Role of immunosuppressive therapy in rheumatic diseases concurrent with covid-19

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. View this table: 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 …