BACKGROUND: The effectiveness of short-term 3,5,3'-triiodothyroacetic acid 
(TRIAC) therapy for the treatment of hyperthyroidism caused by thyroid hormone 
resistance (RTH) has been documented. Here, we report a 3-year course of TRIAC 
therapy in an RTH boy, with a quantitative evaluation of the therapeutic effects 
and pharmacological study of TRIAC.
PATIENT FINDINGS: The gene encoding the thyroid hormone receptor beta (THRB) of 
the patient carries a P453T mutation. During treatment with up to 3.0 mg TRIAC 
per day, reduction in the thyroid volume, resolution of supraventricular 
arrhythmia, and decrease in thyroid-stimulating hormone (TSH) and free-thyroxine 
(FT4) levels were achieved. In addition, attention-deficit hyperactivity 
disorder (ADHD) symptoms improved, with a concomitant decline in the ADHD Rating 
Scale score.
SUMMARY: A TRIAC pharmacokinetic study, conducted using triiodothyronine level 
as a surrogate for TRIAC level, demonstrated that TRIAC disappears from the 
circulation rapidly and has a shorter duration of TSH secretion inhibitory 
effect in the RTH patient compared to that in the control subject. Studies of 
TSH and FT4 levels over a period of 3 years indicated that the TRIAC effect is 
dose dependent.
CONCLUSIONS: TRIAC was effective and safe in ameliorating the effects of 
hyperthyroidism and ADHD symptoms in a child with known genetic RTH. Further, it 
was demonstrated that TRIAC has a short half-life and functions dose 
dependently.