ArticleCureus2025
Iodine Deficiency-Induced Thyrotoxicosis Mimicking Graves' Disease: A Case of Triiodothyronine (T3)-Predominant Hyperthyroidism Without Goiter.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Triiodothyronine (T3)-predominant thyrotoxicosis without goiter is uncommon, with differential diagnoses including Graves' disease, thyroiditis, and iodine deficiency-related autonomy. Diagnostic certainty can be challenging in resource-constrained settings. We describe a 41-year-old man who presented with palpitations, heat intolerance, and weight loss and reported exclusive use of non-iodized rock salt for three years. Examination revealed tachycardia and tremor without goiter or orbitopathy. Thyroid function tests showed suppressed thyroid-stimulating hormone, elevated free T3, normal free thyroxine, and negative thyroid autoantibodies. Ultrasound demonstrated a diffusely enlarged, non-nodular gland with normal echogenicity, while scintigraphy revealed diffuse homogeneous uptake. He was treated with carbimazole (20 mg/day, tapered to 5 mg) and propranolol (40 mg/day, later withdrawn) and was advised to switch to iodized salt at an intake of approximately 5 g/day. After nine months, the patient discontinued carbimazole on his own; two months later, thyroid function was normal, and he remained euthyroid over 24 months of follow-up without medication. Although thyrotropin receptor antibody-negative Graves' disease was initially suspected, the combination of sustained remission after therapy cessation, negative antibodies, and exclusive rock salt use supported a diagnosis of iodine deficiency-induced thyrotoxicosis. This case highlights the importance of dietary history and structured follow-up in evaluating atypical thyrotoxicosis and illustrates how iodine deficiency can mimic autoimmune hyperthyroidism in clinical practice.
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