Sudden severe thrombocytopenia in a patient in the recovery
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A 38-year-old man presented with cough and dyspnoea. A chest CT scan and blood test was positive for moderate COVID-19 and he was admitted to hospital. After admission, he was given antiviral treatment of interferon-α and umifenovir . The patient's symptoms improved, and the pulmonary lesions appeared to have been absorbed after one week. When the COVID-19 nucleic acid test showed negative twice, he met the discharge criteria.

However, on day 29 a blood test showed a decreased platelet count of 2 × 109 cells per L, and fibrinogen concentration remained elevated (4·40 g/L). These results showed a clear, isolated thrombocytopenia. Lymphocyte subset and autoimmune antibody analysis at platelet nadir time showed an increase of the percentage of B cells, from 18·62% on day 21 to 34·80% on day 29 and autoimmune antibodies were negative.

Bone marrow aspiration was done; most cellular lineages were normal except for low numbers of platelet-producing megakaryocytes. A COVID-19 nucleic acid test of the bone marrow aspirate was negative. There were no signs of bleeding or thrombosis during hospital admission or during the time of platelet nadir, and he had never been admitted to the intensive care unit. Our differential diagnosis included complications of acute COVID-19 infection and post-infectious immune thrombocytopenia.

Doctors administered intravenous immunoglobulin and dexamethasone. The patient's platelet count increased to 60 × 109 cells per L 3 days later and dexamethasone was stopped in case of re-activation of viral replication. The platelet count was normal on day 37, so immunoglobulin was ceased. His platelet count remained in the normal range and B-cell percentage gradually decreased. The patient recovered and was discharged on day 46, 4 days after the last chest CT scan.

Thrombocytopenia has been shown to occur in patients with COVID-19, usually noted on admission to hospital, although here thrombocytopenia occurred later in the disease course. The effectiveness of immunoregulatory treatment, the changing concentrations of B lymphocytes, and the results of the bone marrow aspirate, suggest immune-mediated thrombocytopenia in this patient, and the normal prothombin time and activated partial thromboplastin time suggest that other coagulation abnormalities were not the cause of the severe thrombocytopenia.