As of March 12, 2020, 125,048 people worldwide have been diagnosed with coronavirus infection (Covid-19) with a mortality rate of approximately 3.7%, much higher than the mortality rate of less than 1% from influenza.
Increasing evidence suggests that patients with severe Covid-19 may have cytokine storm syndrome.
On March 16, Jessica J Manson's team at the University College London published a newsletter article entitled "Covid-19: consider cytokine storm syndromes and immunosuppression" online in the international top medical journal Lancet. The article suggested using existing, approved Recognized and safe therapies to identify and treat excessive inflammation to reduce mortality.
In summary, laboratory tests (eg, ferritin, platelet count, or erythrocyte sedimentation rate) and HScore (table) should be used to screen all patients with severe Covid-19 hyperinflammation to improve mortality in a subgroup of patients.
Treatment options include steroids, intravenous immunoglobulins, selective cytokine blockers (such as anakinra or tocilizumab), and JAK inhibitors.
In addition, on March 13, 2020, the Wei Haiming team of the University of Science and Technology of China published a research paper entitled "Pathogenic T cells and inflammatory monocytes incite inflammatory storm in severe Covid-19 patients" in the National Science Review online.
This study provides a detailed immunopathological report on SARS-CoV-2, suggesting that the over-activated immune response caused by pathogenic GM-CSF + Th1 cells and inflammatory CD14 + CD16 + monocytes may correlate with lung immunity Pathologically related, leading to harmful clinical manifestations and even acute death.
This study further developed a clinical trial using Tocilizumab to block interleukin 6 receptor (ChiCTR2000029765).
These serious patients recruited now have encouraging clinical results, including a rapid decrease in body temperature and improved respiratory function, which is of great significance for further reducing severe mortality.
Current treatment for Covid-19 is supportive, and respiratory failure caused by acute respiratory distress syndrome (ARDS) is the leading cause of death.
Secondary phagocytic lymphocytic histiocytosis (sHLH) is an under-recognized hyperinflammatory syndrome characterized by explosive and fatal hypercytokineemia and multiple organ failure.
In adults, sHLH is most often caused by a viral infection and occurs in 3.7โ4.3% of cases of sepsis.
The main features of sHLH include persistent fever, hemocytopenia, and hyperferritinemia. Pulmonary involvement (including ARDS) occurs in approximately 50% of patients.
A recent multi-center retrospective death study of 150 Covid-19 cases confirmed in Wuhan, China included ferritin (non-survivors averaged 1297 ยท 6 ng / ml and survivors averaged 614 ยท 0 ng / ml; p <0 ยท 001) and a sharp increase in IL-6, suggesting that the mortality rate may be due to the excessive inflammation caused by the virus.
As with previous severe acute respiratory syndromes and Middle East respiratory syndromes, the routine use of corticosteroids is not recommended because corticosteroids may exacerbate Covid-19-related lung injury.
A reanalysis of data from a phase 3 randomized controlled trial of IL-1 blocker (anakinra) in sepsis revealed a significant survival benefit for patients with hyperinflammation without an increase in adverse events.
A multicenter, randomized controlled trial of tocilizumab (IL-6 receptor blocker) has been approved for clinical trials in patients with Covid-19 pneumonia and elevated IL-6 in China (ChiCTR2000029765).
Inhibition of Janus kinase (JAK) may affect inflammation and entry of cellular viruses in Covid-19.
The article argues that laboratory tests (eg, ferritin, platelet count, or erythrocyte sedimentation rate) and HScore (table) should be used to screen all patients with severe Covid-19 hyperinflammation to improve mortality in a subgroup of patients.
Treatment options include steroids, intravenous immunoglobulins, selective cytokine blockers (such as anakina or tocilizumab), and JAK inhibition.
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