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

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. Methylprednisolone-based 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 qRT-PCR 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 × 109/L, and the pellet count was 61 × 109/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. A CT scanning on day 4 revealed prominently enlarged area of pneumonia. In addition, platelet count of the patient was 18 × 109/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.

Fig. 1

Summary of main clinical features, laboratory parameters, and treatment of the patient (a) Dynamic changes of SARS-COV-2 viral loads evaluated by specific quantitative reverse transcription polymerase chain reaction (qRT-PCR) of the throat swab samples. SARS-COV-2 were continually detected for about 3 weeks. There was a weak positive result on day 26 after two 2 consecutively negative qRT-PCR. (b) Progressive depletion of lymphocytes and platelets during early inpatient days. (c) Clinical features and treatments of the patient. The dosage of the drug: Arbidol (0.2 g, every 8 h); darunavir/cobicistat (0.95 g per day); interferon alfa (500 WU, twice a day, aerosol inhalation); prednisone (10 mg per day); ciclosporin (50 mg, twice a day); methylprednisolone (40 mg per day, intravenously); immunoglobulin (20 g per day, intravenously); platelet transfusion (1 unit per day)

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 of thrombocytopenia and progression of pneumonia in our patient were probably associated with immune-mediated damages. Infection of some viruses has been proposed to immune disorders, such as complement activation and development of antiplatelet IgM antibodies and autoantibodies against endothelial and blood coagulation pathway cells that cross-react with platelets [6]. Furthermore, autopsy of patients with COVID-19 also revealed severe immune-mediated injury [7].

Taken together, we proposed that immune-mediated damages may be activated by SARS-COV-2 and play an important role in the pathogenesis of thrombocytopenia and COVID-19.