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Severe exacerbation of immune thrombocytopenia and COVID-19: the favorable response to corticosteroid-based therapy—a case report

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Dear Editor, Immune thrombocytopenia (ITP) is an immune-mediated hematologic condition, characterized by isolated thrombocytopenia due to immune disorder [1]. Some other reasons were in association with ITP, including viral infection… Click to show full abstract

Dear Editor, Immune thrombocytopenia (ITP) is an immune-mediated hematologic condition, characterized by isolated thrombocytopenia due to immune disorder [1]. Some other reasons were in association with ITP, including viral infection [1, 2]. Many viruses have been identified as a trigger of the autoimmune process. It is reported that thrombocytopenia is common among patients infected with Dengue virus and Zika virus [3]. Recently, the emerged novel coronavirus diseases 2019 (COVID-19) became a serious public health concern [4]. Acute exacerbation of thrombocytopenia during the course of COVID-19 has not been reported yet. Here, we describe a patient with COVID-19 pneumonia who received maintenance immunosuppressive drugs for chronic ITP. There was a fast progression of thrombocytopenia during the initial 4 inpatient days. Methylprednisolonebased treatment was added to treat thrombocytopenia. Thrombocytopenia and pneumonia both relieved quickly. A 72-year-old female patient (51 Kg) was admitted to hospital with productive cough for 5 days and fever for 1 day. Diagnosis of SARS-COV-2 infection was confirmed with positive quantitative reverse transcription polymerase chain reaction (qRT-PCR) result on throat swab samples (Fig. 1A). The qRTPCR was performed every other day to monitor the existence of severe acute respiratory syndrome (SARS)-COV-2 [5]. She had a history of idiopathic thrombocytopenic purpura for about 2 years and currently received immunosuppressive therapy with prednisone (10 mg/d) and cyclosporine (50 mg/d). On admission, the baseline blood lymphocyte count was 2.55 × 10/L, and the pellet count was 61 × 10/L, respectively (Fig. 1B). Chest computed tomography (CT) scanning on day 1 revealed peripheral ground-glass opacity in the right lower lobe. Oral antiviral therapy with arbidol was administrated. However, the treatment did not improve the patient’s clinical symptoms. ACT scanning on day 4 revealed prominently enlarged area of pneumonia. In addition, platelet count of the patient was 18 × 10/L. Thrombocytopenia did not respond to intravenous immunoglobulin and platelet transfusion. Methylprednisolone (40 mg/ d, intravenously) was then included into the treatment. Thrombocytopenia quickly went into remission (Fig. 1B). Chest CT follow-up after 3 days of application of methylprednisolone-based treatment suggested a slightly improvement. Methylprednisolone was administered for a total of 5 days. The platelet count remained normal, and COVID-19 pneumonia continued to improve during the following days despite the persistence of SARS-COV-2 in throat swab samples. The pathophysiology of ITP remains incompletely understood. Immune disorders, such as immune dysfunction, immune-mediated platelet destruction, inhibition of platelet release by megakaryocytes, and abnormalities in T cells, were related to ITP pathogenesis [1]. Glucocorticoid treatment is the standard initial therapy for patients with ITP. The patient’s favorable response to methylprednisolone suggested that acute exacerbation * Wenkui Sun [email protected]

Keywords: immune; thrombocytopenia; treatment; covid; therapy; exacerbation

Journal Title: Annals of Hematology
Year Published: 2020

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