Eficacia del CytoSorb en un paciente en ECMO VV secundario a Síndrome respiratorio agudo severo por corona virus 2 (SARS-CoV-2). Reporte de caso y revisión de la literatura

Resumen El síndrome de dificultad respiratoria del adulto (SDRA) por el virus COVID-19 tiene una alta morbi-mortalidad secundario al severo compromiso pulmonar sumado a una respuesta inmune disregulada causal de una tormenta de citoquinas y disfunción orgánica. La membrana de oxigenación extracorpórea veno venosa (ECMO V-V) es un soporte de rescate que viene demostrando efectividad en casos severos y refractarios de SDRA, no obstante, también puede generar una respuesta inflamatoria sistémica por el contacto de la sangre con la superficie extraña. Por estas razones las estrategias de purificación sanguínea como la hemo-adsorción con CytoSorb son una alternativa terapéutica frente una liberación exagerada de citoquinas. Se describe el caso de un paciente joven con SDRA severo y refractario por SARS CoV-2 con necesidad de soporte ECMO, y posterior clínica de tormenta de citoquinas dado por hipotensión y disfunción multi orgánica, con necesidad de remoción extracorporea de citoquinas con CytoSorb, con los cuales logró una estabilización clínica que permitió retiro del soporte extracorpóreo. Adult respiratory distress syndrome (ARDS) due to the COVID-19 virus has a high morbidity and mortality secondary to severe pulmonary involvement added to a dysregulated immune response that causes a cytokine storm and organ dysfunction. The veno-venous extracorporeal membrane oxygenation (ECMO V-V) is a rescue support that has been demonstrating effectiveness in severe and refractory cases of ARDS, however, it can also generate a systemic inflammatory response due to the contact of blood with the foreign surface. For these reasons, blood purification strategies such as heme adsorption with CytoSorb are a therapeutic alternative to an exaggerated release of cytokines. We describe the case of a young patient with severe and refractory ARDS due to SARS CoV-2 with the need for ECMO support, and subsequent symptoms of cytokine storm due to hypotension and multi-organ dysfunction, with the need for extracorporeal removal of cytokines with CytoSorb, with which he achieved a clinical stabilization that allowed removal of the extracorporeal support.

Anakinra as a potential alternative in the treatment of severe acute respiratory infection associated with SARS-CoV-2 refractory to tocilizumab.

SARS-CoV-2 is a new RNA virus which causes coronavirus disease 2019 (COVID-19), declared a pandemic by the World Health Organization (WHO). It triggers an atypical pneumonia that can progress to multiorgan failure. COVID-19 can cause dysregulation of the immune system, triggering an inflammatory response, and simulate haemophagocytic lymphohistiocytosis. Several studies have proposed that anti-IL-6 receptor antibodies, such as tocilizumab, play an important role in the treatment of severe acute respiratory infection associated with SARS-CoV-2. However, the role of anti-IL-1 receptor antibodies, such as anakinra, in the treatment of COVID-19 has not been established. We present a case report of a 51-year-old man diagnosed with severe respiratory infection associated with SARS-CoV-2 that was refractory to antiviral and anti-IL-6 treatment, with a favourable clinical outcome and analytical improvement after treatment with anti-IL-1 (anakinra).

Caution with the use of dexamethasone in patients with COVID-19 in its initial phases.

INTRODUCTION: The effect of dexamethasone in the initial phase of infection by SARS-CoV-2 and its influence on COVID-19 is not well defined. We describe clinical-radiological characteristics, the cytokine storm parameters, and the clinical evolution of a series of patients treated with dexamethasone in the disease's initial phase. METHOD: A study of 8 patients who received dexamethasone before the development of COVID-19. We evaluate clinical variables, imaging tests, cytokine release parameters, treatment used and patient evolution. RESULTS: All patients received a 6 mg/day dose with a mean duration of 4.5 days before admission. High resolution computed tomography (HRCT) revealed that most of them presented a severe extension; most patients had a slightly elevated level of cytokine release parameters. Three patients required high-flow oxygen therapy due to respiratory failure; none required orotracheal intubation or died. CONCLUSION: Dexamethasone in the early stages of SARS-CoV-2 infection appears to be associated with severe COVID-19.

