PubMed1990
The liver plays a dominant role in the metabolism of the thyroidal hormones; it is here that the 5' deiodase acts to convert part of T4 to T3. There are eight further circulating iodothyronines: the rT3, mainly derived from T4, appears to be the major inhibitor of T4 and T3. Thus, if rT3 increases, the metabolic effects of T3 and T4 can be quite different. In the course of some chronic systemic diseases (e.g. hepatic cirrhosis) rT3 increases simultaneously with the decrease of T3 levels. Therefore we can describe particular alterations of the thyroidal pattern typical of chronic liver diseases: low T3 syndrome, low T3 and T4 syndrome, high T4 syndrome, mixed forms. T3 and T4 diminish due to inefficient hepatic deiodination and defective hepatocellular uptake. Inefficient hepatic deiodination and defective hepatocellular uptake. T4 levels decrease, most likely because of an inefficient production of thyroid binding globulin, or the action of a peripheral binding inhibitor. During acute liver diseases and primitive biliary cirrhosis, we can observe an increase of T4 and TBG together with an increase of the acute phase proteins. Such complex hormonal mechanisms are not influenced by TSH, which appears normal or inhibited, as the TRH stimulus test is normal. The explication can be found in an enhanced conversion of T4 to T3 in the pituitary gland. The biological and clinical significance of these mechanisms might be that of creating a "protective" state for an organism in a catabolic state by reducing the circulating T3. A relationship has been found between circulating thyroidal hormones levels, particularly the T3, rT3 and rT3/T3 ratio, and the state of hepatic functional insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)