MON-455 - Thyrotoxicosis in the Pursuit of Wellness: Off-Label Liothyronine Use in an Euthyroid Patient

Liothyronine is typically reserved as adjunctive therapy in the management of hypothyroidism because of its short half-life and narrow therapeutic index. Its use has increasingly expanded into off-label indications in euthyroid patients, including refractory depression and treatment-resistant bipolar disorder, with emerging evidence also suggesting potential benefits in Alzheimer’s disease. Given its narrow therapeutic index, liothyronine increases the risk of developing hyperthyroidism and thyrotoxicosis. Our case highlights the dangers of off-label liothyronine leading to overt hyperthyroidism in a previously euthyroid patient.

A 67-year-old lady with no pertinent past medical history presented to the hospital for two weeks of shortness of breath and chest palpitations. Throughout the week, her symptoms progressed and became persistent, prompting her visit to the emergency department (ED). Upon arrival to the ED, initial vitals were significant for tachycardia to 136. EKG demonstrated sinus tachycardia, and CT angiography ruled out pulmonary embolism. Her thyroid-stimulating hormone (TSH) was suppressed at 0.008 mcIU/mL (0.35-5.0), free thyroxine (T4) was low at 0.4 ng/dl (0.8-1.5), and free triiodothyronine (T3) was elevated to 10.4 pg/ml (2.2-4.0). She was started on metoprolol 25 mg twice daily and admitted for further evaluation and concerns for thyrotoxicosis.

Upon further interrogation, the patient endorsed taking Liothyronine 15 mcg twice daily since 2010. She was started on this medication for “anti-aging” by her wellness PCP despite no prior biochemical evidence of hypothyroidism. The dose had recently been increased due to persistent fatigue. Endocrinology was consulted and recommended discontinuation of liothyronine. Alternative thyroid hormone replacement was not re-initiated. Repeat testing of her thyroid hormones 48 hours after discontinuation showed drastic decreases in T3 (1.3 pg/ml) and free T4 (0.8 ng/dl). Her symptoms improved, and she was discharged without thyroid replacement hormone. On subsequent clinic follow-up, she reported complete resolution of symptoms. Her thyroid function tests showed improvement, with a free T4 of 0.9 ng/dL and a free T3 of 2.4 pg/ml, without the need for thyroid medication.

This case highlights off-label liothyronine usage as a rare cause of iatrogenic thyrotoxicosis, which can be detrimental. Studies vary regarding the need to use levothyroxine in these patients as a bridge until the pituitary-thyroid axis recovers. Our patient was fortunate that her pituitary-thyroid axis improved spontaneously after stopping liothyronine. Increased liothyronine use for non-thyroid indications in patients with an euthyroid state may increase risks of life-threatening thyrotoxicosis and subsequent thyroid hormone suppression.

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