Retinal Hemorrhage after SARS-CoV-2 Vaccination.

Hyo Song Park,Yong Joon Kim,Yeojue Byun,Christopher Seungkyu Lee,Suk Ho Byeon,Sung Soo Kim

doi:10.3390/jcm10235705

Hyo Song Park, Yong Joon Kim + Show 4 more

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https://doi.org/10.3390/jcm10235705

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Abstract

To report retinal vein occlusion (RVO) and age-related macular degeneration (AMD)-related submacular hemorrhage developing after administration of SARS-CoV-2 vaccines, a single-center, retrospective observational case series was conducted. Clinical data including fundus photographs and optical coherence tomography (OCT) scans were reviewed. Twenty-three eyes of 21 patients were included with the median age at symptom presentation being 77 years (range: 51–85 years). Twelve eyes (52.2%) had submacular hemorrhage and 11 (47.8%) had RVO. Twelve patients (60.9%) had been vaccinated with the Pfizer vaccine (BNT162b2) and 8 with the AstraZeneca (ChAdOx1) vaccine. Sixteen patients (76.2%) experienced ocular disease exacerbation after the first vaccination and 4 (19.0%) after the second vaccination. The median visual acuity (logarithm of the minimal angle of resolution; logMAR) before symptom development was 0.76 (interquartile range: 0.27–1.23); the median logMAR at symptom presentation was 1.40 (interquartile range 0.52–1.70). The median time between vaccination and symptom exacerbation was 2.0 days (interquartile range: 1.0–3.0 days). Five patients (23.8%) underwent tests for hematological abnormalities, including the presence of anti-PF4 antibodies; all were negative. Further studies with larger patient group for evaluation of effect of SARS-CoV-2 vaccination on retinal hemorrhage are necessary.

Highlights

The ongoing coronavirus SARS-CoV-2 pandemic has caused 4 million deaths worldwide among 199 million cases [1]
The mechanisms by which these conditions develop remain unclear, VITT patients seem to have antibodies against platelet factor 4; these mimic the effect of heparin by binding to a similar site on PF4, which allows PF4 to cluster into immune complexes that trigger Fcγ receptor IIa-dependent platelet activation [13]
The mechanism of cardiomyopathy may involve molecular mimicry of the spike protein of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and self-antigens, the triggering of pre-existing dysregulated immune pathways in certain individuals, an immune response to mRNA followed by activation of immunological pathways, and/or dysregulated cytokine expression [12]

Summary

Introduction

The ongoing coronavirus SARS-CoV-2 pandemic has caused 4 million deaths worldwide among 199 million cases [1]. Ad26.COV2.S was given to more than 1.1 million people and mRNA-1273 to 60,000 [4]. The mechanisms by which these conditions develop remain unclear, VITT patients seem to have antibodies against platelet factor 4 (anti-PF4 Ab); these mimic the effect of heparin by binding to a similar site on PF4, which allows PF4 to cluster into immune complexes that trigger Fcγ receptor IIa-dependent platelet activation [13]. The mechanism of cardiomyopathy may involve molecular mimicry of the spike protein of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and self-antigens, the triggering of pre-existing dysregulated immune pathways in certain individuals, an immune response to mRNA followed by activation of immunological pathways, and/or dysregulated cytokine expression [12]

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