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Endocrine Abstracts (2021) 73 AEP760 | DOI: 10.1530/endoabs.73.AEP760

La Mancha Emergency Hospital Center, Endocrinology, Alcázar de San Juan, Spain


Graves’ Disease is an autoimmune syndrome that include hyperthyroidism, goiter, thyroid eye disease, and occasionally, a dermopathy called pretibial or localized myxedema. As each autoinmune ailment to develop in sufferers with genetic susceptibility after a certain environmental exposure (infection, stress…). COVID-19 can cause both pulmonary and systemic inflammation, potentially determining multi-organ dysfunction. Since the outbreak of the SARS-CoV-2 pandemic, there have been many reviews of autoimmune illnesses brought about with the aid or associated with COVID-19. Our objective is to report a case of Graves’ Disease ocurring after recuperation from moderate coronavirus disease 2019 (COVID-19).

Case report

We describe a case of autoinmune hyperthyroidism (Graves’ Disease) ocurring after SARS-CoV 2 infection. A 24-yeas-old woman was admitted to hospital emergency department on October 29, 2020 reporting fever, myalgia, cough and general malaise for three days. Naso-pharyngeal swab test for SARS-CoV-2 was positive and chest X-ray turned into normal. She did not require hospitalisation and was discharged symptomatically. A week later she returned to the emergency room beacause of a sense of dizziness, tremor and palpitations. The EKG confirmed sinus rhythm at one hundred thiry beats per minute without others alterations. Thyroid function was assessed, showing suppressed serum TSH with increased free thyroxine. Also this analysis showed IgM and IgG against SARS-CoV-2 were positive. The female pronounced having lost 3-5 kgs in the last month, sweating and distant tremor. No goiter was found and she referred no cervical pain. She denied Family history of thyroid diseases. We requested thyroid antibodies and treatment with a combination of methimazole and beta blocker was started on Nov 13th, 2020. The patient started follow-up. On Dec 15th, 2020 and refered clinical improvement. The laboratory testing results included suppressed TSH, normal free T4 and free triiodothyronine, TSH receptor antibodies were positive. Clinical presentation, ultrasound and positive TSH receptor antibodies are well matched with a diagnosis of Graves’ disease.


We file the development of Graves’ Disease in a patient 1 week after the medical onset of SARS-CoV-2 infection. Previous chencking out of thyroid function was normal, and she had no medical signs or symptoms of hyperthyroidism previous to her contamination with COVID-19. Whether COVID-19 contributes to the development of Graves’ Disease, or the occurrence is coincidental, calls for definitive studies. This presentation may also align with the idea of a viral link in the development of autoimmune thyroid disease in people with genetic predisposition.

Volume 73

European Congress of Endocrinology 2021

22 May 2021 - 26 May 2021

European Society of Endocrinology 

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