• lupus erythematosus
• systemic
• hydroxychloroquine
• autoimmune diseases

We thank Kondo et al 1 for their interest in our study reporting on the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) in a case series of patients with systemic lupus erythematosus (SLE) under long-term treatment with hydroxychloroquine.2 Currently, there are no data that identify SLE as a risk factor for COVID-19-related immunological complications. Kondo et al 1 report a patient with SLE experiencing an exacerbation of immune thrombocytopaenic purpura (ITP) likely triggered by COVID-19. This case raises several subjects for discussion. In the cohort of patients with SLE that we reported, there were no manifestations of lupus activity during the course of COVID-19, except for one patient who had a tenosynovitis at the onset of SARS-CoV-2 infection.2 Similar to our observations, other studies reported that the occurrence of COVID-19 in patients with SLE was not accompanied by a flare of the autoimmune disease, at least in the short term.3–5 This finding is rather surprising considering the fact that SARS-CoV-2 is clearly a type I interferon-inducing virus,6 and that this family of cytokines has a key role in the pathogenesis of SLE flares.7 The latter consideration notwithstanding, it is expected that the secretion of interferons over a relatively short period of time, as in the course of COVID-19, is unlikely to be sufficient to induce a sustained activation of the immune system leading to an SLE flare. In this regard, we noticed that thrombocytopaenia was the only clinical manifestation of lupus activity in the case reported by Kondo et al.1 This observation is reminiscent of cases of ITP in patients without SLE, reported recently in the context of SARS-CoV-2 infection8 9 and previously for coronavirus HKU1 infections,10 which suggests an immunological mechanism common to patients with or without lupus that might be directly linked to the viral impact on the immune response mediated by a type I interferon-independent mechanism. An example for such a mechanism is the increased platelet clearance caused by coating of these cells with non-specific immune complexes or platelet antibodies produced during the immune response against SARS-CoV-2.

While thrombocytopaenia is prominent in severe cases of COVID-19 and clearly associated with poor outcomes and mortality,11 the occurrence of an ITP during the course of this disease does not seem to be linked with the severity of the viral infection, given that most of the reported cases of COVID-19 in this condition were mild or moderate.1 8 9 Finally, it is important to note that in the course of this infectious disease, which presents a major thrombotic risk,12 glucocorticoids and/or eltrombopag were used, without complications, neither infectious nor thrombotic, in patients who were poorly responsive or non-responsive to intravenous immunoglobulin.8 9 In conclusion, we recommend that new-onset thrombocytopaenia in SLE should be screened for the presence of SARS-CoV-2 during the current COVID-19 epidemic.