A Grave Turn on Hashimoto’s Thyroiditis - A Case Series on Four Patients With Autoimmune Hypothyroidism that Converted to Grave’s Disease

Disclaimer: The view(s) expressed herein are those of the author(s) and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, or the Department of Defense or the U.S. Government. Introduction: The most common cause of hypothyroidism is Hashimoto’s thyroiditis, a destructive autoimmune injury to the thyroid gland. Rarely, autoimmune hypothyroidism can be caused by thyroid-stimulating hormone (TSH) receptor blocking antibodies (TSHRab), and can be difficult to differentiate clinically from Hashimoto’s. Grave’s disease is the most common etiology of hyperthyroidism, and is typically caused by activation from TSHRab acting as an agonist for the TSH receptor. Patients with autoimmune thyroiditis, whether from TSHRab or Hashimoto’s, have been infrequently reported to convert to Grave’s disease1–3. Presentation: We present four cases whom initially presented with typical symptoms of hypothyroidism, were diagnosed with autoimmune hypothyroidism and started on levothyroxine. All four cases were later found to be hyperthyroid and ultimately diagnosed and treated for Grave’s disease. Conclusion: Primary hypothyroidism can rarely transition to a hyperthyroid state, although these cases may be underreported. The mechanism isn’t well understood, but is hypothesized to be from a switch of a predominance of TSH receptor blocking antibodies (TBAb) to that of thyroid stimulating antibodies (TSAb)1. Assays using competitive binding for TSH receptor antibodies will not differentiate between blocking and stimulating antibodies4. A high index of suspicion is needed to diagnose these individuals. References: 1. McLachlan SM, Rapoport B. Thyrotropin-blocking autoantibodies and thyroid-stimulating autoantibodies: Potential mechanisms involved in the pendulum swinging from hypothyroidism to hyperthyroidism or vice versa. Thyroid. 2013;23(1). doi:10.1089/thy.2012.03742. Takasu N, Matsushita M. Changes of TSH-stimulation blocking antibody (TSBAb) and thyroid stimulating antibody (TSAb) over 10 years in 34 TSBAb-positive patients with hypothyroidism and in 98 TSAb-positive graves’ patients with hyperthyroidism: Reevaluation of TSBAb and TSAb in TSH-receptor-antibody (TRAb)-positive patients. J Thyroid Res. 2012;2012. doi:10.1155/2012/1821763. Gonzalez-Aguilera B, Betea D, Lutteri L, et al. Conversion to graves disease from hashimoto thyroiditis: A study of 24 patients. Arch Endocrinol Metab. 2018;62(6). doi:10.20945/2359-39970000000864. Li Y, Kim J, Diana T, Klasen R, Olivo PD, Kahaly GJ. A novel bioassay for anti-thyrotrophin receptor autoantibodies detects both thyroid-blocking and stimulating activity. Clin Exp Immunol. 2013;173(3). doi:10.1111/cei.12129