RESUMEN
The effects of a single oral dose of liothyronine (L-T3) on thyroid stimulating hormone (TSH) and other related thyroid system parameters are partly understood despite therapeutic use of this hormone over many decades. We characterize individualized responses of the hypothalamus-pituitary-thyroid (HPT) axis and its related temporal hormonal profile using an electrical network model. Based on thyroid hormone responses from blood samples using a single 50 µg oral dose of liothyronine in healthy persons with a normal operating euthyroid feedback HPT system, we derived an equivalent electrical circuit model for the system's responses. The mathematical model was tested with a circuit simulator and validated with individualized clinical data. This signal processing technique makes the evaluation of bioequivalence and bioavailability of various preparations of liothyronine at an individualized level a feasible endeavor for clinical application.
RESUMEN
BACKGROUND: As changes in thyroid stimulating hormone (TSH), thyroid hormones, and vital signs after administration of a single dose of liothyronine have typically only been documented for 24 hours, we documented these parameters more than 96 hours. METHODS: Blood samples were obtained for 4 days after administration of 50-mcg liothyronine to 12 healthy euthyroid participants. Concentrations of total and free triiodothyronine, free and total thyroxine, and TSH were measured. Vital signs were documented. RESULTS: Triiodothyronine concentrations peaked at 2.5 hours after liothyronine administration. Heart rate (HR) increased by 5 hours after liothyronine administration, subsequently reaching a value higher than baseline (P = 0.009). Suppression of TSH concentrations began at 2 hours. The nadir TSH value at 12 hours was significantly different from baseline (P < 0.001) and remained lower than the baseline value for 2-3 days. CONCLUSIONS: A single dose of liothyronine has both short-term and long-term effects. There is clearly a different lag time between the serum concentrations of triiodothyronine and its effects on the heart and pituitary, respectively. The increase in serum triiodothyronine concentration occurred within hours and was then followed by an increase in HR. The increased HR was transient and was followed by a reduction in TSH concentration. The suppression of TSH was delayed but was more sustained. Thus, sustained TSH reduction beyond 24 hours was achieved by a single dose of liothyronine that produced only brief increases in serum triiodothyronine levels and transient increases in HR.