[The low triiodothyronine syndrome--the cause or the result of a critical state?].

A comprehensive review of the deiodinating pathway of thyroxine (T4) metabolism including its conversion to triiodothyronine (T3) and reverse triiodothyronine (rT3) presented with special attention to intracellular events and their regulation. In addition, present knowledge on T3 syndrome in nonthyroidal diseases (definition, pathophysiology, clinical stages, differential diagnosis of thyroid disorders, treatment) is briefly reviewed. The question is being raised whether low T3 syndrome should be considered the consequence or rather the cause of critical stages of major nonthyroidal diseases. Though the view of some authors considering this syndrome a homeostatic mechanism enabling survival of the organism under critical conditions is fully observed, it is hypothesized that, under certain conditions, a stepwise decrease of T3 formation becomes irreversible. Considering the role of T3 in the expression of essential metabolic enzymes, such an irreversible stage may result in very unfavorable metabolic conditions of vital organs, an assumption supported by the high mortality rate of critically ill patients with very low plasma T3 and T4 levels reported by several authors. This problem warrants further attention involving attempts to find appropriate methods of treatment. Finally a brief review of the author's own experimental approach to the study of the regulation of T4 deiodination in rat liver in vivo based on the determination of billiary excretion of T4, T3 and rT3 by radioimmunoassay is presented. As published elsewhere, the excretion of rT3 was acutely increased after administration of adrenaline (which was mediated by alpha 1-adrenoceptors) and of other glycogenolytic and gluconeogenic hormones such as glucagon, vasopressin and angiotensin II. These findings lead to the conclusion that 5'-monodeiodination in the liver is inhibited under conditions of prevailing gluconeogenesis which may explain the decrease of T3 formation under fasting and under reduced caloric intake in severe nonthyroidal diseases. (Fig. 6, Ref. 64).