mortality, but they also entail an increased risk of shock and, contrary to what they state in their article, they lead to a worse outcome and a greater need for tocilizumab. De Los Pulsos De Corticoides En Pacientes Con Síndrome De Liberación De Citoquinas Inducido Por Infección Por Sars-Cov-2 Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury The role of interleukin 6 during viral infection Innate immune evasion strategies of DNA and RNA viruses Viral dynamics in mild and severe cases of COVID-19