We read the article regarding COVID-19 in patients with systemic lupus erythematosus (SLE) by Mathian et al 1 with great interest. We would like to report a case with SLE with COVID-19 who presented severe relapse of thrombocytopaenia. Mild thrombocytopaenia during COVID-19 is frequently observed, and immune thrombocytopaenia (ITP) has also been reported. 2 3 Management of ITP during active COVID-19 can be difficult as immunosuppressive therapies can exacerbate infections, and the recovery of platelet count may lead to thrombosis due to coagulopathy caused in COVID-19. 4 Here, we report a case with severe ITP relapse in patients with SLE during a course of COVID-19.

A 58-year-old woman with a nearly 20-year history of SLE was admitted to our hospital with COVID-19. Her main manifestation of SLE was ITP, and her platelet count was low but stable at approximately 60× 109/L with 5 mg of prednisolone (PSL) since the administration of 12 years before. On 2 days before admission, she presented with chest discomfort, and her chest CT scan showed patchy ground-glass opacities in the both lungs. Her oxygen saturation was 95% on room air. A reverse transcription PCR test of a nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was positive. Laboratory examinations on admission revealed normal white cell count (6020/µL) with lymphocytopaenia (650/µL) and slightly elevated C reactive protein (0.5 mg/dL). Her platelet count was 10× 109/L, which was acutely decreased from 6.1× 109/L of 3 months before, with a highly elevated immature platelet fraction (36.0%). Her lupus anticoagulant test was positive with a prolonged activated partial thromboplastin time of 41.3 s, and her rapid plasma regain test showed a biologic falsepositive with a negative Treponema pallidum hemagglutination test, which had never been observed at previous examinations. On day 3, her platelet count decreased to 8× 109/L, and the PSL dose was increased from 5 mg/day to 10 mg/day. On day 6, her platelet count was further decreased to 5× 109/L with continued gingival bleeding. Daily 20 g doses of intravenous immunoglobulin (IVIg) were administered for 5 days, and her platelet count increased to 121× 109/L on day 13 with cessation of bleeding. The patient’s COVID-19 remained mild throughout her clinical course with ciclesonide inhalation, and no thrombosis was developed. To our knowledge, this is the first description of a case with severe ITP exacerbation induced by COVID-19. She was successfully treated with IVIg without worsening of respiratory symptoms and thrombosis. Mild thrombocytopaenia is a common feature of COVID-19, while a count below 100× 109/L has been found only in only 5% of hospitalised patients. 5 Our case’s chronic ITP, although stable, might have been volatile to such a viral infection; however, rheumatologists should be awere that autoimmune disease flares can be triggered by COVID-19. Standard first-line therapy for new or relapsed acute ITP is usually the use of PSL; however, concerns remain that the COVID-19 disease may worsen. Thrombopoietin receptor agonists are alternative therapeutic options for ITP; however, they have a potential to increase the risk of thrombosis in patients with COVID-19, which causes vascular endothelial damage. Therefore, as our case suggests, IVIg would be a good option for patients with severe ITP who acquire COVID-19, although accumulation of more cases is needed. 6 Interestingly, our patient showed newly detected lupus anticoagulant and biological false positivity, indicating the presence of antiphospholipid antibodies …