srpski
Abstract
Graves’ orbitopathy (GO), the most common extrathyroidal manifestation of autoimmune hyperthyroidism, typically occurs within the first year after diagnosis, although it may rarely develop in euthyroid and hypothyroid patients as well. Following total thyroidectomy, GO may develop in approximately 10–20% of patients, symptoms usually appear several months to one year after surgery. The risk is higher in patients with elevated thyrotropin receptor antibodies (TRAb), smokers, and patients who do not initiate levothyroxine replacement therapy promptly. Intravenous corticosteroid therapy represents the first-line treatment. A 69-year-old female patient with autoimmune thyroid disease initially presented with autoimmune hyperthyroidism and received antithyroid drug therapy for five years without developing orbitopathy during treatment. Failure to achieve sustained disease control, second-line treatment was implemented, and total thyroidectomy was performed, resulting in hypothyroidism and hypoparathyroidism. Subsequently, she was adequately substituted with levothyroxine, alfacalcidol, and calcium supplementation. The patient also underwent surgery for colon adenocarcinoma and received chemotherapy postoperatively. Nine years after thyroidectomy, despite regular vaccination, she developed COVID-19 infection and was treated with biologic therapy consisting of a monoclonal antibody targeting the SARS-CoV-2 spike protein, together with antiviral treatment. Eleven years after total thyroidectomy, the patient developed moderate-to-severe GO with moderate clinical activity, intermittent diplopia, and elevated TRAb levels. Intravenous corticosteroids resulted in a satisfactory therapeutic response. The occurrence of GO, as the most common extrathyroidal manifestation of autoimmune hyperthyroidism, is exceptionally rare several years after the onset of hyperthyroidism and even more uncommon following surgical treatment of autoimmune hyperthyroidism. COVID-19 infection, biologic therapy, and coexisting comorbidities may have acted as potential triggers for reactivation of autoimmune processes in this patient.
References
2. Tay WL, Loh WJ, Lee LAL, Chng CL. Persistent hyperthyroidism and de novo Graves’ ophthalmopathy after total thyroidectomy. Endocrinol diabetes Metab case reports. 2017;2017.
3. Eckstein AK, Plicht M, Lax H, Neuhäuser M, Mann K, Lederbogen S, et al. Thyrotropin receptor autoantibodies are independent risk factors for Graves’ ophthalmopathy and help to predict severity and outcome of the disease. J Clin Endocrinol Metab. 2006 Sep;91(9):3464–70.
4. Bartalena L, Kahaly GJ, Baldeschi L, Dayan CM, Eckstein A, Marcocci C, et al. The 2021 European Group on Graves’ orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves’ orbitopathy. Eur J Endocrinol. 2021 Aug;185(4):G43–67.
5. Khoo TK, Bahn RS. Pathogenesis of Graves’ Ophthalmopathy: The Role of Autoantibodies. 2014;17(10):1013–8.
6. Macovei ML, Azis Ű, Gheorghe AG, Burcea M. A systematic review of euthyroid Graves ’ disease ( Review ). 2021;
7. Eckstein A, Dekowski D, Führer-Sakel D, Berchner-Pfannschmidt U, Esser J. [Graves’ ophthalmopathy]. Ophthalmologe. 2016 Apr;113(4):346–9.
8. Čivrný J, Karhanová M, Hübnerová P, Schovánek J, Heřman M. MRI in the assessment of thyroid-associated orbitopathy activity. Clin Radiol. 2022 Dec;77(12):925–34.
9. Jespersen S, Nygaard B, Østergaard L. Methylprednisolone Pulse Treatment of Graves ’ Ophthalmopathy Is Not Associated with Secondary Adrenocortical Insufficiency. 2015;222–5.
10. Wang L, Chen L. Emerging therapeutic approaches in Graves’ ophthalmopathy : an update on pharmacological interventions. 2025;(July):1–8.