Endocrine Abstracts

Hyperthyroidism in Graves’ disease (GD) is caused by thyroid-stimulating autoantibodies to the TSH receptor. Hypothyroidism in Hashimoto’s thyroiditis (HT) is associated with thyroid peroxidase and thyroglobulin autoantibodies. Transformation of HT to GD has been rarely reported. We report a woman with history of HT, who then developed GD.

Case presentation: A 50-year-old female with a past history of hypothyroidism due to HT treated with Levothyroxine from 2016 to 2018, presented in March 2020 with palpitations, dyspnea on slightest effort and dizziness. Thyroid gland was symmetrically normal, without any bruit. There were no ocular manifestations. Initial thyroid function tests revealed: TSH: < 001 mUI/l (0.27–4.20), FT4:37 pmol/l (12–22), TPO antibodies: 216 UI/ml (<34), TG antibodies: 202 UI/ml (< 34); TSH receptor antibodies: 10 U/l (< 1). Thyroid ultrasonography showed a multinodular gland with a nodule of 17 mm located in the left lobe. 99 m Tc pertechnetate scan showed a normal sized gland with increase uptake of radiocontrast, typical image of GD.

Comment: HT and GD represent the main two types of autoimmune thyroid disease. The conversion to GD from HT is a rare phenomenon which needs further immunological and genetic studies to explain this unusual autoimmune disorder and the time between hypothyroidism and the occurrence of hyperthyroidism. In our case, hyperthyroidism appeared 4 years after hypothyroidism due to HT.

References

1. Gonzalez-Aguilera B. Lutteri D. et al., Conversion of Graves’ disease from Hashimoto’s thyroiditis: a study of 24 patients. Archives of Endocrinology and Metabolism, 2018 62(6).

2. McMarcello M, Nagayama Y, et al. The link between Graves’ disease and Hashimoto’s thyroiditis: A role for regulatory T cell. Endocrinology, 2007 148.