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Cited by 61Thyroid Disorders and TreatmentsThyroid Cancer Diagnosis and TreatmentDrug-Induced Hepatotoxicity and Protection

Nongoitrous (Type I) Amiodarone-Associated Thyrotoxicosis: Evidence of Follicular Disruption In Vitro and In Vivo

BRENNAN, MICHAEL D., ERICKSON, DANA Z., CARNEY, J. AIDAN, BAHN, REBECCA S.·1995·Thyroid
DOI 10.1089/thy.1995.5.177
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Abstract

Treatment with the antiarrhythmic agent amiodarone results in alterations in thyroid hormone metabolism, and can induce either hypothyroidism or hyperthyroidism (amiodarone-associated thyrotoxicosis, AAT). AAT occurs in patients both with and without preexisting goiter. In our study of the nongoitrous variety, the effect in vitro of amiodarone treatment and of concurrent treatment with potential inhibitors on thyroid cells (FRTL-5) was assessed by measuring the release of radiolabeled chromium (51Cr). In addition, thyroid histopathology was evaluated in autopsy specimens from six amiodarone-treated patients who had no pretreatment evidence of thyroid disease. Histopathologic examination revealed minimal or no evidence of thyroid follicular damage in specimens from amiodarone-treated euthyroid patients (n = 4). In contrast, moderate to severe follicular damage and disruption were present in glands from patients with AAT (n = 2). Studies in vitro showed amiodarone to be cytotoxic to thyroid cells; this effect was inhibited by treatment with dexamethasone (10(-3) mmol) or perchlorate (2.5 micrograms/mL). In summary, we demonstrate evidence in vitro and in vivo of amiodarone-induced thyroid follicular damage and disruption in specimens from patients with nongoitrous AAT and in cultured normal thyroid cells. In addition, we demonstrate inhibition of this effect following treatment in vitro with dexamethasone or perchlorate. Our findings support the concept that nongoitrous (type I) AAT results from direct drug toxicity with disruption of thyroid follicles and subsequent release of preformed thyroid hormone.

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Crossref · 10.1089/thy.1995.5.177

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  • Two distinct mechanisms have been proposed in the development of AIT: an iodine-induced form of hyperthyroidism (type 1 AIT) due to the high iodine content of amiodarone (37% by molecular weight) and a destructive thyroiditis (type 2 AIT) due to direct toxicity of amiodarone on follicular cells.

    “Two distinct mechanisms have been proposed in the development of AIT, including an iodine-induced form of hyperthyroidism (type 1 AIT) due to the high iodine content of amiodarone (37% by molecular weight) and a destructive thyroiditis (type 2 AIT) due to direct toxicity of amiodarone on follicular cells.”

    From 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis (2016) · cites this paper as [579]

  • Type 1 AIT tends to occur in patients with underlying thyroid autonomy in a nodular goiter or GD, whereas type 2 AIT occurs as a result of direct damage or induction of apoptosis in thyrocytes by amiodarone.

    “Type 1 AIT tends to occur in patients with underlying thyroid autonomy in a nodular goiter, or GD, whereas type 2 AIT occurs as a result of direct damage or induction of apoptosis in thyrocytes by amiodarone (579-582).”

    From 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis (2016) · cites this paper as [579]

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Authors
BRENNAN, M. D., ERICKSON, D. Z., CARNEY, J. A., & BAHN, R. S.
Affiliations
Mayo Clinic (US)
ORCID
Venue
Thyroid
Publisher
SAGE Publications
Published
1995-06
Volume
5
Issue
3
Pages
177-183
ISSN
  • 1050-7256 (ISSN-L)
  • 1557-9077
DOI
10.1089/thy.1995.5.177
OpenAlex
W1535986052
Cited by
61
References
29
Citations by year
2022: 2 · 2021: 2 · 2020: 1 · 2019: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 4 · 2012: 5
FWCI
2.11
Type
journal article
Language
en
Open access
closed
Licence
www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/ (tdm)
Locations
  • Thyroid (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
amiodarone, FRTL-5 cells, dexamethasone, perchlorate, thyroid hormone secretion, thyroid histopathology
MeSH terms
Adult, Aged, Amiodarone, Cell Line, Chromium Radioisotopes, Cytotoxins, Dexamethasone, Female, Glucocorticoids, Humans, Hyperthyroidism, Male, Middle Aged, Perchlorates, Thyroid Gland, Thyrotoxicosis, Survival Analysis, Sodium Compounds

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