Alterations in Circulating Thyroid Hormones and Thyrotropin in Hepatic Cirrhosis: Evidence for Euthyroidism Despite Subnormal Serum Triiodothyronine

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Abstract
We studied serum concentrations of thyroid hormones and thyrotropin (TSH) in 23 clinically euthyroid patients with hepatic cirrhosis. The mean serum total thyroxine T4 concentration of 7.5 μg per 100 ml was modestly but significantly lower than the corresponding normal mean value of 8.4 μg per 100 ml. However, since the dialyzable fraction of serum T4 in patients with hepatic cirrhosis was considerably above normal (0.055% vs 0.030%), their mean serum free T4 concentration of 3.9 ng per 100 ml was significantly greater than the mean normal value of 2.8 ng per 100 ml. The mean serum concentration of triiodothyronine (T3) of 33 ng per 100 ml in patients with cirrhosis was markedly lower than the normal mean of 126 ng per 100 ml. The mean serum concentration of free T3, 163 pg per 100 ml, was also significantly lower than the mean of 375 pg per 100 ml in normal subjects; this was the case even though the mean dialyzable fraction of serum T3, 0.52, was significantly higher than that of 0.34 in normal subjects. The mean serum TSH concentration of 8.0 μU per ml in patients with cirrhosis was significantly greater than the corresponding normal value of 4.6 μU per ml. The mean serum TSH in patients with cirrhosis did not differ significantly from that in the newborn (cord serum); just as in cirrhosis, serum T3 in the newborn is much less than that in the normal adult. The clinical impression of euthyroidism was strengthened by the finding of normal serum TSH response to iv administration of thyrotropinreleasing hormone (TRH) in 5 of 6 patients so studied. Normal Achilles reflex time and an index of myocardial contractility assessed by sphygomorecording also supported the clinical diagnosis of euthyroidism in a majority of patients studied. Since serum free T3 concentration was in the hypothyroid range our data suggested that euthyroidism in our patients was maintained predominantly by the high normal or high serum free T4 concentration. Elevated serum free T4 in our patients was considered a result of a compensatory increase in the activity of pituitary-thyroid axis in response to the low serum free T3. When thyroidal secretion of T3 was assessed by a study of serum T3 responses to administration of TRH, data indicated that thyroid reserve is well maintained in patients with hepatic cirrhosis. These findings suggested that low serum free T3 in these patients is probably a result of a substantial reduction in extrathyroidal conversion of T4 to T3 in hepatic cirrhosis.

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