Drugs that suppress TSH or cause central hypothyroidism
Open accessAbstract
Many different drugs affect thyroid function. Most of these drugs act at the level of the thyroid in patients with normal thyroid function, or at the level of thyroid hormone absorption or metabolism in patients requiring exogenous levothyroxine. A small subset of medications including glucocorticoids, dopamine agonists, somatostatin analogues and rexinoids affect thyroid function through suppression of TSH in the thyrotrope or hypothalamus. Fortunately, most of these medications do not cause clinically evident central hypothyroidism. A newer class of nuclear hormone receptors agonists, called rexinoids, cause clinically significant central hypothyroidism in most patients and dopamine agonists may exacerbate 'hypothyroidism' in patients with non-thyroidal illness. In this review, we explore mechanisms governing TSH suppression of these drugs and the clinical relevance of these effects.
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Several other drugs (e.g., glucocorticoids, anti-epileptics, somatostatin) have transient or controversial TSH-suppressive effects.
“Several other drugs (e.g., glucocorticoids, anti-epileptics, somatostatin) have transient or controversial TSH-suppressive effects [1, 38] (see Table 3).”
From 2018 European Thyroid Association (ETA) Guidelines on the Diagnosis and Management of Central Hypothyroidism (2018) · cites this paper as [38]
The Somatostatin analogs section describes TSH suppression as primarily transient, and Other medications that may affect TSH levels says whether antiepileptics affect TSH remains controversial. The Glucocorticoids section confirms TSH suppression but does not characterize that effect as transient or controversial; it says long-term use does not appear to cause clinically evident central hypothyroidism. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSerum TSH concentrations may be altered by patient demographic characteristics, comorbidities, concomitant drug use, and assay interference.
“It is worth noting that serum TSH concentrations may be altered by the patient’s demographic characteristics and comorbidities, concomitant drug use, assay interference and so on (3, 4).”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [4]
The Glucocorticoids and Summary sections report that medications can alter serum TSH, and the Dopamine/bromocryptine section describes additional TSH suppression in patients with nonthyroidal illness. These passages support the drug-use component and a condition-specific aspect of comorbidity, but the paper does not address demographic characteristics or assay interference. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredOral estrogen therapy increases circulating cortisol-binding globulin through a hepatic first-pass effect, leading to increased total cortisol levels; this does not occur with transdermal estrogen therapy.
“Oral estrogen therapy increases circulating CBG (through a hepatic first-pass effect), leading to increased total cortisol levels; this does not occur with transdermal estrogen therapy (189,190).”
From Hormonal Replacement in Hypopituitarism in Adults: An Endocrine Society Clinical Practice Guideline (2016) · cites this paper as [190]
The Glucocorticoids section (page unavailable) discusses cortisol and glucocorticoid effects on TSH, not estrogen therapy. Searches for oral and transdermal estrogen, cortisol-binding globulin, and hepatic first-pass effects found no passage addressing the claimed difference in total cortisol levels. (LLM, conf=0.76)
Experimental — accuracy not yet measuredAlthough dopamine and its agonists, somatostatin analogs, dobutamine, amphetamines and corticosteroids inhibit TSH, patients taking chronically these medications have no sustained decreases of thyroid function tests; consequently, central hypothyroidism does not develop.
“Though dopamine and its agonists (bromocriptine, cabergoline), somatostatin analogs (octreotide), dobutamine, amphetamines and corticosteroids inhibit TSH, patients taking chronically these medications have no sustained decreases of TFTs. Consequently, CH does not develop (34, 85).”
From L-T4 therapy in the presence of pharmacological interferents (2020) · cites this paper as [34]
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References 51 · Cited by 252
- Authors
- Haugen, B. R.
- Affiliations
- University of Colorado Anschutz (US)
- Corresponding author
- Haugen, Bryan R.
- ORCID
- Haugen, Bryan R.
- Venue
- Best Practice & Research Clinical Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 23
- Issue
- 6
- Pages
- 793-800
- ISSN
- 1521-690X (ISSN-L)
- PMC
- PMC2784889
- OpenAlex
- W2065558920
- Cited by
- 252
- References
- 51
- Citations by year
- 2026: 14 · 2025: 7 · 2024: 18 · 2023: 13 · 2022: 20 · 2021: 17 · 2020: 21 · 2019: 20 · 2018: 16 · 2017: 17 · 2016: 15 · 2015: 14 · 2014: 18 · 2013: 16 · 2012: 12
- FWCI
- 1.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Best Practice & Research Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK054383)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Keywords
- TSH suppression, central hypothyroidism, drug-induced thyroid dysfunction, glucocorticoids, dopamine agonists, somatostatin analogues, rexinoids, low T3 syndrome, hypothalamic-pituitary-thyroid axis, levothyroxine, thyroid hormone metabolism
- MeSH terms
- Bexarotene, Aged, Glucocorticoids, Humans, Hypothyroidism, Male, Metformin, Somatostatin, Tetrahydronaphthalenes, Thyrotropin, Lymphoma, T-Cell, Dopamine Agonists, Retinoid X Receptors
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