From Hashimoto's Thyroiditis to Graves' Disease: Autoimmune Thyroid Disease, a Dynamic Spectrum
Recommended Citation
Taleb M, Faber A, Simon R. From Hashimoto's Thyroiditis to Graves' Disease: Autoimmune Thyroid Disease, a Dynamic Spectrum. J Endocr Soc 2025; 9:A1161.
Document Type
Conference Proceeding
Publication Date
10-22-2025
Publication Title
J Endocr Soc
Keywords
atenolol, iodine, levothyroxine, teprotumumab, thyroid hormone, thyroid peroxidase, thyroid stimulating immunoglobulin, thyrotropin, thyrotropin receptor antibody, adult, adverse drug reaction, autoimmune thyroiditis, case report, clinical article, conference abstract, diagnosis, drug therapy, endocrine ophthalmopathy, exophthalmos, female, Graves disease, Hashimoto disease, human, hyperemia, hyperthyroidism, hypothyroidism, thyroid disease, thyroiditis
Abstract
Background: Hashimoto's thyroiditis (HT) and Graves' disease (GD) represent two kinds of thyroid-related autoimmune disorders, and while the two are related, they are clinically distinct. The shift from HT to GD is rare but possible. HT is the most common type of hypothyroidism in iodine-sufficient areas. It is characterized by the presence of high concentrations of antibodies to thyroid peroxidase (TPO). GD, on the other hand, is the most common cause of hyperthyroidism; characterized by TSH receptor antibodies (TRAbs), with a degree of anti-Tg and anti-TPO antibodies present in some. TRAbs, specifically thyroid-stimulating immunoglobulin (TSI), lead to the stimulation of the thyroid gland and the overproduction of thyroid hormones. Given the significant overlap in the types of antibodies present in the two disorders, the major difference lies in the predominance of one kind over the other. Although rare, a shift in this predominance is the mechanism through which the switch from HT to GD can occur. Clinical Case: This is a case of a 36-year-old female with a past medical history of hypothyroidism, presumably due to HT, diagnosed at the age of 26. After the initial diagnosis of hypothyroidism, the patient remained on levothyroxine for around 8 years. TSH was then found to be consistently suppressed, even with weaning levothyroxine completely off. Shortly afterward, the patient began to note exophthalmos (more so in the left eye). Antibody testing revealed elevated TRAb at 28 IU/L (normal <0.10 IU/L) with TSI elevated at 10.90 IU/L (normal <0.10 IU/L). Neck US showed a diffusely heterogeneous, hyperemic, and lobular thyroid with increased vascularity consistent with thyroiditis. The patient was started on Methimazole for the treatment of GD and Atenolol for symptomatic management which helped improve symptoms. However, she continued to experience worsening thyroid ophthalmopathy in the left eye. The patient was seen by an Oculoplastic specialist who started the patient on Teprotumumab for the treatment of severe thyroid eye disease. Conclusion: Autoimmune thyroid disorder is a spectrum with its dynamic nature stemming from the delicate balance of different characteristic antibodies. This case is a cardinal reminder of this, and it documents the rare but possible phenomenon of transitioning from a diagnosis of HT to GD. Furthermore, it underscores the importance of the close monitoring of thyroid studies and antibody profiles in patients with an autoimmune thyroid disease.
Volume
9
First Page
A1161
