SUN-576 Thyrotoxicosis Due to Liothyronine Therapy for Treatment-Resistant Bipolar Disorder

Abstract A. Newman: None. G.K. Adler: None. Exogenous thyrotoxicosis is caused by excess consumption of thyroid hormone preparations, primarily levothyroxine (T4) or mixed T4-T3 preparations (e.g. desiccated thyroid). Herein, we report the case of a 42-year-old man with bipolar II disorder and anxiety who presented with muscle weakness and inability to stand. Medications were notable for lithium carbonate, alprazolam, doxepin, hydroxyzine, and propranolol (80 mg/day in divided doses). In addition, he had been started on liothyronine for treatment-resistant bipolar II disorder 3 months prior to admission. Liothyronine had been titrated up to 150 mcg daily according to a protocol recommending initiation at 25 mcg daily with weekly dose escalation by 25 mcg increments until psychiatric response, thyrotoxic adverse effects or 150 mcg maximum daily dose. Medications were taken as prescribed based on the patient’s family’s count of remaining pills. TSH on lithium and prior to starting liothyronine ranged from 3.4 to 6.3 mIU/mL (assay reference range: 0.28 – 3.89) with normal free T4, consistent with euthyroidism to mild subclinical hypothyroidism. Physical exam on presentation was notable for normal vital signs with heart rate of 88 bpm, BMI of 36.3 kg/m2, bilateral upper extremity action tremor, no hyperreflexia, and mild, diffuse muscle weakness with proximal predominance. Labs revealed TSH < 0.01 mIU/mL (0.50-5.70), low free T4 of 0.5 ng/dL (0.9-1.7), total T3 > 500 ng/dL (80-200), negative thyroid peroxidase and TSH receptor antibodies, and lithium level in the therapeutic range. Liothyronine was discontinued and thyroid function tests were repeated every 12 hours. His total T3 fell rapidly, with an initial half-life of about 12 hours. The patient was discharged after 2 days, with a total T3 of 123 ng/dL (80-200). Due to concern for transient iatrogenic central hypothyroidism, levothyroxine was initiated on discharge. In outpatient telemedicine follow up, he reported improvement in muscle strength and ambulation over a 2–4-week timeframe. TSH levels normalized and levothyroxine was tapered. This is an unusual case of isolated T3 thyrotoxicosis due to chronic excess liothyronine use. Propranolol likely masked the signs and symptoms of thyrotoxicosis expected with liothyronine supplementation at a dose four times higher than his predicted daily endogenous triiodothyronine production. However, his presenting weakness may represent thyrotoxic myopathy, previously described only in T4 thyrotoxicosis such as Graves disease. This case demonstrates that the cardiovascular masking effect of beta-blockade in T3 thyrotoxicosis may not extend to other adverse effects of chronic excess liothyronine use, such as thyrotoxic myopathy, and that any supraphysiologic treatment with thyroid hormone should be undertaken with care and close monitoring. Sunday, June 2, 2024