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1.
EJHaem ; 3(2): 453-456, 2022 May.
Article in English | MEDLINE | ID: covidwho-1739178

ABSTRACT

Over the last 2 years, different cases of immune thrombocytopenia (ITP) in patients affected by SARS-CoV2 have been reported. The management of SARS-CoV2 in subjects with simultaneous or previous ITP can be challenging because of the great involvement of the haemostatic system in this viral infection. In this report, we describe the management and outcome of patients with newly diagnosed (ND), chronic and previous ITP, infected by COVID-19, referred to the Haematology Institute of University Hospital Policlinico Umberto I in Rome. Steroids + immunoglobulins for ND or relapsed ITP and continuation of home therapy for chronic ITP are advised, although further knowledge is required.

3.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-309242

ABSTRACT

Background: Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare syndrome of unclear aetiology occurring after DNA-based vaccinations against COVID-19. The aim of this study was to investigate the DNA vaccine-encoded Sars-cov-2 soluble spike protein (SP). as a potential trigger of platelet activation in VITT. Methods. We studied three VITT patients and seven healthy controls (HCs) within 3 weeks from the first dose of ChAdOx1 nCoV-19, and one non vaccinated HC. Serum levels of SP and soluble angiotensin-converting enzyme 2 (sACE2), ACE2 expression in platelets and platelet response to VITT serum stimulation were studied. A thrombus retrieved during mechanical thrombectomy from one VITT patients, was analysed by immunohistochemistry for SP and ACE2. Neutrophil extracellular traps (NETs) markers and coagulation parameters were also measured. Results. We detected serum SP (up to 35 days post-vaccination) and sACE2 in all VITT patients, and respectively in two and three out of 7 vaccinated HCs. Only platelets from one non-vaccinated HC expressed ACE2. VITT sera markedly activated platelets and this activation was inhibited by both anti-SP and anti-FcγRIIA blocking antibodies. The thrombus showed positive immunohistochemical labelling of platelets using an anti-SP antibody with reduced ACE2 expression, compared to a thrombus from a pre-pandemic stroke patient. Markers of endothelial dysfunction, NETs and hypercoagulability state were present in all VITT sera. Conclusions. The present data provides first evidence that DNA vaccine-encoded Sars-cov-2 SP is detectable in VITT sera (several weeks post-vaccination) and in a platelet-rich thrombus, and that may contribute to the initial platelet stimulation in VITT patients.

4.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-309241

ABSTRACT

Vaccine induced thrombotic thrombocytopenia is a new syndrome recently described in young adults within two weeks from the first dose of the ChAdOx1 nCoV-19 vaccine and characterized by cerebral venous thrombosis. We report two cases of malignant middle cerebral artery (MCA) infarct and thrombocytopenia within 10 days after vaccination with ChAdOx1 nCoV-19. Patient 1 was a 57-year-old woman who underwent decompressive craniectomy despite two successful mechanical thrombectomies. Patient 2 was a 55-year-old woman who developed a fatal bilateral malignant MCA infarct. Both the patients had pulmonary and portal vein thrombosis and high level of antibodies to platelet factor 4-polyanion complexes.

6.
J Thromb Thrombolysis ; 52(1): 105-110, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1002136

ABSTRACT

Patients with Coronavirus-associated disease-2019 (COVID-19) display alterations of the hemostatic system and the presence of a prothrombotic status frequently leading to vascular complications. However, the impact of COVID-19 on platelet activity, aggregation and agglutination still needs to be clarified. We measured total levels of von Willebrand factor (vWF) and vWF binding to the platelet glycoprotein (Gp) complex (GPIb-IX-V), in a cohort of COVID-19 patients admitted to the intensive care unit of our Institution. Moreover, we evaluated platelet aggregation in response to agonists (ADP, collagen, arachidonic acid) and platelet agglutination in response to ristocetin. We found that levels of vWF antigen and the active form of vWF binding to platelets (vWF:RCo), were markedly increased in these patients. These results were associated with higher agglutination rates induced by ristocetin, thereby indirectly indicating an increased capability of vWF to bind to platelets. Conversely, we found that platelet aggregation in response to both ADP and collagen was lower in COVID-19 patients compared to healthy volunteers. This study shows that COVID-19 is associated with increased vWF-induced platelet agglutination but reduced platelet responsivity to aggregation stimuli. Our findings have translational relevance since platelet adhesion to vWF may represent a marker to predict possible complications and better delineate therapeutic strategies in COVID-19 patients.


Subject(s)
Blood Platelets/metabolism , COVID-19/blood , Platelet Aggregation , von Willebrand Factor/metabolism , Adult , Aged , Aged, 80 and over , Agglutination , Blood Platelets/virology , COVID-19/diagnosis , COVID-19/virology , Female , Host-Pathogen Interactions , Humans , Male , Middle Aged , Platelet Function Tests , Protein Binding , SARS-CoV-2/pathogenicity , Thrombosis/blood , Thrombosis/diagnosis , Thrombosis/virology
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