Amiodarone-Induced Thyroid Dysfunction: A Clinical Update

Elnaggar, Mohamed Nabil; Jbeili, Kahtan; Nik-Hussin, Nik; Kozhippally, Mohandas; Pappachan, Joseph M

doi:10.1055/a-0577-7574

Cited by 28 publications

(22 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Rarely, inflammatory cells are noted within the thyroid parenchyma (Type I). On the other hand if the thyroid is histologically normal (Type II), the pathologic lesions show much milder follicular damage (73–75). These changes are similar to those seen in amiodarone induced pulmonary and liver toxicity (76, 77).…”

Section: Drug Associated Hyperthyroidismmentioning

confidence: 99%

The Pathology of Hyperthyroidism

LiVolsi

Baloch

2018

Front. Endocrinol.

View full text Add to dashboard Cite

This article reviews those pathologic lesions which are associated with clinical and/or biochemical hyperthyroidism. Beginning with the descriptive pathology of classical Graves' disease and the less common toxic nodular goiter and hyper-functioning thyroid nodules, this paper describes the effects of non-thyroidal hormones, glandular function (including pituitary and hypothalamic lesions), ectopic production of thyroid stimulating proteins by non-thyroidal neoplasms, exogenous drug reactions causing hyper-function and finally conditions associated with a mechanic- destructive cause of hyperthyroidism.

show abstract

Section: Drug Associated Hyperthyroidismmentioning

confidence: 99%

The Pathology of Hyperthyroidism

LiVolsi

Baloch

2018

Front. Endocrinol.

View full text Add to dashboard Cite

show abstract

“…In our opinion, the best way to treat this condition would be as with any other case of AIT: withdrawal of the amiodarone, a pertechnetate scan, and the use of anti-thyroid drugs. In addition, it may be helpful to use high-dose steroids while waiting to see if the anti-thyroid drugs work (3). In this situation, ablative radioactive iodine therapy may also have helped.…”

Section: Discussionmentioning

confidence: 99%

Amiodarone-Induced Thyrotoxicosis After Total Thyroidectomy for Metastatic Follicular Thyroid Cancer

Charles

Dhatariya

2020

AACE Clinical Case Reports

View full text Add to dashboard Cite

Objective: To describe the case of a man who developed amiodarone-induced thyrotoxicosis (AIT) after a total thyroidectomy for metastatic follicular thyroid cancer because of the effect of the drug on metastasis. To the best of our knowledge this is the first reported case of this condition. Methods: We completed a retrospective review of medical records and laboratory results including thyroid function tests as well as imaging reports including plain radiographs, positron emission tomographs, computed tomographs, and histology reports. Results: A 78-year-old man had undergone a total thyroidectomy for follicular thyroid cancer. He had meta-static disease in his chest and vertebrae, and after the operation he was started on suppressive levothyroxine treatment prior to ablative radioactive iodine treatment. Prior to thyroidectomy, his thyroid-stimulating hormone (TSH) concentration was 3.21 mU/L (reference range is 0.35 to 3.50 mU/L). On suppressive thyroxine replacement, his TSH concentration was 0.02 mU/L, his free thyroxine was 13 pmol/L (reference range is 8 to 12 pmol/L), and free triiodothyronine was 5.8 pmol/L (reference range is 3.8 to 6.0 pmol/L). He subsequently had a myocardial infarction and required antiarrhythmic treatment with amiodarone. Eleven days later he developed the clinical and biochemical features of thyrotoxicosis (TSH <0.01 mU/L, free thyroxine of 41 pmol/L, and free triiodothyronine of 14.7 pmol/L). His thyroxine dose was reduced and then discontinued 3 days later. AIT was the principal differential diagnosis, but before being able to determine the nature of the condition he died 18 days after his myocardial infarction. Conclusion: AIT can still occur after total thyroidectomy if metastatic tissue is present.

show abstract

“…Endocrine-Related Cancer Elnaggar et al 2018). In addition, ultrasonography may be particularly useful through providing representative information of Graves' disease with diffuse, bilateral or isthmic goiter, heterogeneous and hypoechogenicity parenchyma and hypervascularization with the classical aspect so called 'thyroid inferno', and describing the characteristics of malignant thyroid nodule, including taller than wide shape, hypoechogenicity, irregular margins, calcifications, vascularity and extrathyroidal extension (Alzahrani et al 2012, Bogazzi et al 2012, Goichot et al 2018.…”

Section: :7mentioning

confidence: 99%

“…Before performing RAIU, patients are needed to exclude the influence of iodine, which could induce false-negative or -positive results. In addition, 99m Tc sestamibi ( 99m Tc-MIBI) scans have been reported to be helpful in differentiating between the two principal types of AIT, with normal or increased uptake in AIT1 and decreased uptake in AIT2 due to the destruction of thyroid follicular cells by amiodarone (Piga et al 2008, Elnaggar et al 2018.…”

Section: Diagnosismentioning

confidence: 99%

“…In addition, amiodarone with a half-life of up to 100 days, is accumulated within the adipose tissue and should be interrupted for at least 6 months to be eliminated (Bogazzi et al 2010). Moreover, despite interruption of amiodarone administration, spontaneous remission of thyrotoxicosis is rare (Elnaggar et al 2018). Thus, one can suggest that its interruption or continuation might not influence AIT management.…”

Section: Treatmentmentioning

confidence: 99%

See 1 more Smart Citation

Thyrotoxicosis with concomitant thyroid cancer

Cheng

Jin

et al. 2019

Endocrine-Related Cancer

View full text Add to dashboard Cite

Thyrotoxicosis with concomitant thyroid cancer is rare and poorly recognized, which may result in delayed diagnosis, inappropriate treatment and even poor prognosis. To provide a comprehensive guidance for clinicians, the etiology, pathogenesis, diagnosis and treatment of this challenging setting were systematically reviewed. According to literatures available, the etiologies of thyrotoxicosis with concomitant thyroid cancer were categorized into Graves’ disease with concurrent differentiated thyroid cancer (DTC) or medullary thyroid cancer, Marine–Lenhart Syndrome with coexisting DTC, Plummer’s disease with concomitant DTC, amiodarone-induced thyrotoxicosis with concomitant DTC, central hyperthyroidism with coexisting DTC, hyperfunctioning metastases of DTC and others. The underlying causal mechanisms linking thyrotoxicosis and thyroid cancer were elucidated. Medical history, biochemical assessments, radioiodine uptake, anatomic and metabolic imaging and ultrasonography-guided fine-needle aspiration combined with pathological examinations were found to be critical for precise diagnosis. Surgery remains a mainstay in both tumor elimination and control of thyrotoxicosis, while anti-thyroid drugs, beta-blockers, 131I, glucocorticoids, plasmapheresis, somatostatin analogs, dopamine agonists, radiation therapy, chemotherapy and tyrosine kinase inhibitors should also be appropriately utilized as needed.

show abstract

Amiodarone-Induced Thyroid Dysfunction: A Clinical Update

Cited by 28 publications

References 65 publications

The Pathology of Hyperthyroidism

The Pathology of Hyperthyroidism

Amiodarone-Induced Thyrotoxicosis After Total Thyroidectomy for Metastatic Follicular Thyroid Cancer

Thyrotoxicosis with concomitant thyroid cancer

Contact Info

Product

Resources

About