New-Onset Graves’ Thyrotoxicosis Following Long-Standing Autoimmune Hypothyroidism

A bstract Hashimoto’s thyroiditis (HT) and Graves’ disease (GD) are opposing conditions within the autoimmune thyroid disease spectrum, with spontaneous conversion from GD to HT being common but conversion from HT to GD being rarely seen. Here, I am reporting the case of a 27-year-old lady of Bangladeshi origin, a known case of primary hypothyroidism for the last 7 years, who was receiving treatment with 75 µg levothyroxine (LT4) once daily. Her initial thyroid-stimulating hormone (TSH) was 43 µIU/mL (normal: 0.35–5.5 µIU/mL). Additionally, she tested positive for anti-thyroid peroxidase (TPO) autoantibody (anti-TPO: 430.04 IU/mL; normal: <35 IU/mL). Everything was going well until the last 5–7 months, when the patient began experiencing excessive sweating, heat intolerance, and palpitations with significant weight loss (lost 7 kg) without any recent changes in her dietary habits. Thyroid function tests (TFTs) indicated biochemical thyrotoxicosis. The administration of LT4 was stopped for 3 months, but the patient was still thyrotoxic (TSH < 0.01 µIU/mL and T4: 15.2 µg/dL; normal: 4.5–12.0 µg/dL). She did not exhibit definitive signs of GD, such as orbitopathy, pretibial myxedema, or thyroid bruits. There was no evidence of thyroiditis or tenderness over the thyroid gland; she merely had a mild, diffuse goiter. TSH receptor antibody (TRAb) was found to be very high-titer-positive (TRAb: 15.39 IU/L; normal: <1.5 IU/L), indicating GD. Treatment was initiated with carbimazole 30 mg daily in divided doses. After 2 months of treatment, all clinical symptoms of thyrotoxicosis resolved, she gained 3 kg of weight, and her TFT reports almost normalized.