Iatrogenic Thyrotoxicosis Secondary to Compounded Liothyronine

A 71-year-old woman presented with ST segment elevation myocardial infarction (STEMI) associated with hypotension (100/70 mm Hg) and dizziness. Her husband stated that she appeared confused and was experiencing visual hallucinations. Her medical history was significant for hypertension, pulmonary embolism, hypothyroidism, and gastroesophageal reflux disease. Preadmission medications were reported as amlodipine 2.5 mg daily and pantoprazole 40 mg daily. She denied any recreational drug use or history of mental illness (including hallucinations). She was living independently at home with her husband. The patient’s atypical cardiac symptoms prompted referral to the neurology service. However, neurogenic causes such as Hashimoto encephalitis and cerebrovascular accident were ruled out by negative results on thyroid antibody testing and computed tomography of the head. Incidentally, the laboratory panel for Hashimoto encephalitis included measurement of thyroid hormones, which showed that the level of free tri-iodothyronine was greater than 50 pmol/L (normal range 3–6.8 pmol/L). Thyroidstimulating hormone was 0.03 mIU/L (normal range 0.34–5.6 mIU/L) and free thyroxine was 15 pmol/L (normal range 10–23 pmol/L). The thyroid was not examined, and Grave disease was ruled out on the basis of the normal thyroxine level. In light of the laboratory results, a more detailed investigation for an exogenous iatrogenic cause was initiated. The only discrepancy between the patient’s in-hospital medications and her preadmission medications was a compounded product that she had been taking before the admission, specifically compounded liothyronine capsules (25 μg of liothyronine in hydroxypropyl methylcellulose [hypromellose] for once-daily dosing). The diagnosis was iatrogenic thyrotoxicosis secondary to a compounding error involving liothyronine. The patient’s symptoms, her history related to the current illness, and the supratherapeutic level of tri-iodothyronine were consistent with acute toxicity. She was given supportive care until her mental status and hemo dynamics returned to normal and was then discharged to home. The consequences of the poisoning included STEMI, acute renal injury secondary to hypotension (with serum creatinine twice her baseline value), and a 13-day hospital stay for delirium. Hospital staff contacted the patient’s outpatient pharmacy and alerted them to these findings.

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