The Effect of Hepatic Enzyme-Inducing Drugs on Thyroid Hormones and the Thyroid Gland*

CURRAN, PETER G.; DEGROOT, LESLIE J.

doi:10.1210/edrv-12-2-135

Cited by 226Thyroid Disorders and TreatmentsPharmacogenetics and Drug MetabolismEffects and risks of endocrine disrupting chemicals

The Effect of Hepatic Enzyme-Inducing Drugs on Thyroid Hormones and the Thyroid Gland*

CURRAN, PETER G., DEGROOT, LESLIE J.·1991·Endocrine Reviews

DOI 10.1210/edrv-12-2-135

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Abstract

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)

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Examples of drugs that have either been shown to increase hepatic metabolism of T4 and T3 via induction of conjugation enzymes, or are presumed or hypothesized to have this effect, include phenobarbital, phenytoin, carbamazepine, rifampin, sertraline, and possibly imatinib.
“Examples of drugs that have either been shown to increase hepatic metabolism of T4 and T3 via their induction of these enzymes, or are presumed or hypothesized to have this effect, include phenobarbital, phenytoin, carbamazepine, rifampin, sertraline, and possibly imatinib (172).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [172]
The effect of phenobarbital to increase T4 and T3 metabolism has been documented in rodents and humans, but effects on thyroid function are more notable in rats.
“The effect of phenobarbital to increase T 4 and T3 metabolism has been documented in rodents (173) and humans (174,175), but effects on thyroid function are more notable in rats (172).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [172]
Treatments with phenobarbital, phenytoin, carbamazepine, and rifampin induce an increase in the levels of the enzyme responsible for the glucuronidation of LT4.
“Treatments with phenobarbital, phenytoin, carbamazepine, and rifampin induce an increase in the levels of the enzyme responsible for the glucuronidation of LT4 [ 116 , 117 ].”
From Factors influencing the levothyroxine dose in the hormone replacement therapy of primary hypothyroidism in adults (2022) · cites this paper as [116]

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Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement
Jonklaas, J., Bianco, A. C., Bauer, A. J., Burman, K. D., Cappola, A. R., Celi, F. S., Cooper, D. S., Kim, B. W., Peeters, R. P., Rosenthal, M. S., et al. (2014) · Thyroid® · doi:10.1089/thy.2014.0028 · Cited by 1,928 · see citing works
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Anti-epileptic Drugs and Thyroid Function
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Authors: CURRAN, P. G., & DEGROOT, L. J.
Affiliations: University of Chicago Medical Center (US)
Corresponding author: DEGROOT, LESLIE J.
Venue: Endocrine Reviews
Publisher: The Endocrine Society
Published: 1991-05
Volume: 12
Issue: 2
Pages: 135-150
ISSN: 0163-769X (ISSN-L)
1945-7189
DOI: 10.1210/edrv-12-2-135
OpenAlex: W1977833798
Cited by: 226
References: 142
Citations by year: 2026: 3 · 2025: 6 · 2024: 5 · 2023: 4 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 3 · 2018: 7 · 2017: 8 · 2016: 5 · 2015: 8 · 2014: 4 · 2013: 12 · 2012: 12
FWCI: 3.59
Type: journal article
Language: en
Open access: closed
Locations: Endocrine Reviews (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (2r01dk013377-21a1)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK027384, DK 13 377, DK27384, DK-07011-17, T32DK007011)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
Keywords: thyroid hormones, biliary excretion, thyroid hormone metabolism, thyroid-stimulating hormone, hypothalamic-pituitary-thyroid axis, phenobarbital, nicardipine, phenytoin, rifampicin, carbamazepine, leukotriene antagonists, polycyclic aromatic hydrocarbons, imidazole, thyroid hyperplasia, thyroid cancer, goiter, thyroid hormone clearance, free thyroxine
MeSH terms: Animals, Enzyme Induction, Humans, Liver, Thyroid Gland, Thyroid Hormones

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The Effect of Hepatic Enzyme-Inducing Drugs on Thyroid Hormones and the Thyroid Gland*

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