SAT-367 Thyroid Storm Following Methimazole Discontinuation in a Patient With Persistent Postpartum Hyperthyroidism

Abstract Disclosure: K. Sanu: None. A. Al-thunaibat: None. P. Sidhu: None. A. Abualnil: None. C. Penaherrera: None. A 23 year old female with a history of hyperthyroidism initially attributed to postpartum thyroiditis, previously on Methimazole, presented to the emergency department with symptoms of tremors, anxiety, and palpitations. Her thyroid function tests (TFT) at that time revealed suppressed Thyroid-stimulating hormone (TSH) (0.04 mIU/L), normal Free T4 (1.56 ng/dL) and elevated free T3 (4.91 pg/mL). Thyroid receptor antibodies (TRAb), thyroid-stimulating immunoglobulin (TSI), and thyroid peroxidase antibodies (TPO) which were previously checked were undetectable. Her clinical presentation was highly concerning for thyroid storm with a Burch-Wartofsky Point Scale (BWPS) of 55. She was admitted to the intensive care unit (ICU), where she was treated with propylthiouracil (PTU), propranolol, and potassium iodide. Treatment with methimazole was also reinitiated which led to symptomatic improvement. Patient was discharged with endocrinology follow up and was referred for radioactive iodine (RAI) ablation which she has completed. She subsequently developed hypothyroidism and was started on levothyroxine 88 mcg daily, with ongoing improvement in symptoms and normalization of TFTs. This case highlights several key considerations in the management of antibody-negative hyperthyroidism. The development of thyrotoxicosis after discontinuation of Methimazole supports a diagnosis of Graves' disease rather than postpartum thyroiditis. As the medication is stopped, the underlying autoimmune process begins overproducing thyroid hormones which leads to a recurrence of thyrotoxicosis. Although rare, there are documented cases of patients with clinical features of Graves' disease without detectable TRAb. These negative results may be attributed to the conventional assays used. One study, Iliciki et al. reported that a small number of patients with Graves' disease did not have detectable TRAb but developed these antibodies after treatment (1). In cases of low antibody titers, the antibody assays may lack sensitivity resulting in false-negative results. A study performed by Ng HP and Kung AW demonstrated that immunization with a specific T cell epitope of thyroid peroxidase (TPO) can induce autoimmune thyroiditis in animal models (2). This highlights the role of T cell-mediated mechanisms in the pathogenesis of hyperthyroidism, bypassing the need for detectable antibodies. Increased vigilance is also needed in considering other causes of hyperthyroidism in these cases. Employing a multifaceted diagnostic approach which integrates clinical presentation, laboratory tests, and imaging play a valuable role in diagnosing and managing these patients. Presentation: Saturday, July 12, 2025