Immune thrombocytopenia in a patient with COVID-19
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CASE REPORT
Immune thrombocytopenia in a patient with COVID‑19 Emilie Deruelle1 · Omar Ben Hadj Salem1 · Sonnthida Sep Hieng2 · Claire Pichereau1 · Hervé Outin1 · Matthieu Jamme1,3 Received: 15 May 2020 / Revised: 3 July 2020 / Accepted: 7 July 2020 © Japanese Society of Hematology 2020
Abstract This case report describes immune thrombocytopenic purpura in a 41-year-old man hospitalized in the intensive-care unit for COVID-19, 13 days after the onset of COVID-19 symptoms with respiratory failure at admission. Acute respiratory distress syndrome was treated with, among other drugs, low-molecular-weight heparin. On day 8, his platelet count began descending rapidly. On day 10, heparin treatment was replaced by danaparoid sodium, but by day 13, the continued low platelet count made a diagnosis of heparin-induced thrombocytopenia unlikely. Normocytic nonregenerative anemia gradually developed. On day 13, a bone marrow aspiration showed numerous megakaryocytes and a few signs of hemophagocytosis. Corticosteroids were introduced on day 14, and platelets began rising after 3 days and then fell again on day 19. Intravenous immunoglobulin (IV Ig) was then administered. Two days later, the platelet count returned to normal. The immune cause was confirmed by ruling out the differential diagnoses and the excellent and rapid response to intravenous immunoglobulins. Finally, the patient’s respiratory state improved. He was discharged to a respiratory rehabilitation unit on day 38. Our case suggests that an immunological cause should be considered in patients with thrombocytopenia during COVID-19.
Introduction Thrombocytopenia has recently been described as a frequent feature during the pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes COVID-19, identified in up to 36% of patients [1]. The severity of thrombocytopenia has since been linked to the severity of COVID-19 and to its mortality [2–5]. Several physiopathological processes leading to thrombocytopenia during COVID-19 disease have been proposed [6–8]. It has been postulated that hematopoiesis dysfunction and alterations of megakaryocytic differentiation and maturation could occur through infection of hematopoietic stem cells and megakaryocytes, alterations of medullar microenvironment mediated by inflammation, and decrease of TPO production by liver cells which are susceptible to * Matthieu Jamme Matthieu.Jamme@ght‑yvelinesnord.fr 1
Intensive Care Unit, Poissy Saint Germain Hospital, 9‑10 rue du champ Gaillard, 78300 Poissy, France
2
Laboratory of Hematology, Poissy Saint Germain Hospital, 9‑10 rue du champ Gaillard, 78300 Poissy, France
3
INSERM U-1018, CESP, Team 5 (EpReC, Renal and Cardiovascular Epidemiology), UVSQ, Villejuif, France
SARS-CoV-2 infection. Lung injury mediated by SARSCoV-2 infection could also affect megakaryocyte fragmentation and platelet formation, which takes place in pulmonary vessels [9]. Moreover, pro-inflammatory mechanisms including cytokine and chemokine release have been docume
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