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Author: Admin | 2025-04-28
Ranging from 1500 to 3750 μg. None of the children had any serious adverse event. Pharmacokinetics of thyroid hormones Levothyroxine is thyroxine (T4) analog, which is the predominant circulating form of thyroid hormone. In the peripheral tissues, T4 is partially converted to liothyronine (T3), a more biologically active thyroid hormone. Since T4 is pharmacologically inactive, T3 is the substance responsible for the development of toxic symptoms. It is clear that if any symptoms appear, they are delayed in onset as levothyroxine must achieve peripheral conversion to T3. Pharmacological data also show that Tmax of levothyroxine is reached at 5–6 h after oral intake. Elimination half-life (T1/2) is 7 d for T4 and 0.8 d for T3. Exogenously administered thyroid hormone indirectly suppresses the thyroid gland activity, decreases the TSH level. Lewander et al.[2] specifically studied the pharmacokinetics of T4 and T3 in acute T4 intoxication in 7 patients. Their findings indicate a mean T1/2 for T4 of 2.8 d, which is shorter than the T1/2 observed in physiologic concentrations (7 d in children) and a T1/2 for T3 of 6 d, which is almost five times longer than in physiologic concentrations. Furthermore, the peak concentration of T3 is reached at >24 h after the ingestion. This favors the conclusion that delay in onset of symptoms and duration of toxicity is due to the conversion from levothyroxine to T3 and prolonged elimination time of T3 in acute overdose. In our patient, the peak concentration of T3 was on day 2, with T3 reaching normal values after 14 days. This explains the occurrence of a delay in symptoms after levothyroxine overdose. The usual dose of levothyroxine in hypothyroid pediatric patients is 2–6 μg/kg/d in one dose. Our patients ingested 50 μg/kg to 200 μg/kg, 25–35 times the standard dose, and they were
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