Abstract
The acute toxicity of levothyroxine ingestion is influenced by the dose ingested, the rate of conversion of thyroxine (T4) to triiodothyronine (T3), and the level of medical intervention. Approximately 21 million prescriptions for thyroid products were dispensed in the United States in 1986, accounting for 1.4% of all prescriptions. This wide availability leads to frequent acute overdoses. In 1986, the American Association of Poison Control Centers Data Collection System documented 2,231 acute toxic exposures to thyroid preparations.1 Several articles have appeared in the past few years concerning the relative toxicity and treatment of a patient with an acute ingestion of levothyroxine preparations.2-7
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