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We read the article regarding COVID-19 in patients with systemic lupus erythematosus (SLE) by Mathian et al1 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 false-positive 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. Antiphospholipid antibodies are frequently observed in patients with SLE, but our patient previously presented as negative. Since the presence of antiphospholipid antibodies with coagulopathy has been reported in patients with COVID-19,7 special attention should be provided to patients with SLE and COVID-19.
Contributors YaK and YuK drafted the manuscript. TO, HF, SS, MO and HK were responsible for the clinical care of the patients. MI, NH, KF and TT supervised the conduct of researchers involved in the study and made critical revisions to the paper to enhance intellectual content. All authors read and approved the final manuscript.
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 consent for publication Obtained.
Provenance and peer review Not commissioned; internally peer reviewed.
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