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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The effect of hepatic enzyme-inducing drugs on thyroid hormones and the thyroid gland.

With the understanding that various drugs, industrial chemicals, and chemicals of environmental importance can increase thyroid hormone hepatic metabolism and excretion, it is important to consider whether compensation by the thyroid gland for this increased excretion can lead to stimulation of the hypothalamic-pituitary-thyroid axis and possibly secondary hyperplastic or neoplastic changes in the thyroid. The compounds discussed in this review all affect thyroid function by increasing biliary excretion of thyroid hormone metabolites. Numerous studies have been performed to elucidate the effect of these drugs on thyroid hormone equilibrium. Animals given PB compensate for the increased biliary excretion with an elevated TSH allowing maintenance of a euthyroid state. Human studies demonstrate increased thyroid hormone plasma clearance, but without an increased TSH. The effects of an experimental leukotriene antagonist are similar. In humans, diphenylhydantoin has been conclusively shown to cause a decrease in peripheral thyroid hormone levels, although without evident hypothyroidism or increase in TSH. Limited studies of rifampin and carbamazepine reveal similar results. Nicardipine in rats causes reproducible decreases in free T4 levels, although it does not clearly stimulate a rise in TSH levels. An experimental imidazole caused reversible lowering of peripheral thyroid hormone levels in rats; in this study TSH was not measured. Studies with aromatic hydrocarbons administered to rats reveal a general decrease in T4 levels, with a compensatory increase of TSH. The effects of chronic administration of a compound that can cause increased thyroid hormone metabolism with compensation via increased TSH production are of more than theoretical interest, as it has been well documented that constant stimulation of the thyroid gland in rats with supraphysiological levels of TSH causes goiter, thyroid hyperplasia, adenomas, and carcinomas. In humans with congenital metabolic thyroid deficiencies there is an increased incidence of thyroid neoplasia, suggesting an association with chronic increased TSH levels. In contrast, however, large epidemiological studies of areas of endemic goiter do not show an association of human thyroid cancer with iodine deficiency and presumed chronic thyroid gland stimulation. Histological evidence of thyroid follicular hyperplasia has been noted in rats after administration of phenobarbital, nicardipine, polycyclic hydrocarbons, and possibly an experimental imidazole. Increased thyroid gland size has been demonstrated in rats given phenobarbital, nicardipine, a leukotriene antagonist, and various polycyclic hydrocarbons. Thyroid carcinoma in rats has been associated with treatment with nicardipine and after exposure to several aromatic hydrocarbons.(ABSTRACT TRUNCATED AT 400 WORDS)[1]


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