FUNCTIONAL RELATIONSHIPS BETWEEN THE LIVER, THE THYROXINE-BINDING PROTEIN OF SERUM, AND THE THYROID*

Abstract

Various aspects of the effect of liver damage on thyroid function were studied in 35 cases of liver disease (with 30 normal controls) and in a group of thyroidectomized rats made toxic with carbon tetrachloride. Acute, severe, diffuse liver damage (as in infectious hepatitis) temporarily provokes a statistically significant increase in the level of serum protein-bound iodine (PBI), associated with a higher rate of fixation of thyroxine to the serum thyroxine-binding protein (TBP). These abnormal findings are caused by different mechanisms, such as disturbance of biliary thyroxine excretion, and lack of deiodination and glucuroconjugation of thyroxine in the damaged liver cell. Under these conditions, the thyroxine turnover is slower and thyroxine accumulates in the circulation. The increased serum PBI level is not associated with hyperthyroidism, although the content of the PBI in infectious hepatitis is practically built from chromatographically demonstrable pure thyroxine. The data do not confirm the hypothesis of a pathologic binding of thyroxine to plasma protein, but the high TBP level in hepatitis could contribute to the non-utilization of thyroxine in the tissues. On the other hand, experiments in rats show that the damaged liver cell is also the cause of the lack of metabolic response in this particular type of hyperthyroxinemia.