<abstract xmlns="http://www.w3.org/1999/xhtml">

<sec><h3>Introduction</h3>
<p>The immune response in patients with SARS-CoV2 infection is an incompletely elucidated pathophysiological challenge. There are more and more cases in which COVID-19 vaccination induces autoimmune side effects, of course, in a selected population. What are the criteria that induce such a response? How can it be prevented? These are questions that the medical world must answer.</p>
</sec>
<sec><h3>Material and Methods</h3>
<p>A 28-year-old male patient presented with repeated small hemoptysis accompanied by pleuritic pain, which started suddenly 2 days prior. From the patient’s history, we note autoimmune thyrotoxicosis triggered by the administration of the second dose of the anti-SARS-CoV2 vaccine, but also a recent COVID-19 episode. At the time of hospitalization, slightly elevated serum values of D-dimers were noted, and the CT examination identified multiple unilateral filling defects in the middle and small right pulmonary arteries, accompanied by a ground-glass opacity suggestive of a pulmonary infarction and possible bilateral stenosis of the subclavian arteries. The extended immunological panel was negative, but genetic tests have identified two thrombophilic gene mutations. Functionally, a discrete decrease in lung volumes and a slight impairment of alveolo-capillary diffusion was observed. The clinical, imaging and functional evolution was favorable under anticoagulant treatment.</p>
</sec>
<sec><h3>Discusions</h3>
<p>The predisposition for thrombosis in COVID-19 is determined by at least two distinct processes, subsegmental and segmental vessel occlusion and microvascular in situ immunothrombosis. Pulmonary thromboembolism occurs more frequently in the first weeks after diagnosis, but cases farther from the acute moment have also been reported in literature, including in patients with mild forms of the disease.</p>
<p>Certain adjuvant components of the vaccines, as well as the SARS-CoV2 virus itself, can trigger autoimmune reactions in genetically predisposed individuals.</p>
</sec>
<sec><h3>Conclusion</h3>
<p>Patients with active or recently recovered COVID-19 should be considered at an increased risk of pulmonary embolism when they present with specific symptoms, even without the existence of other risk factors.</p>
</sec>
</abstract>

Introduction
The immune response in patients with SARS-CoV2 infection is an incompletely elucidated pathophysiological challenge. There are more and more cases in which COVID-19 vaccination induces autoimmune side effects, of course, in a selected population. What are the criteria that induce such a response? How can it be prevented? These are questions that the medical world must answer.

Material and Methods
A 28-year-old male patient presented with repeated small hemoptysis accompanied by pleuritic pain, which started suddenly 2 days prior. From the patient’s history, we note autoimmune thyrotoxicosis triggered by the administration of the second dose of the anti-SARS-CoV2 vaccine, but also a recent COVID-19 episode. At the time of hospitalization, slightly elevated serum values of D-dimers were noted, and the CT examination identified multiple unilateral filling defects in the middle and small right pulmonary arteries, accompanied by a ground-glass opacity suggestive of a pulmonary infarction and possible bilateral stenosis of the subclavian arteries. The extended immunological panel was negative, but genetic tests have identified two thrombophilic gene mutations. Functionally, a discrete decrease in lung volumes and a slight impairment of alveolo-capillary diffusion was observed. The clinical, imaging and functional evolution was favorable under anticoagulant treatment.

Discusions
The predisposition for thrombosis in COVID-19 is determined by at least two distinct processes, subsegmental and segmental vessel occlusion and microvascular in situ immunothrombosis. Pulmonary thromboembolism occurs more frequently in the first weeks after diagnosis, but cases farther from the acute moment have also been reported in literature, including in patients with mild forms of the disease.
Certain adjuvant components of the vaccines, as well as the SARS-CoV2 virus itself, can trigger autoimmune reactions in genetically predisposed individuals.

Conclusion
Patients with active or recently recovered COVID-19 should be considered at an increased risk of pulmonary embolism when they present with specific symptoms, even without the existence of other risk factors.

Autoimmunity in context of exposure to SARS-Cov2 virus

University of Medicine and Pharmacy of Craiova

University of Medicine and Pharmacy “Carol Davila”

Pneumologia

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

{"article-title":"Autoimmunity in context of exposure to SARS-Cov2 virus"}

Introduction
The immune response in patients with SARS-CoV2 infection is an incompletely elucidated pathophysiological challenge. There are more and more cases...

Autoimmunity in context of exposure to SARS-Cov2 virus

Publicado en línea: 10 jun 2024

Páginas: 71 - 78

DOI: https://doi.org/10.2478/pneum-2024-0011

Palabras clave
SARS-CoV2 vaccine, COVID-19, immunothrombosis, Basedow-Graves thyroiditis, pulmonary thromboembolism

© 2023 Iris-Andreea Negoescu et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Autoimmunity in context of exposure to SARS-Cov2 virus

Publicado en línea: 10 jun 2024

Páginas: 71 - 78

DOI: https://doi.org/10.2478/pneum-2024-0011

Palabras claveSARS-CoV2 vaccine, COVID-19, immunothrombosis, Basedow-Graves thyroiditis, pulmonary thromboembolism

© 2023 Iris-Andreea Negoescu et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Palabras clave
SARS-CoV2 vaccine, COVID-19, immunothrombosis, Basedow-Graves thyroiditis, pulmonary thromboembolism