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Role of immunosuppressive therapy in rheumatic diseases concurrent with COVID-19
  1. Chenyang Lu1,
  2. Shasha Li2,
  3. Yi Liu1
  1. 1 Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China
  2. 2 Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA
  1. Correspondence to Professor Yi Liu, rheumatology and immunology, Sichuan University West China Hospital, Chengdu, Sichuan, China; Yi2006liu{at}163.com

https://doi.org/10.1136/annrheumdis-2020-217460

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    The COVID-19 has been declared a pandemic by WHO since 11 March 2020.1 The cumulative incidence of COVID-19 cases is showing similar trends in European Union and USA, and the UK confirmed that, while at a different stage depending on the country, the COVID-19 pandemic is progressing rapidly in all countries.2 As of 10 April 2020, COVID-19 has been confirmed in 1521252 people worldwide, carrying a mortality of approximately 6.1%.3 With tens of millions of individuals suffering rheumatic diseases (RDs) around the world who routinely receive glucocorticoids and disease-modifying anti-rheumatic drugs (DMARDs) (table 1), RD patients with compromised immune systems make up a large population of susceptible patients in which novel coronavirus infection may cause devastating consequences.

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    Table 1

    Summary of drugs commonly used in rheumatic diseases and their mechanisms of action

    Accumulating evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome represented by acute respiratory distress syndrome (ARDS) and secondary haemophagocytic lymphohistiocytosis, which are two of main causes of mortality.4 Disease severity of COVID-19 was correlated with hypercytokinaemia, characterised by increased serum interleukin (IL)-2, IL-7, IL-10, granulocyte colony-stimulating factor (G-CSF), IP10/CXCL10, monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1), tumour necrosis factor-α (TNF-α), ferritin and IL-6.5–8 In addition, decreased monocyte count was found in patients with COVID-19,9 low levels of CD4+ T and CD8+ T cells were more common in severe cases,7 while numbers of leucocytes, B cells and NK cells were similar between patients and healthy controls.9 On the novel coronavirus infection, CD4+ T cells were activated to become pathogenic Th1 cells and generate granulocyte-macrophage colony-stimulating factor, augmenting the expression of IL-6 in CD14+CD16+ monocytes.9

    As hyperinflammation …

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    Footnotes

    • Handling editor Josef S Smolen

    • CL and SL contributed equally.

    • Contributors CL and SL contributed equally to this work. CL and YL generated the idea; SL collected data and made the table and graph. CL wrote the manuscript, and YL supervised the project.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Patient consent for publication Not required.

    • Provenance and peer review Not commissioned; externally peer reviewed.