Iodine Deficiency-Induced Thyrotoxicosis Mimicking Graves’ Disease: A Case of Triiodothyronine (T3)-Predominant Hyperthyroidism Without Goiter

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 He was treated with carbimazole (20 mg/day, tapered to 5 mg) and propranolol (40 mg/day, later withdrawn) and was advised to switch to iodized salt at an intake of approximately 5 g/day.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.