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ODP531 Worsening of pretibial myxedema following repeated doses of radioiodine treatment in a patient with hyperthyroid Graves’ disease

INTRODUCTION: The development of new-onset pretibial myxedema following radioiodine (RAI) treatment has been occasionally reported from the probable influences of thyrotropin receptor antibodies (TRAbs) similar to the RAI-associated Graves’ ophthalmopathy (GO). However, the worsening of pre-existing...

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Detalles Bibliográficos
Autores principales: Thewjitcharoen, Yotsapon, Chatchomchuan, Waralee, Wanothayaroj, Ekgaluck, Veerasomboonsin, Veekij, Nakasatien, Soontaree, Himathongkam, Thep
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9627694/
http://dx.doi.org/10.1210/jendso/bvac150.1630
Descripción
Sumario:INTRODUCTION: The development of new-onset pretibial myxedema following radioiodine (RAI) treatment has been occasionally reported from the probable influences of thyrotropin receptor antibodies (TRAbs) similar to the RAI-associated Graves’ ophthalmopathy (GO). However, the worsening of pre-existing pretibial myxedema after RAI treatment has never been reported. Herein, we report an interesting case of fluctuating clinical course of pretibial myxedema following treatments of hyperthyroid Graves’ disease for over 3 years. CASE REPORT: A 49-year-old Thai woman with underlying hyperthyroid Graves’ disease with GO and pretibial myxedema for 1 year came to our hospital for relapsed hyperthyroidism and active, moderate-to-severe GO in 2019. A plague form of pretibial myxedema with indurated hyperpigmented lesion was found on both legs. Intravenous pulse methylprednisolone (IVMP) was given to control her active GO. Both GO and pretibial myxedema significantly improved after IVMP treatments. Then, RAI (30 mCi) was administered at 1 month later as a definitive treatment. Low dose of oral prednisolone (20 mg/ day) was also given before and after RAI treatment. Transient hypothyroidism developed at 4 months post-RAI and the estimated weights of the thyroid decreased from 60 grams to 30 grams. However, hyperthyroidism relapsed again within 6 months post-RAI treatment. At that time, her pretibial myxedema flared up slightly but her GO was still inactive. Eventually, a second dose of RAI (20 mCi) was given at 11 months apart from the first RAI administration. Low dose of oral prednisolone was also given. She developed post-radiation thyroiditis at 4 months after RAI with worsening of pretibial myxedema and mild exacerbation of GO. Topical corticosteroid ointment was given for pretibial myxedema and only local supportive measures was applied to treat GO. Finally, permanent hypothyroidism was achieved at 6 months after the second course of RAI. Currently, her pretibial myxedema is stable without further flareup. CONCLUSION: Our case highlights the potential of RAI treatment to precipitate both GO and pretibial myxedema in patients with pre-existing skin lesions. Low dose prednisolone prophylaxis might not ensure preventative effect in exacerbation. Whether the risk of worsening of pretibial myxedema is higher in patients with persistent hyperthyroidism requiring a second dose of RAI is a question that warrants further studies. Presentation: No date and time listed