Alteration in thyroid functions and nuclear T3 receptors [Nt3R] pinding capacity in chronic nonthyroidal illnesses

ABSTRACT

This study was carried out on 30 chronically ill patients and 10 normal control subjects. 10 patients were with chronic liver disease, 10 with chronic renal failure [CRF] and 10 were diabetics on insulin therapy. Thyroid functions and NT3R were measured by radioimmunoassay [R.I.A.]. The main objective of this study was to examine if changes in nuclear binding capacity for T3 might explain the maintenance of clinical euthyroidism during chronic illness. Hepatic and renal patients had significant decrease in T3 and a significant increase in TSH, whereas no significant changes in T4 could be detected, a condition known as low T3 syndrome. In diabetics, a non-significant decrease in T3 and T4 was observed together with a slightly significant increase in TSH. Binding of lymphocyte nuclei to [125I] T3 in hepatic and renal patients revealed decreased binding sites and increased binding capacity which could be explained as a compensated hypometabolic state which might be achieved by increased binding capacity for NT3R. In diabetics binding sites were increased while binding capacity were decreased. The explanation for these diverse hormonal changes may be related to the stress situation as a whole rather than to a particular disease. Moreover, these changes represent a beneficial adaptive homeostatic mechanism, and alteration by therapy with thyroid hormones in such cases interrupt physiological adaptive changes and is not recommended