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Endocrine Abstracts (2024) 99 EP1029 | DOI: 10.1530/endoabs.99.EP1029

ECE2024 Eposter Presentations Thyroid (198 abstracts)

Methimazole-Resistant graves’ disease: a case report

Meriem Adel 1 , Marwa Chiboub 1 , 2 , Ons Smairi 1 , Manel Jemel 1 & Ines Kammoun 1


1National Institute of Nutrition and Food Technology, Endocrinology, Tunis; 2Tunisia, Endocrinology, Tunis, Tunisia


Introduction: Graves’ disease (GD), the most common cause of hyperthyroidism, is an organ-specific autoimmune disease. Initial treatment of GD is based on antithyroid drugs (ATDs). However, few cases of resistance to ATDs have been described in the literature. Here, we report a GD patient who suffered from resistance to ATDs requiring an early definitive therapy.

Case presentation: A 30-year-old female patient was referred to our institution for management of resistant thyrotoxicosis. She had no significant medical or surgical history. The diagnosis of Graves' disease was established based on clinical signs of thyrotoxicosis, goiter and eye signs. Laboratory findings objective high free thyroxine (FT4) concentrations, low TSH concentration and positive levels of TSH receptor autoantibody. Initial treatment involved prescribing 1 mg of Methimazole and 1 mg of Propranolol. However, despite good compliance, FT4 levels remained elevated for few months. Corticosteroid therapy at a dose of 30 mg of prednisolone was added for one month but thyroid function tests remained unchanged. Therefore, the patient was given 3 boluses of 1 mg of Solumedrol per day in combination with Methimazole 40 mg/d. seven days later, FT4 levels decreased to 39.8 pmol/l. In the presence of a FT4 level close to the normal range, the patient underwent definitive treatment. She received 15 mCi of radioactive iodine. The biological control one month after radioiodine therapy revealed a normal level of FT4 with decreasing clinical signs.

Discussion: For many years, ATDs have been the primary treatment for Graves' disease due to their ability to swiftly achieve euthyroidism with a lower likelihood of progressing to permanent hypothyroidism compared to alternative therapies. The occurrence of resistance to ATDs is uncommon, and the mechanisms behind such resistance remain unclear due to limited cases. Potential etiologies encompass malabsorption, elevated metabolism, drug antibodies, and irregularities in the intrathyroidal accumulation or action of the drugs. The approach to handling resistance to ATDs is not yet clearly defined. Alternative approaches have been suggested for such situations, including Lugol's solution, lithium carbonate, cholestyramine, and plasma exchange. These aim to achieve prompt euthyroidism before administering definitive treatment.

Conclusion: Managing resistance to ATDs in GD remains a complex issue due to the lack of well-defined diagnostic methods and established secure treatment approaches.

Volume 99

26th European Congress of Endocrinology

Stockholm, Sweden
11 May 2024 - 14 May 2024

European Society of Endocrinology 

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