SUN-372 - From Hashimoto'S to Graves': A Case Report on A Rare Autoimmune Thyroid Disease Conversion

Introduction/

Background:
Autoimmune thyroid diseases (AITD), mainly Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), have distinct clinical manifestations and biochemical phenotypes responsible for overt hyperthyroidism and hypothyroidism, respectively. About 2–5% of the Western population is affected with marked female predominance. Pathophysiology involves autoantibodies causing glandular destruction in HT or hypersecretion in GD. Early HT may present with hyperthyroidism, complicating diagnosis, although antibody differences may assist. While transition from GD to HT is described, the reverse is rare, highlighting this case.

Case Presentation:
A 37-year-old hispanic female with prediabetes, alopecia areata, vitamin D deficiency and thyroid disorder presented for follow-up of abnormal thyroid tests. In 2021, labs showed negative TSI on two occasions, positive anti-TPO (227 IU/mL), TSH < 0.01, FT4 1.6 and TT3 126, consistent with Hashimoto’s thyroiditis in a thyrotoxic phase. She was asymptomatic and treated with methimazole for six months with monitoring. Four years later, testing demonstrated recurrent thyrotoxicosis with TSH < 0.01, FT4 2.00 and TT3 204. Antibodies revealed positive thyroglobulin antibodies (91 IU/mL) and markedly elevated TSI (205%), diagnostic of Graves’ disease. She reported 4-lb weight loss and intermittent fatigue. Methimazole was restarted with biochemical improvement. Due to lack of medical insurance, the patient was never able to undergo either conventional or nuclear medicine thyroid imaging.

Discussion:
This case illustrates a rare conversion from HT to GD supporting AITD as a dynamic spectrum rather than fixed entities. The initial presentation was consistent with Hashitoxicosis, a transient hyperthyroid phase from inflammatory hormone release rather than sustained TSH receptor stimulation. The later development of elevated TSI with overt thyrotoxicosis represented a clear immunologic shift toward Graves' disease. Prior studies report similar transitions, underscoring antibody evolution unpredictability in AITD. Coexisting autoimmune disease supports broader immune dysregulation. The mild clinical presentation despite biochemical hyperthyroidism aligns with reports of less severe disease following autoimmune hypothyroidism. This case emphasizes limitations of single-time-point antibody testing and the importance of serial assessment when patterns evolve.

Conclusion:
This case highlights diagnostic and therapeutic challenges of conversion from hypothyroidism to hyperthyroidism. Although conversion from Hashimoto's thyroiditis to Graves' disease is rare, awareness is critical, emphasizing close monitoring of fluctuating thyroid function, nonspecific symptoms and patient-centered therapy. Meticulous biochemical evaluation is essential to guide appropriate treatment.

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