Journal of Clinical Neurology (Seoul, Korea) | 2021

Vaccine-Induced Immune Thrombotic Thrombocytopenia: First Case Report in South Korea

 
 
 
 
 

Abstract


Dear Editor, The coronavirus disease 2019 (COVID-19) pandemic is an ongoing global crisis. Among 11 vaccines recently introduced worldwide, vaccines using adenoviral vectors such as ChAdOx1 nCov-19 (AstraZeneca) and Ad26.COV2.S (Janssen) have been reported to rarely cause vaccine-induced immune thrombotic thrombocytopenia (VITT).1 As at June 2021, approximately 7.9 million people had received the AstraZeneca vaccination in South Korea, and we have identified the first case of VITT presenting with cerebral venous sinus thrombosis.2 A previously healthy, 33-year-old male patient presented with recurrent successive generalized tonic–clonic seizures with prolonged confusion. Four days before admission he experienced worsening exploding headache confined to the left frontotemporal area, accompanied by nausea, vomiting, and general weakness. He had received the AstraZeneca vaccination 15 days prior to the headache onset. On arrival, he showed stuporous mentality, impaired awareness, and neck stiffness with no lateralizing neurological deficits. Emergent CT disclosed a small amount of intracranial hemorrhage in the left frontal lobe and high density lesions in the superior sagittal sinus. Subsequent diffusion-weighted imaging also showed dark signal lesions in the corresponding areas on a gradient recalled echo sequence (Fig. 1A). Cerebral venous thrombosis of the superior sagittal sinus was suggested, which was subsequently confirmed by CT venography (Fig. 1B). Laboratory tests revealed mild thrombocytopenia (platelet count, 75,000/mm3) and markedly elevated D-dimer (>20 mg/L fibrinogen equivalent unit [FEU], reference range <0.5 mg/L FEU). The laboratory results for coagulopathy including fibrinogen, protein C activity, protein S activity, antithrombin III, antiphospholipid antibody IgM/IgG, anti-cardiolipin antibody IgM/IgG, anti-platelet antibody, and platelet-associated antibody were all negative or within normal ranges. Intravenous antiepileptic drugs (levetiracetam 1,500 mg and lacosamide 400 mg) and 20% mannitol (200 mL) were immediately administered to prevent recurrent generalized seizures and reduce the raised intracranial pressure. Anticoagulation treatment with oral edoxaban (60 mg/day) was also commenced under the impression of probable VITT, in compliance with the VITT guideline (http://ncov. mohw.go.kr/upload/ncov/file/202104/1618802689481_20210419122449.pdf). The screening test for antibodies against the platelet factor 4 (PF4)–heparin complex using a chemiluminescent immunoassay was negative but strongly positive when using an enzyme-linked immunosorbent assay (3.1 optical-density units, normal range <0.4 optical-density units). The patient regained consciousness the next day and no further seizures occurred. An electroencephalogram showed regional sharp-waves in the left frontal area on a normal background. Thrombocytopenia and elevated D-dimer gradually improved to normal over the following 2 weeks (Fig. 1D). Repeat CT venography on hospital day 14 showed reductions in the hematoma size and perilesional edema as well as a marked resolution of venous thrombosis (Fig. 1C). He remained on an oral anticoagulant and was discharged to home on hospital day 19 without any neurological sequelae. Min Kyung Kim Seongsoo Jang Sang-Hoon Na Soo-Mee Bang Ji Hyun Kim

Volume 17
Pages 570 - 572
DOI 10.3988/jcn.2021.17.4.570
Language English
Journal Journal of Clinical Neurology (Seoul, Korea)

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