COVID-19: a new etiological factor of Graves’ disease?

Authors

DOI:

https://doi.org/10.22141/2224-0721.16.7.2020.219014

Keywords:

Graves’ disease, COVID-19, thyrotoxicosis, angiotensin-converting enzyme 2 receptors, reinfection, recurrence

Abstract

SARS-CoV-2 rapidly became a pandemic and has affected millions of people worldwide. Even though the main target of the coronavirus is the respiratory system, researchers all over the world are increasingly concerned about the problem of the impact of COVID-19 on other organs and systems. There is a possibility that coronavirus can affect the thyroid gland because angiotensin-converting enzyme type 2 receptors, through which coronavirus enters cells, were detected in this organ. Recently, there has been an increasing number of reports about subacute thyroiditis and Graves’ disease developing after COVID-19. In our clinical practice, we had a first-onset of Graves’ disease with severe thyrotoxicosis after coronavirus. Severe thyrotoxicosis required the prescription of antithyroid drugs and glucocorticosteroids. Six months later, the patient was reinfected by COVID-19, after which Graves’ disease recurred and endocrine ophthalmopathy developed. We assume that coronavirus altering immunological tolerance can trigger autoimmune mechanisms that provoke autoaggression against various tissues in the human body. One such example is Graves’ disease, recurrence of which might occur due to reinfection of COVID-19. The authors suggest that because the coronavirus alters immunological tolerance in the human body, it can trigger autoimmune mechanisms, which provokes autoaggression against various organs and systems. One such manifestation is Graves’ disease, the onset and manifestation of which may occur after infection or reinfection with COVID-19. The clinical case describes a patient without previous thyroid pathology in whom coronavirus infection was a trigger for the development of Graves’ disease with overt severe thyrotoxicosis requiring glucocorticosteroids. Reinfection with COVID-19 six months after the first infection led to a recurrence of the autoimmune disease and the need for increased antithyroid therapy. Besides reinfection caused the development of endocrine ophthalmopathy, which did not exist at the beginning of Graves’ disease.

References

WHO. Coronavirus disease (COVID-19) Weekly Epidemiological Update and Weekly Operational Update. Available from: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/situation-reports.

Guo YR, Cao QD, Hong ZS, et al. The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak - an update on the status. Mil Med Res. 2020 Mar 13;7(1):11. doi:10.1186/s40779-020-00240-0.

Reguera J, Mudgal G, Santiago C, Casasnovas JM. A structural view of coronavirus-receptor interactions. Virus Res. 2014 Dec 19;194:3-15. doi:10.1016/j.virusres.2014.10.005.

Yan R, Zhang Y, Li Y, Xia L, Guo Y, Zhou Q. Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2. Science. 2020 Mar 27;367(6485):1444-1448. doi:10.1126/science.abb2762.

Li MY, Li L, Zhang Y, Wang XS. Expression of the SARS-CoV-2 cell receptor gene ACE2 in a wide variety of human tissues. Infect Dis Poverty. 2020 Apr 28;9(1):45. doi:10.1186/s40249-020-00662-x.

Plow EF, Haas TA, Zhang L, Loftus J, Smith JW. Ligand binding to integrins. J Biol Chem. 2000 Jul 21;275(29):21785-8. doi:10.1074/jbc.R000003200.

Xiong JP, Goodman SL, Arnaout MA. Purification, analysis, and crystal structure of integrins. Methods Enzymol. 2007;426:307-36. doi:10.1016/S0076-6879(07)26014-8.

Davis PJ, Goglia F, Leonard JL. Nongenomic actions of thyroid hormone. Nat Rev Endocrinol. 2016 Feb;12(2):111-21. doi:10.1038/nrendo.2015.205.

Davis PJ, Lin HY, Hercbergs A, Keating KA, Mousa SA. Coronaviruses and Integrin αvβ3: Does Thyroid Hormone Modify the Relationship? Endocr Res. 2020 Aug;45(3):210-215. doi:10.1080/07435800.2020.1767127.

Muller I, Cannavaro D, Dazzi D, et al. SARS-CoV-2-related atypical thyroiditis. Lancet Diabetes Endocrinol. 2020 Sep;8(9):739-741. doi:10.1016/S2213-8587(20)30266-7.

Desailloud R, Hober D. Viruses and thyroiditis: an update. Virol J. 2009 Jan 12;6:5. doi:10.1186/1743-422X-6-5.

De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet. 2016 Aug 27;388(10047):906-918. doi:10.1016/S0140-6736(16)00278-6.

Lania A, Sandri MT, Cellini M, Mirani M, Lavezzi E, Mazziotti G. Thyrotoxicosis in patients with COVID-19: the THYRCOV study. Eur J Endocrinol. 2020 Oct;183(4):381-387. doi:10.1530/EJE-20-0335.

Kam YW, Ahmed MY, Amrun SN, et al. Systematic analysis of disease-specific immunological signatures in patients with febrile illness from Saudi Arabia. Clin Transl Immunology. 2020 Aug 22;9(8):e1163. doi:10.1002/cti2.1163.

Pacheco Y, Acosta-Ampudia Y, Monsalve DM, Chang C, Gershwin ME, Anaya JM. Bystander activation and autoimmunity. J Autoimmun. 2019 Sep;103:102301. doi:10.1016/j.jaut.2019.06.012.

Alberti P, Beretta S, Piatti M, et al. Guillain-Barré syndrome related to COVID-19 infection. Neurol Neuroimmunol Neuroinflamm. 2020 Apr 29;7(4):e741. doi:10.1212/NXI.0000000000000741.

Toscano G, Palmerini F, Ravaglia S, et al. Guillain-Barré Syndrome Associated with SARS-CoV-2. N Engl J Med. 2020 Jun 25;382(26):2574-2576. doi:10.1056/NEJMc2009191.

Virani A, Rabold E, Hanson T, et al. Guillain-Barré Syndrome associated with SARS-CoV-2 infection. IDCases. 2020 Apr 18;20:e00771. doi:10.1016/j.idcr.2020.e00771.

Zulfiqar AA, Lorenzo-Villalba N, Hassler P, Andrès E. Immune Thrombocytopenic Purpura in a Patient with Covid-19. N Engl J Med. 2020 Apr 30;382(18):e43. doi:10.1056/NEJMc2010472.

Nathan N, Prevost B, Corvol H. Atypical presentation of COVID-19 in young infants. Lancet. 2020 May 9;395(10235):1481. doi:10.1016/S0140-6736(20)30980-6.

Jones VG, Mills M, Suarez D, et al. COVID-19 and Kawasaki Disease: Novel Virus and Novel Case. Hosp Pediatr. 2020 Jun;10(6):537-540. doi:10.1542/hpeds.2020-0123.

Verdoni L, Mazza A, Gervasoni A, et al. An outbreak of severe Kawasaki-like disease at the Italian epicentre of the SARS-CoV-2 epidemic: an observational cohort study. Lancet. 2020 Jun 6;395(10239):1771-1778. doi:10.1016/S0140-6736(20)31103-X.

Smith TJ, Hegedüs L. Graves' Disease. N Engl J Med. 2016 Oct 20;375(16):1552-1565. doi:10.1056/NEJMra1510030.

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. J Endocrinol Invest. 2020 Oct;43(10):1527-1528. doi:10.1007/s40618-020-01366-7.

Jiménez-Blanco S, Pla-Peris B, Marazuela M. COVID-19: a cause of recurrent Graves' hyperthyroidism? J Endocrinol Invest. 2020 Oct 6:1–2. doi:10.1007/s40618-020-01440-0.

Published

2020-10-01

Issue

Section

Clinical Case