Ethanol, Thyroid Hormones and Acute Liver Injury: Is There a Relationship?

Abstract

Alcoholic liver disease continues to be an important cause of morbidity and mortality, and the hypermetabolic hypothesis continues to be an attractive area for research. However, the current state of knowledge does not allow unequivocal acceptance or rejection of the role of thyroid hormone and antithyroid medication in alcoholic hepatitis. Clinical trials will help to establish or disprove the veracity of this hypothesis. What has been established is that chronic ethanol ingestion enhances EMR (19-22) which probably reflects the degree of hepatocellular necrosis, at least when relatively mild (25). The influence of thyroid hormone or a hyperthyroid-like state on EMR would be established if it could be shown that different antithyroid medications inhibit the enhanced EMR in chronic alcoholics. This effect has been shown in rats (125), but not in man. It is not apparent that events in the rat model can be readily applied to man. Furthermore, proof that antithyroid medications can inhibit enhanced EMR in chronic ethanol-consuming patients may allow this feature to be used to select patients who may best benefit from such treatment. A controlled randomized clinical trial using different anti-thyroid medications in alcoholic hepatitis may shed light on this important question. At the very least, demonstration of inhibition of enhanced EMR by antithyroid medications may provide the rationale for research concerning the role of thyroid hormone (or a similar hypermetabolic factor) in alcohol-mediated hepatocellular injury.