The association between severe COVID‐19 and low platelet count: evidence from 31 observational studies involving 7613 participants

Jiang, Shiqin; Huang, Qiming; Xie, Wei‐Ming; Lv, Chao; Quan, Xiao‐Qing

doi:10.1111/bjh.16817

Cited by 117 publications

(118 citation statements)

References 8 publications

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“…Thrombocytopenia has been identified as a frequent feature [1][2][3][4][5], reported in 18-36% of patients in different cohorts. It has also been associated with severe disease [2,5] and mortality [3][4][5]. It was also a frequent feature of the SARS-CoV infectious epidemic of 2003 when it was reported in 40-50% of the patients [12,13].…”

Section: Discussionmentioning

confidence: 99%

Immune thrombocytopenia in a patient with COVID-19

et al. 2020

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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.

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Section: Discussionmentioning

confidence: 99%

Immune thrombocytopenia in a patient with COVID-19

et al. 2020

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“…A meta-analysis of 7,613 COVID-19 patients revealed that patients with severe disease had a lower platelet count than those with non-severe disease. Additionally, the non-survivors had a much lower platelet count than the survivors [ 25 , 36 ]. However, not all studies have found platelet counts to be a predictor of COVID-19 mortality [ 37 ].…”

Section: Plateletsmentioning

confidence: 99%

The Impact of COVID-19 Disease on Platelets and Coagulation

2020

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Coronavirus disease 2019 (COVID-19) causes a spectrum of disease; some patients develop a severe proinflammatory state which can be associated with a unique coagulopathy and procoagulant endothelial phenotype. Initially, COVID-19 infection produces a prominent elevation of fibrinogen and D-dimer/fibrin(ogen) degradation products. This is associated with systemic hypercoagulability and frequent venous thromboembolic events. The degree of D-dimer elevation positively correlates with mortality in COVID-19 patients. COVID-19 also leads to arterial thrombotic events (including strokes and ischemic limbs) as well as microvascular thrombotic disorders (as frequently documented at autopsy in the pulmonary vascular beds). COVID-19 patients often have mild thrombocytopenia and appear to have increased platelet consumption, together with a corresponding increase in platelet production. Disseminated intravascular coagulopathy (DIC) and severe bleeding events are uncommon in COVID-19 patients. Here, we review the current state of knowledge of COVID-19 and hemostasis.

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“…3,5 Thrombocytopenia and increased levels of D-dimers have proved as early predictors of outcome in critically ill COVID-19 patients. 3,[6][7][8][9][10][11] However, the pathophysiological mechanisms underlying COVID-19-associated hypercoagulability are still to be defined.…”

Section: Introductionmentioning

confidence: 99%

Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19

Hottz

Azevedo-Quintanilha

Palhinha

et al. 2020

Blood

636

754

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an emergent pathogen responsible for the coronavirus disease 2019 (COVID-19). Since its emergence, the novel coronavirus has rapidly achieved pandemic proportions causing remarkably increased morbidity and mortality around the world. A hypercoagulability state has been reported as a major pathologic event in COVID-19, and thromboembolic complications listed among life-threatening complications of the disease. Platelets are chief effector cells of hemostasis and pathological thrombosis. However, the participation of platelets in the pathogenesis of COVID-19 remains elusive. This report demonstrates that increased platelet activation and platelet-monocyte aggregate formation are observed in severe COVID-19 patients, but not in patients presenting mild COVID-19 syndrome. In addition, exposure to plasma from severe COVID-19 patients increased the activation of control platelets ex vivo. In our cohort of COVID-19 patients admitted to the intensive care unit, platelet-monocyte interaction was strongly associated with tissue factor (TF) expression by the monocytes. Platelet activation and monocyte TF expression were associated with markers of coagulation exacerbation as fibrinogen and D-dimers, and were increased in patients requiring invasive mechanical ventilation or patients who evolved with in-hospital mortality. Finally, platelets from severe COVID-19 patients were able to induce TF expression ex vivo in monocytes from healthy volunteers, a phenomenon that was inhibited by platelet P-selectin neutralization or integrin αIIb/β3 blocking with the aggregation inhibitor abciximab. Altogether, these data shed light on new pathological mechanisms involving platelet activation and platelet-dependent monocyte TF expression, which were associated with COVID-19 severity and mortality.

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The association between severe COVID‐19 and low platelet count: evidence from 31 observational studies involving 7613 participants

Cited by 117 publications

References 8 publications

Immune thrombocytopenia in a patient with COVID-19

Immune thrombocytopenia in a patient with COVID-19

The Impact of COVID-19 Disease on Platelets and Coagulation

Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19

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