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Thrombosis and thrombocytopaenia after ChAdOx1 nCoV-19 vaccination: a single UK centre experience
Fehmida Bano1, Buddikha Badugama2, Deepak Chandra2
1Haematology, University Hospitals of North Staffordshire NHS Trust, Stoke-on-Trent, UK fehmida.bano@uhnm.nhs.uk.
Insights
Three patients developed vaccine-induced thrombotic thrombocytopaenia (VITT) after the ChAdOx1 nCoV-19 vaccine, presenting with thrombosis and low platelets. High-titre anti-PF4 antibodies confirmed VITT, a rare but serious adverse event.
Area of Science:
- Immunology
- Hematology
- Vaccinology
Background:
- The ChAdOx1 nCoV-19 vaccine (Vaxzevria) is a critical tool for controlling the SARS-CoV-2 pandemic.
- Rare adverse events following vaccination require thorough investigation and characterization.
Observation:
- Three patients presented with severe thrombosis and thrombocytopaenia 10-16 days post-first ChAdOx1 nCoV-19 vaccine dose.
- Patients exhibited high-titre antibodies against platelet factor 4 (PF4) without prior heparin exposure.
- Clinical presentation included extensive venous thrombosis, thrombocytopaenia, elevated D-dimer, and low fibrinogen.
Findings:
- Two patients experienced fatal intracerebral hemorrhage secondary to cavernous venous sinus thrombosis.
- One patient had a pulmonary embolism (PE).
- Laboratory analysis confirmed the presence of anti-PF4 antibodies, leading to a diagnosis of vaccine-induced thrombotic thrombocytopaenia (VITT).
Implications:
- This case series highlights VITT as a rare but severe complication associated with the ChAdOx1 nCoV-19 vaccine.
- Early recognition and management, including the use of intravenous immunoglobulin and corticosteroids for PE, can be beneficial.
- Further research is needed to understand the pathogenesis and optimize treatment strategies for VITT.
Abstract:
We report clinical findings of three patients presenting with thrombosis and thrombocytopaenia 10-16 days following the first dose of the ChAdOx1 nCoV-19 vaccine against SARS-CoV-2. All patients presented to a major university teaching hospital in the UK over a 5-day period and were found to have high-titre antibodies against platelet factor 4 (PF4) without previous exposure to heparin. All three patients presented with extensive venous thrombosis, significant thrombocytopaenia, elevated D-dimer and borderline low fibrinogen. Two had fatal intracerebral haemorrhage secondary to cavernous venous sinus thrombosis and one had PE. Reference laboratory testing of serum demonstrated anti-PF4 antibodies in all three patients. The clinical and laboratory findings confirmed vaccine-induced thrombotic thrombocytopaenia (VITT) which was poorly described at the time of presentation. We were able to manage successfully one patient with PE with intravenous immunoglobulin and corticosteroids.
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