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A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism

Background: Autoimmune hyperthyroidism also known as Graves’ disease is the leading cause of hyperthyroidism. The pathogenesis of Graves’ disease is still an area of active research. We present a case of Graves’ disease, which developed following SARS-CoV2 infection. Clinical Case: A 43-year-old man...

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Autores principales: Matos, Moises, Merino-Chavez, Hilda Maria, Martinez, Suzanne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089878/
http://dx.doi.org/10.1210/jendso/bvab048.1863
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author Matos, Moises
Merino-Chavez, Hilda Maria
Martinez, Suzanne
author_facet Matos, Moises
Merino-Chavez, Hilda Maria
Martinez, Suzanne
author_sort Matos, Moises
collection PubMed
description Background: Autoimmune hyperthyroidism also known as Graves’ disease is the leading cause of hyperthyroidism. The pathogenesis of Graves’ disease is still an area of active research. We present a case of Graves’ disease, which developed following SARS-CoV2 infection. Clinical Case: A 43-year-old man with no prior history of thyroid disease, presented for evaluation due to fatigue palpitations, tremors, and hair loss in June 2020. Earlier that month, he was diagnosed with SARS-CoV2 infection and his thyroid function tests (TFTs) during a visit to the emergency department revealed thyroid stimulating hormone (TSH) level of <0.010 mIU/L (0.35-4.94) with a free T4 (FT4) 1.4 ng/dL (0.7-1.5); consistent with subclinical hyperthyroidism. He continued to report palpitations and tremors and further workup was done. A thyroid ultrasound showed two sub-centimeter nodules. A thyroid uptake scan followed, which showed heterogeneous activity in the thyroid gland, (12% and 32% uptake at 6 and 24 hours respectively) with focal increased uptake in the medial lobes, without cold nodules or hot nodules. Repeat TFTs one month later showed a suppressed TSH <0.010 mIU/L, and a normal FT4 1.3 ng/dL. Given suspicion for Graves’ disease, further labs were ordered. Thyroid stimulating immunoglobulin (TSI) were found to be elevated at 173 % baseline (<=140). Thyroid peroxidase (TPO) antibodies and thyroglobulin antibodies were also elevated at 362 IU/mL H* (<=9) and 2 IU/mL H* (<=1) respectively. The overall picture was consistent with evolving early Graves’ disease. Conclusion: Multiple factors are frequently cited in the pathogenesis of autoimmune hyperthyroidism including viral and bacterial infections(1) and there have been several reported cases of autoimmune disease related to SARS-CoV2 infection(2). This case is one of several emerging cases of autoimmune hyperthyroidism possibly linked to COVID-19. References: 1. Smith, T. J . Graves’ Disease. New England Journal of Medicine. 2016 October 20; 375:1552-1565 2. Mateu-Salat, M., Urgell, E., Chico, A. SARS-COV-2 as a trigger for autoimmune disease: report of two cases of Graves’ disease after COVID-19. Journal of Endocrinological Investigation. 2020 July 19
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spelling pubmed-80898782021-05-06 A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism Matos, Moises Merino-Chavez, Hilda Maria Martinez, Suzanne J Endocr Soc Thyroid Background: Autoimmune hyperthyroidism also known as Graves’ disease is the leading cause of hyperthyroidism. The pathogenesis of Graves’ disease is still an area of active research. We present a case of Graves’ disease, which developed following SARS-CoV2 infection. Clinical Case: A 43-year-old man with no prior history of thyroid disease, presented for evaluation due to fatigue palpitations, tremors, and hair loss in June 2020. Earlier that month, he was diagnosed with SARS-CoV2 infection and his thyroid function tests (TFTs) during a visit to the emergency department revealed thyroid stimulating hormone (TSH) level of <0.010 mIU/L (0.35-4.94) with a free T4 (FT4) 1.4 ng/dL (0.7-1.5); consistent with subclinical hyperthyroidism. He continued to report palpitations and tremors and further workup was done. A thyroid ultrasound showed two sub-centimeter nodules. A thyroid uptake scan followed, which showed heterogeneous activity in the thyroid gland, (12% and 32% uptake at 6 and 24 hours respectively) with focal increased uptake in the medial lobes, without cold nodules or hot nodules. Repeat TFTs one month later showed a suppressed TSH <0.010 mIU/L, and a normal FT4 1.3 ng/dL. Given suspicion for Graves’ disease, further labs were ordered. Thyroid stimulating immunoglobulin (TSI) were found to be elevated at 173 % baseline (<=140). Thyroid peroxidase (TPO) antibodies and thyroglobulin antibodies were also elevated at 362 IU/mL H* (<=9) and 2 IU/mL H* (<=1) respectively. The overall picture was consistent with evolving early Graves’ disease. Conclusion: Multiple factors are frequently cited in the pathogenesis of autoimmune hyperthyroidism including viral and bacterial infections(1) and there have been several reported cases of autoimmune disease related to SARS-CoV2 infection(2). This case is one of several emerging cases of autoimmune hyperthyroidism possibly linked to COVID-19. References: 1. Smith, T. J . Graves’ Disease. New England Journal of Medicine. 2016 October 20; 375:1552-1565 2. Mateu-Salat, M., Urgell, E., Chico, A. SARS-COV-2 as a trigger for autoimmune disease: report of two cases of Graves’ disease after COVID-19. Journal of Endocrinological Investigation. 2020 July 19 Oxford University Press 2021-05-03 /pmc/articles/PMC8089878/ http://dx.doi.org/10.1210/jendso/bvab048.1863 Text en © The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Thyroid
Matos, Moises
Merino-Chavez, Hilda Maria
Martinez, Suzanne
A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
title A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
title_full A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
title_fullStr A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
title_full_unstemmed A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
title_short A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
title_sort grave case of covid-19: sars-cov-2 induced autoimmune hyperthyroidism
topic Thyroid
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089878/
http://dx.doi.org/10.1210/jendso/bvab048.1863
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