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Background: Subacute thyroiditis (SAT) is a transient inflammatory disorder of the thyroid gland, whereas Hashimoto thyroiditis (HT) is an autoimmune disorder. These two disease entities have quite different pathogenic mechanisms and typically do not co-occur. The objective of this report is to describe a patient with HT with eventual evolution into SAT to euthyroid. We review the diagnostic challenges of an uncommon presentation of Hashimoto thyroiditis with SAT. Clinical Case:52-year old female diagnosed with Hashimoto thyroiditis with subsequent development of hypothyroidism 10 years ago presented to our endocrinology clinic for the management of hyperthyroidism. She was diagnosed previously 10 years ago with reported elevated TSH, low FT4 and positive antibody testing assumed to include elevated anti-thyroid peroxidase. Therefore, at the time of her diagnosis she was started on levothyroxine 25 mcg daily and increased over time to 75 mcg daily. Approximately several months prior to her clinic visit with us, she began having a sore throat with subsequent development of voice hoarseness and tachycardia associated with palpitations lasting persistently for 1 month. She endorsed symptoms 2 months prior with having pain in her lower anterior neck described as non-radiating, intermittent and sharp associated with voice hoarseness, palpitations, racing heart and jitteriness that was exacerbated while palpating area. Her symptoms have since improved to having mild voice hoarseness. Her past medical history aside from hypothyroidism is Celiac disease and migraines. Her medications included Erenumab 70 mg once monthly and sumatriptan 100 mg as needed. During her evaluation, her blood pressure was 120/75, heart rate 72 bmp, temperature 36.0 C. Her physical exam was remarkable for mild tenderness of the anterior inferior midline neck without obvious masses or lesions. Ultrasound of her neck revealed heterogenous echotexture of the entire thyroid gland is noted with diffuse increased vascularity. The right thyroid lobe measured 4.2 x 1.0 x 1.5 cm and left thyroid lobe measures 4.0 x 1.0 x 1.3 cm without focal lesion is noted within either lobe. The soft tissues of the neck are unremarkable. There are no abnormal masses or fluid collections. Visualized lymph nodes are unremarkable in size and did not demonstrate increased vascularity. These findings were consistent with thyroiditis. Laboratory values obtained during her initial symptoms revealed slight hyperthyroidism with a TSH 0.05 mU/L (normal range, 0.8 to 1.7 mU/L) and FT4 2.0 ng/dL (normal range, 0.45 - 4.50 ng/dL), therefore her treatment with levothyroxine was discontinued. She was not started on any additional treatment as her symptoms were self-resolving. Repeat laboratory values in 4 weeks showed completely normal thyroid laboratory value with TSH 4.36 mU/L (normal range, 0.8 to 1.7 mU/L) and FT4 1.1 ng/dL (normal range, 0.45 - 4.50 ng/dL). Conclusion: HT is thought to be autoimmune in origin with lymphocytic infiltration and fibrosis. Early in the disease course, hyperthyroidism may result from destruction of the thyroid gland cells. HT is known to be a life-long disorder with essentially a non-functional thyroid. It is well established that SAT may evolve to HT and that HT may transform in Grave’s disease. Additionally, painful HT mimicking SAT has also been reported. There have been few reported cases of HT progressing into hyperthyroidism secondary to SAT and further resolution to euthyroid function.

SUN-LB89 Resolution of Hashimoto Thyroiditis: A Case of Hashimoto Thyroiditis Evolving Into Subacute Thyroiditis and Euthyroidism