MON-344 - Severe Iodine Deficiency Mimicking Graves Disease: A Case of Hypervascular Goitre with Paradoxical Thyroid Function Tests

Severe iodine deficiency is uncommon in industrialised settings and may produce paradoxical biochemical patterns that resemble autoimmune thyroid disease. A 38-year-old man with longstanding restrictive eating behaviour was referred after abnormal thyroid function tests were noted on routine review (free T4 3.1 pmol/L (10–22) and TSH 8 mIU/L). His BMI was 14.8 kg/m² (weight 36.6 kg; height 157 cm). Apart from cholecalciferol 400 IU twice daily and calcium carbonate 1.25 g twice daily, he used no supplements. Dietary review demonstrated extremely low intake of iodine-containing foods, and there was no family history of thyroid-related disorders. He reported no symptoms of thyroid dysfunction. Examination revealed no clinical features of thyrotoxicosis, with a regular pulse of 76 beats per minute, but there was diffuse thyromegaly with an audible bruit. There were no eye signs or dermopathy to suggest Graves’ disease. Initial testing showed free T4 4 pmol/L (10–22), free T3 3.4 pmol/L (3.1–6.8), and TSH 6.3 mIU/L. Repeat assessment on a different platform showed concordant results, reducing the likelihood of assay interference. Sex hormone binding globulin (SHBG) was mildly elevated at 58 nmol/L, arguing against significant tissue hypothyroidism. The remainder of the pituitary profile including calculated free testosterone was normal, and thyroid autoantibodies were undetectable. Ultrasound demonstrated a bulky, markedly hyperperfused thyroid. A Tc-99m pertechnetate scan showed strikingly increased diffuse uptake of 43% (reference 0.2–3.5%), initially raising concern for Graves’ disease but physiologically compatible with severe iodine depletion. A 24-hour urinary iodine concentration (UIC) was profoundly low at 0.02 µmol/24 h (0.60–4.30). Thyroglobulin (Tg) was markedly elevated (607.7 µg/L) with negative Tg antibodies, consistent with TSH-driven thyroidal stimulation. The combination of elevated TSH, low T4, relatively preserved T3, raised Tg, and diffuse hyper-uptake reflects preferential T3 synthesis due to its lower iodine requirement. The increased T3/T4 ratio is a key adaptive response, as T3 has greater metabolic potency but requires less iodine for synthesis. Iodine supplementation at 300 µg/day led to normalisation of thyroid function (free T4 11.5 pmol/L, free T3 3.6 pmol/L, TSH 1.4 mIU/L), a marked fall in Tg to 26.5 µg/L, and regression of goitre and hypervascularity. UIC reflects recent iodine intake, Tg reflects intermediate changes, and thyroid size reflects long-term iodine status. Thyroid size may take months or years to return to normal following repletion. This case illustrates that profound iodine deficiency persists even in developed settings and may closely mimic autoimmune hyperthyroidism. Measurement of urinary iodine and thyroglobulin should be considered when thyroid function tests and imaging are discordant with typical etiologies.

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