Abstract
The interaction of thyroid hormones with specific nuclear receptors in target cells is generally thought to be the site of initiation of hormone action. We investigated nuclear triiodothyronine (T3) binding in lymphocytes of 4 patients with partial generalized THR. The patients had a chronological age of 3.5, 13, 2.3 and 26 years, respectively, were clinically euthyroid and exhibited goiters of different sizes. Total and free thyroxine (T4) and T3 were significantly elevated in the presence of inappropriately increased TSH. The mode of inheritance was autosomal dominant in patients III and IV (father and son).
Affinity constants (Ka) derived from Scatchard analyses of the T3 binding data were significantly decreased in the patients compared to controls. Our data suggest that THR is caused by a defective receptor affinity for T3. They are in contrast to published data (JCEM, 55, 502, 1982). Biochemically, THR seems to be a heterogeneous disorder with receptor and post-receptor defects.
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Heidemann, P., De Neyer, P., Rabl, W. et al. 10 NUCLEAR T3, RECEPTORS OF LYMPHOCYTES IN THYROID HORMONE RESISTANCE (THR). Pediatr Res 19, 605 (1985). https://doi.org/10.1203/00006450-198506000-00030
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DOI: https://doi.org/10.1203/00006450-198506000-00030