SUN-560 Thyrotoxic Hashimoto's Disease: Is It Graves' Thyrotoxicosis or "Hashitoxicosis"?

Abstract

Introduction: Hashimoto's Thyroiditis (HT) and Graves' Disease (GD) reflect two extremes in the spectrum of autoimmune thyroid diseases. In HT, there are anti-thyroid peroxidase antibodies thought, but not proven, to be destructive to thyroid follicles as well as thyroid stimulating hormone (TSH) stimulation-blocking antibodies which block the action of TSH and cause damage and atrophy of the thyroid gland leading to hypothyroidism. On the other hand, GD is characterized by primary hyperthyroidism due to stimulating autoantibodies against TSH receptors. While some of the patients with GD can develop spontaneous hypothyroidism due to HT, development of GD with hyperthyroidism following HT is unusual (1). We report a case of development of GD in a case of long standing HT. Case Report: A 55-year-old woman with a 20-year history of HT on stable doses of levothyroxine was found to be hyperthyroid on routine follow up. She presented with clinical signs of hyperthyroidism including weight loss of 40 pounds over 1 year and periorbital edema. The dose of levothyroxine was tapered and ultimately stopped over six months. Despite discontinuation of thyroid hormone, she continued to remain hyperthyroid. Labs were significant for elevated free T4 2.28 (0.82-1.77 ng/dL), elevated free T3 9.2, (2.0-4.4 pg/mL) and suppressed TSH, 0.006 (0.0-0.55 IU/L). Further testing revealed elevated thyroid antibodies including TSI of 10.4 (0.0-0.55 IU/L), Thyroglobulin Ab of 50.6 (0.0-0.9 IU/mL), TSH receptor Ab of 6.1 (>1.5 U/L positive) and TPO Ab of > 600 (0.0-34 IU/mL). Thyroid ultrasound disclosed an enlarged, heterogenous and hyperemic thyroid parenchyma. The 24-hour radioactive iodine uptake was elevated at 52% (8-35%) indicative of hyperthyroidism, most likely from GD. She was treated with methimazole and atenolol, followed by total thyroidectomy. Surgical pathologyrevealed diffuse chronic lymphocytic thyroiditis with lymphoid aggregates, fibrosis, adenomatous nodules with oncocytic changes and reactive nuclear atypia. Conclusion: Although development of GD following HT is rare, it can occur suggesting that HT does not always result in irreversible destruction of the thyroid gland. Patients with thyroid autoimmune disease have both thyroid hormone receptor stimulating and thyroid hormone receptor blocking antibodies and clinical manifestations depend upon the level of these antibodies and the state of the thyroid gland. Because patients with HT can transform to GD at any point due to a change of blocking to stimulating antibodies, clinicians should be aware of the potential for this transformation.