SAT-375 From Hypothyroidism to Hyperthyroidism: Interplay Between Hashimoto’s Thyroiditis and Graves’ Disease in a Case of Coexisting Autoimmune Thyroiditis

Abstract Disclosure: R.G. Vaca: None. A.N. Delgado Nieves: None. P.A. Goulden: None. Background:Autoimmune thyroiditis encompasses a spectrum of conditions ranging from hypothyroidism to hyperthyroidism, primarily Hashimoto’s thyroiditis (HT) and Graves’ disease (GD). These conditions often coexist, and transitions between them, though rare, offer insight into their pathophysiology. Case Presentation: A 63-year-old woman with a history of asymptomatic chronic HT, initially euthyroid, presented with a mildly elevated TSH (4.262 uIU/mL) and low free T4 (0.70 ng/dL). Levothyroxine (88 mcg) was initiated but caused diarrhea, leading to discontinuation. Her TSH normalized without treatment but fluctuated over time, warranting lower-dose levothyroxine (25 mcg), stabilizing her thyroid function. A year later, following a COVID-19 diagnosis, she developed symptoms of insomnia, anxiety, and suppressed TSH (0.008 uIU/mL) with normal free T4 (1.29 ng/dL). Further testing revealed positive thyroid-stimulating immunoglobulin (TSI, 4.09 IU/L), thyroid peroxidase antibodies (TPO, 53.1 IU/mL), and hyperemic thyroid parenchyma on ultrasound. A radioactive iodine uptake (RAIU) scan showed diffusely heterogeneous uptake (13.9% at 24 hours). Despite stopping levothyroxine, TSH remained suppressed, free T4 normalized, and she experienced worsening anxiety and osteoporosis (T-score -2.7). Thyrotropin receptor antibody (TRAb, 2.58 IU/L) positivity confirmed Graves’ disease, and low dose methimazole with propranolol was initiated. Discussion: This case illustrates the rare transition from Hashimoto’s thyroiditis to Graves’ disease, highlighting the interplay between antibody profiles. Both conditions share TPO antibodies in up to 70% of cases, but TRAb, typically associated with Graves’ disease, was the key diagnostic marker. The patient’s preserved thyroid function, evidenced by RAIU uptake, suggests sufficient thyroid tissue capable of responding to TRAb stimulation. SARS-CoV-2 may have triggered GD onset through thyroid antigen release, a mechanism seen with other viruses. While progression from Graves’ disease to Hashimoto’s thyroiditis occurs in 20% of cases, Hashimoto’s to Graves transitions are uncommon due to the chronic damage induced by TPO antibodies. This case underscores the need for close monitoring in autoimmune thyroiditis patients, particularly after viral illnesses, as shifts in thyroid function may have significant clinical implications. Conclusion: This case highlights the dynamic nature of autoimmune thyroid diseases and the potential influence of external triggers like SARS-CoV-2. Further research is needed to elucidate mechanisms underlying the rare transition from Hashimoto’s thyroiditis to Graves’ disease and the role of viral infections in triggering such changes. Presentation: Saturday, July 12, 2025