[Glucocorticoids alone versus tocilizumab alone or glucocorticoids plus tocilizumab in patients with severe SARS-CoV-2 pneumonia and mild inflammation]. / Glucocorticoides solos versus tocilizumab solo o glucocorticoides más tocilizumab en pacientes con neumonía grave por SARS-CoV-2 e inflamación moderada.

AIM: To assess clinical outcomes according to the immunosuppressive treatment administered to patients with severe SARS-CoV-2 pneumonia and moderate inflammation. METHODS: A retrospective observational cohort study involving 142 patients with severe COVID-19 pneumonia and moderate inflammation divided into three treatment groups (pulses of methylprednisolone alone [groupI], tocilizumab alone [groupII] and methylprednisolone plus tocilizumab [groupIII]). The aim was to assess intergroups differences in the clinical course with a 60-day follow-up and related analytical factors. RESULTS: 14 patients (9,8%) died: 8 (10%) in groupI and 6 (9,5%) in groupsII andIII. 15 (10,6%) were admitted to ICU: 2 (2,5%) from groupI, 4 (28,5%) from groupII and 9 (18,4%) from groupIII. The mean hospital stay was longer in groupII and clinical outcome was not associated with treatment. CONCLUSIONS: Tocilizumab seems to be not associated with better clinical outcomes and should be reserved for clinical trial scenario, since its widespread use may result in higher rate of ICU admission and longer mean hospital stay without differences in mortality rate and potentially adverse events.

Liver transplant immunosuppression during the covid-19 pandemic. / Inmunosupresión en el trasplante hepático en la era covid-19.

SARS-CoV-2 infection has produced a pandemic with serious consequences for our health care system. Although liver transplant patients represent only a minority of the population, the hepatologists who follow these patients have tried to coordinate efforts to produce a protocol the management of immunosuppression during SARS-CoV-2 infection. Although there are no solid studies to support general recommendations, experiences with other viral infections (hepatitis C, cytomegalovirus) suggest that management of immunosuppression without mycophenolate mofetil or m-Tor inhibitors (drugs that are also associated with leukopenia and lymphopenia) may be beneficial. It is also important to pay attention to possible drug interactions, especially in the case of tacrolimus, with some of the treatments with antiviral effect given in the context of COVID 19 (lopinavir/ritonavir, azithromycin). Finally, the immunosuppressive effect of immunomodulating drugs (tocilizumab and similar) administered to patients with severe lung disease should be taken into account. The mechanisms of action of the different immunosuppressive drugs are reviewed in this article, as well as their potential effect on SARS-CoV-2 infection, and suggests guidelines for the management of immunosuppression.

Impact of SARS-CoV-2 infection on neurodegenerative and neuropsychiatric diseases: a delayed pandemic? / Influencia de la infección SARS-CoV-2 sobre enfermedades neurodegenerativas y neuropsiquiátricas: ¿una pandemia demorada?

INTRODUCTION: SARS-CoV-2 was first detected in December 2019 in the Chinese city of Wuhan and has since spread across the world. At present, the virus has infected over 1.7 million people and caused over 100 000 deaths worldwide. Research is currently focused on understanding the acute infection and developing effective treatment strategies. In view of the magnitude of the epidemic, we conducted a speculative review of possible medium- and long-term neurological consequences of SARS-CoV-2 infection, with particular emphasis on neurodegenerative and neuropsychiatric diseases of neuroinflammatory origin, based on the available evidence on neurological symptoms of acute SARS-CoV-2 infection. DEVELOPMENT: We systematically reviewed the available evidence about the pathogenic mechanisms of SARS-CoV-2 infection, the immediate and lasting effects of the cytokine storm on the central nervous system, and the consequences of neuroinflammation for the central nervous system. CONCLUSIONS: SARS-CoV-2 is a neuroinvasive virus capable of triggering a cytokine storm, with persistent effects in specific populations. Although our hypothesis is highly speculative, the impact of SARS-CoV-2 infection on the onset and progression of neurodegenerative and neuropsychiatric diseases of neuroinflammatory origin should be regarded as the potential cause of a delayed pandemic that may have a major public health impact in the medium to long term. Cognitive and neuropsychological function should be closely monitored in COVID-19 survivors.