7683 Tipping the Balance: Development of Graves’ Disease in a Patient with Longstanding Hashimoto’s Thyroiditis

Abstract Disclosure: K.S. Hazen: None. B.J. Gigliotti: None. Background: Development of persistent Graves’ hyperthyroidism in patients with hypothyroidism from Hashimoto’s thyroiditis is a rare phenomenon that is presumed to be due to a shift in the shift in the balance of inhibitory, neutral, and stimulatory thyroid stimulating hormone (TSH) receptor autoantibodies. Clinical Case: A 70-year-old female with a history of obstructive sleep apnea, hypertension, hyperlipidemia, osteopenia, positive antinuclear antibody, positive antinuclear ribonucleoprotein antibody, and hypothyroidism on relatively stable dose of levothyroxine 75 mcg 6 days weekly for about 20 years was slowly weaned off levothyroxine over 3 years by her primary care physician due to persistently low TSH levels. Symptoms included increased thirst, cold intolerance, dry skin, increased appetite, and fatigue. Exam showed no thyromegaly. Despite levothyroxine discontinuation, her TSH remained suppressed at 0.21 uIU/mL (0.27-4.20 uIU/mL) with normal free T4 1.0 ng/dL (0.9-1.7 ng/dL) and total T3 122 ng/dL (80-200 ng/dL). The patient had been taking biotin, but thyroid function testing remained unchanged after discontinuation. Additional testing revealed a thyroid stimulating immunoglobulin (TSI) 29.30 IU/L (<= 0.54 IU/L), TSH receptor antibody 33.40 IU/L (<= 1.75 IU/L), thyroglobulin Ab >2,500.0 IU/ml (0.0-3.9 IU/mL), and thyroid peroxidase Ab 2,792.8 IU/mL (0.0-8.9 IU/mL). After remaining off the levothyroxine for several months, her TSH rose to 11.20 uIU/ml (0.27-4.20 uIU/mL) and she was restarted on low dose levothyroxine with a subsequent decrease in TSH to 0.11 uIU/ml (0.27-4.20 uIU/mL) after 5 weeks. Conclusion: This case demonstrated a rare situation in which a patient with hypothyroidism from Hashimoto’s thyroiditis subsequently developed hyperthyroidism from Graves’ disease. Given she was not on a weight-based levothyroxine replacement dose, it is suspected she still had underlying active thyroid tissue that was able to respond to stimulatory antibodies. Elevation of the TSH receptor antibody and TSI suggest that the patient also had underlying Graves’ disease with either new onset, or a possible shift of antibodies from inhibitory or neutral to stimulatory, resulting in decreased levothyroxine requirement and subsequent endogenous hyperthyroidism. This demonstrates the importance of considering non-iatrogenic causes of dramatic changes in levothyroxine dose requirements and close monitoring required for such patients. Presentation: 6/2/2024