[Low T4 syndrome in alcoholism: role of the decrease in TBG].

Controversial data concerning thyroid function in chronic alcoholics prompted us to evaluate some aspects of thyroxine transport and metabolism in these patients. We studied 45 patients with a history of alcohol consumption of at least 160 g a day for 10 years or more. Only patients without clinical and histopathological evidence of chronic liver disease have been included in the study. All patients were clinically euthyroid and there was no history of thyroid disease. Serum thyroxine (T4), free thyroxine (FT4) and thyroxine-binding globulin (TBG) were measured by radioimmunoassay methods within 48 hours of admission and after 30 day of alcohol abstinence. At admission the mean values of T4 and TBG in alcoholics were significantly reduced when compared to those of healthy controls (6.8 +/- 1.4 vs 8.4 +/- 1.2 micrograms/dl; p less than 0.01 and 17.5 +/- 3.2 vs 20.5 +/- 1.2 micrograms/ml; p less than 0.01). Contrarily FT4 levels did not differ significantly between the groups (9.8 +/- 1.6 vs 10.8 +/- pg/ml). A close relationship between T4 and TBG (r = 0.684; p less than 0.0001) demonstrated that the decrease of T4 in alcoholics depended on a decrease in circulating TBG. We could not find any correlation between TBG and serum albumin, gamma-glutamyl-transpeptidase, aspartate aminotransferase, alanine aminotransferase and mean corpuscular volume. Indeed there was a strong relationship between TBG and mean daily alcoholic intake (r = 0.712; p less than 0.0001). T4 and TBG increase rapidly during withdrawal and after 30 days of abstinence their values did not differ significantly from those of healthy controls. In conclusion these data provide evidence that alcohol abuse causes a decrease in T4 which depends on a decrease in circulation TBG and is not associated with a reduction of FT4. Such "low TBG syndrome" seems to be due more probably to a primary effect of alcoholic on TBG synthesis that to the liver injury secondary to the alcohol abuse.