Mechanism of thrombocytopenia in COVID-19 patients

Xu, Panyang; Zhou, Qi; Xu, Jiancheng

doi:10.1007/s00277-020-04019-0

Cited by 512 publications

(548 citation statements)

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“…There have been multiple proposed mechanisms for how COVID-19 causes thrombocytopaenia. 17 The first mechanism is through a cytokine storm and macrophage activation which possibly results in decreased haematopoietic progenitor cells. The second mechanism is by direct infection of haematopoietic and BM stromal cells.…”

Section: Discussionmentioning

confidence: 99%

“… 18 It may also include persistent hypertension and hypoxaemia, which result in areas of lung fibrosis, and therefore less surface area for platelet biogenesis. 17 The fourth mechanism is via an increase in autoantibodies resulting in platelet destruction: SARS-specific IgG antibodies are produced in the late acute stage (at around 2 weeks) and gradually increase with the course of the disease. 19 As the thrombocytopaenia was first recorded in our case in the latter disease stages on day 10, we propose that autoantibody platelet destruction may be a prominent mechanism.…”

Section: Discussionmentioning

confidence: 99%

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Severe thrombocytopaenia secondary to COVID-19

et al. 2020

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The SARS-CoV-2 infection has caused a pandemic with a case rate of over 290 000 lab-confirmed cases and over 40 000 deaths in the UK. There is little evidence to inform the optimal management of a patient presenting with new or relapsed acute idiopathic thrombocytopaenic purpura with concurrent SARS-CoV-2 infection. We present a case of severe thrombocytopaenia complicated by subdural haematoma and rectal bleed associated with COVID-19. A 67-year-old man, admitted with a non-productive cough and confusion, was found to be positive for COVID-19. Ten days after admission, his platelets decreased from 146×109/L to 2×109/L. His platelets did not increase despite receiving frequent platelet transfusions. He was non-responsive to corticosteroids and intravenous immunoglobulins. Romiplostim and eltrombopag were given and after 9 weeks of treatment, his platelet count normalised. He was deemed medically fit with outpatient follow-up in a haematology clinic.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Severe thrombocytopaenia secondary to COVID-19

et al. 2020

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“…Furthermore, a shift in platelet-lymphocyte ratio may indicate the occurrence of an acute inflammatory or thrombotic event and therefore have prognostic value (Qu et al, 2020). Thus, thrombocytopaenia may reflect (a) alteration in thrombopoiesis due to the bone marrow or lungs (and potentially spleen) being inflamed or receiving inflammatory and trauma-related thrombopoietic cues; (b) localised lung recruitment of platelets as a facet of their role in the immune response or alveolar coagulation; (c) disseminated intravascular coagulation (DIC) throughout the body (Xu, Zhou, & Xu, 2020); or (d) platelet-viral interaction, although this remains hypothetical as an engagement of platelets with SARS-CoV-2 has not been described (Amgalan & Othman, 2020 Results of studies in mice modelling influenza agree on the necessity for platelets in the immune response and inflammation but conflict as to whether this is beneficial (Campbell et al, 2019;Guo et al, 2017), or detrimental (Boilard et al, 2014;Lê et al, 2015). Additionally, platelets respond to influenza virus by increasing complement availability and encourage the release of NETs into blood, and so platelets may be important integrators linking viral infection to neutrophil responses that are associated with coagulopathy and venous thrombosis (Koupenova et al, 2019).…”

Section: Platelet Responses Coagulopathy and Hyperinflammationmentioning

confidence: 99%

Animal models of mechanisms of SARS‐CoV‐2 infection and COVID‐19 pathology

Cleary

Pitchford

Amison

et al. 2020

British J Pharmacology

177

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The coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 infections has led to a substantial unmet need for treatments, many of which will require testing in appropriate animal models of this disease. Vaccine trials are already underway, but there remains an urgent need to find other therapeutic approaches to either target SARS-CoV-2 or the complications arising from viral infection, particularly the dysregulated immune response and systemic complications which have been associated with progression to severe COVID-19. At the time of writing, in vivo studies of SARS-CoV-2 infection have been described using macaques, cats, ferrets, hamsters, and transgenic mice expressing human angiotensin I converting enzyme 2 (ACE2). These infection models have already been useful for studies of transmission and immunity, but to date only partly model the mechanisms involved in human severe COVID-19. There is therefore an urgent need for development of animal models for improved evaluation of efficacy of drugs identified as having potential in the treatment of severe COVID-19. These models need to reproduce the key mechanisms of COVID-19 severe acute respiratory distress syndrome and the immunopathology and systemic sequelae associated with this disease. Here, we review the current models of SARS-CoV-2 infection and COVID-19-related disease mechanisms and suggest ways in which animal models can be adapted to increase their usefulness in research into COVID-19 pathogenesis and for assessing potential treatments.

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“… 2 Thrombocytopenia can occur secondary to sepsis, disseminated intravascular coagulation or drug-induced, 3 as well as direct bone marrow suppression or immune-mediated destruction. 4 …”

Section: Introductionmentioning

confidence: 99%