MON-361 - When Hashimoto Strikes Back: Hashitoxicosis Taking over the Heart

Hashitoxicosis represents the transient hyperthyroid phase of Hashimoto’s thyroiditis and results from inflammatory destruction of thyroid follicles with subsequent release of preformed thyroid hormones into the bloodstream. This phase may be precipitated by inflammatory stressors such as infection, systemic illness, or physiological stress. In patients with pre-existing hypothyroidism receiving levothyroxine therapy, Hashitoxicosis may be challenging to recognize and is often misattributed to iatrogenic hyperthyroidism, resulting in delayed diagnosis and management.
We report the case of a 41-year-old woman with a long-standing history of hypothyroidism on levothyroxine who was admitted with severe symptomatic anemia and atrial fibrillation with rapid ventricular response. Physical examination revealed no exophthalmos or goiter. Laboratory evaluation on admission showed a profoundly suppressed thyroid-stimulating hormone (TSH) level of 0.005 μIU/mL and a markedly elevated free thyroxine (T4) level of 7.55 ng/dL. Levothyroxine therapy was discontinued, and beta-blocker treatment was switched from metoprolol to propranolol; however, the patient’s clinical response remained suboptimal.
The hospital course was complicated by high-output heart failure, volume overload, acute respiratory failure requiring mechanical ventilation, bacteremia, and septic shock. Given the patient’s poor outpatient follow-up, iatrogenic hyperthyroidism from hormone over-replacement was initially suspected. However, despite cessation of levothyroxine, the patient demonstrated continued elevation of free T4 levels and cardiovascular deterioration requiring electrical cardioversion. Thyroglobulin and thyroid peroxidase antibodies were positive, consistent with underlying Hashimoto’s thyroiditis and supportive of a diagnosis of Hashitoxicosis. TSH receptor antibodies and thyroid-stimulating immunoglobulin (TSI) were obtained to assess for possible overlapping Graves’ disease. In light of ongoing severe thyrotoxicosis and clinical instability, treatment with propylthiouracil, dexamethasone, and cholestyramine were initiated. Targeted management resulted in both biochemical improvement and clinical stabilization. Management of tachyarrhythmia proved particularly challenging given the hyperthyroid state and cardiac complications, and iodine-containing antiarrhythmic agents, such as amiodarone, were avoided to prevent exacerbation of thyrotoxicosis via the Jod-Basedow phenomenon
This case highlights the importance of regular follow-up in patients with Hashimoto’s thyroiditis, early recognition of Hashitoxicosis, evaluation for coexisting Graves’ disease, and the complexity of managing thyrotoxicosis in patients with significant cardiovascular involvement.

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