Endocrine Abstracts

Radio-active iodine (RAI) therapy is effective in managing hyperthyroidism due to solitary toxic thyroid nodule, in which 90% efficacy is observed. The most common side effects of RAI include hypothyroidism, transient neck pain and dry mouth and eyes. Occasionally, transient worsening of hyperthyroidism or the development of new-onset Graves’ orbitopathy (GO) has been reported in patients with GD after RAI therapy. However, there is scant literature regarding the risk of developing new Graves’ disease following RAI. We report a case of a patient who was treated with RAI for mild hyperthyroidism due to solitary toxic thyroid nodule who developed severe hyperthyroidism and GO. A 38-year-old male patient was incidentally noted to have mild T3 toxicosis due to a solitary toxic thyroid nodule, based on negative TRAb and TPOAb levels and characteristic increased uptake on 99m-technetium scan and corresponding nodule on thyroid ultrasound. He had no family history of thyroid disorder and was a non-smoker. After discussion and obtaining written consent, and as per NICE guidelines, he received treatment with RAI 400MBq. About six weeks after his therapy, he complained of unexplained weight loss, palpitations, frequent stools and eye irritation. He was noted to be clinically and biochemically thyrotoxic (TSH of <0.01, FT4 64 pmol/l, FT3 24.5 pmol/l) with raised TRAb levels of 27.5U/l(reference range <1.8). He had evidence of inflammation in both eyes (clinical activity score or CAS of 1). He was commenced on propranolol, carbimazole, eye-lubricants, selenium and was reviewed regularly in clinic. Over the next few weeks, his thyroid hormones normalised but there was worsening of TRAb levels (72 U/l) and severity of GO (CAS of 4). Due to marked peri-orbital oedema, an urgent MRI of orbits was performed that demonstrated severe oedema and peri-orbital inflammation but no compression of the optic nerves. He was commenced on weekly intravenous methylprednisolone and his thyroid function remains stable on ‘block and replacement doses’ of carbimazole and levothyroxine. The GO is gradually responding to steroid therapy and the CAS score is now ranging between 2-3.

Conclusion: There are few reported cases of radioiodine induced de novo Graves’ disease in the literature. This case highlights the dual importance of clinicians being aware of and informing patients that RAI may induce Graves’ disease in a small group of patients. The exact mechanisms of how RAI leads to Graves’ disease are not well elucidated but may involve leakage of thyroid antigenic material following RAI treatment.