Amiodarone-Induced Thyrotoxicosis Is a Predictor of Adverse Cardiovascular Outcome

Yiu, Kai‐Hang; Jim, Man‐Hong; Siu, Chung‐Wah; Lee, Chi H.; Yuen, Mantak; Mok, Maggie Ming Yee; Shea, Yet-Fung; Fan, Kang-Hsien; Tse, Hung‐Fat; Chow, Wing‐Hing

doi:10.1210/jc.2008-1907

Cited by 82 publications

(63 citation statements)

References 15 publications

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“…AIT has been associated with increased morbidity and mortality, especially in older patients with impaired left ventricular function [31][32][33]. Thus, in the majority of cases, particularly in the elderly, prompt restoration and stable main- tenance of euthyroidism should be achieved as quickly as possible, and in selected categories of patients, detailed below, emergency management of AIT should be considered to obtain a prompt resolution of thyrotoxicosis.…”

Section: Is Ait Always An Emergency Situation?mentioning

confidence: 99%

2018 European Thyroid Association (ETA) Guidelines for the Management of Amiodarone-Associated Thyroid Dysfunction

Bartalena¹,

Bogazzi²,

Chiovato³

et al. 2018

Eur Thyroid J

188

193

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Treatment with amiodarone is associated with changes in thyroid function tests, but also with thyroid dysfunction (amiodarone-induced hypothyroidism, AIH, and amiodarone-induced thyrotoxicosis, AIT). Both AIH and AIT may develop in apparently normal thyroid glands or in the presence of underlying thyroid abnormalities. AIH does not require amiodarone withdrawal, and is treated with levothyroxine replacement if overt, whereas subclinical forms may be followed without treatment. Two main types of AIT are recognized: type 1 AIT (AIT 1), a form of iodine-induced hyperthyroidism occurring in nodular goitres or latent Graves disease, and type 2 AIT (AIT 2), resulting from destructive thyroiditis in a normal thyroid gland. Mixed/indefinite forms exist due to both pathogenic mechanisms. AIT 1 is best treated with thionamides that may be combined for a few weeks with sodium perchlorate to make the thyroid gland more sensitive to thionamides. AIT 2 is treated with oral glucocorticoids. Once euthyroidism has been restored, AIT 2 patients are followed up without treatment, whereas AIT 1 patients should be treated with thyroidectomy or radioiodine. Mixed/indefinite forms of AIT are treated with thionamides. Oral glucocorticoids can be added from the beginning if a precise diagnosis is uncertain, or after a few weeks if response to thionamides alone is poor. The decision to continue or to stop amiodarone in AIT should be individualized in relation to cardiovascular risk stratification and taken jointly by specialist cardiologists and endocrinologists. In the presence of rapidly deteriorating cardiac conditions, emergency thyroidectomy may be required for all forms of AIT.

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Section: Is Ait Always An Emergency Situation?mentioning

confidence: 99%

2018 European Thyroid Association (ETA) Guidelines for the Management of Amiodarone-Associated Thyroid Dysfunction

Bartalena¹,

Bogazzi²,

Chiovato³

et al. 2018

Eur Thyroid J

188

193

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“…Patients with amiodarone-induced thyrotoxicosis (AIT) are at a high risk of developing adverse cardiac events (72). In a recent study, the presence of AIT and impaired left ventricular ejection fraction has been associated with a particularly high risk of developing major adverse cardiovascular events such as cardiovascular mortality, myocardial infarction, stroke and HF or ventricular arrhythmias with a hazard ratio (HR) of 3.18 (72). These results suggest that amiodarone should be used with caution, especially in patients with hyperthyroidism and impaired left ventricular ejection fraction.…”

Section: Hf and Amiodarone-induced Hyperthyroidismmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction

Biondi

2012

European Journal of Endocrinology

245

187

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Context: Heart failure (HF) is a major cause of morbidity and mortality in Europe and in the United States. The aim of this review article was to assess the results of the prospective studies that evaluated the risk of HF in patients with overt and subclinical thyroid disease and discuss the mechanism of this dysfunction. Evidence Acquisition: Reports published with the following search terms were searched:, thyroid, hypothyroidism, hyperthyroidism, subclinical hyperthyroidism, subclinical hypothyroidism, levothyroxine, triiodothyronine, antithyroid drugs, radioiodine, deiodinases, clinical symptoms, heart rate, HF, systolic function, diastolic function, systemic vascular resistance, endothelial function, amiodarone and atrial fibrillation. The investigation was restricted to reports published in English. Evidence Synthesis: The outcome of this analysis suggests that patients with untreated overt thyroid dysfunction are at increased risk of HF. Moreover, persistent subclinical thyroid dysfunction is associated with the development of HF in patients with serum TSH !0.1 or O10 mU/l. Conclusions: The timely recognition and effective treatment of cardiac symptoms in patients with thyroid dysfunction is mandatory because the prognosis of HF may be improved with the appropriate treatment of thyroid dysfunction.

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“…AIT bears a threefold increased rate of major adverse cardiovascular events compared to euthyroid patients, hence prompt implementation of treatment is important [38,49,50]. The decision regarding the continuation or otherwise of AMIO is difficult, with no definitive answer.…”

Section: Management Of Amiodarone-induced Thyrotoxicosismentioning

confidence: 99%

“…Nadczynność tarczycy indukowana amiodaronem niesie za sobą 3-krotnie większe ryzyko ciężkich powikłań sercowo-naczyniowych niż u osób w eutyreozie, z tego powodu najważniejsze jest szybkie włączenie odpowiedniego leczenia [38,49,50]. Decyzja dotycząca kontynuowania lub zaprzestania stosowania AMIO jest trudna i nie ma w tym względzie jednoznacznego konsensusu.…”

Section: Postępowanie W Nadczynności Tarczycy Indukowanej Amiodaronemunclassified

Amiodaron i tarczyca

Jabrocka‐Hybel

Bednarczuk

Bartalena

et al. 2015

Endokrynologia Polska

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Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15-20% of cases. Amiodarone can cause both hypothyroidism (AIH, amiodarone-induced hypothyroidism) and thyrotoxicosis (AIT, amiodarone-induced thyrotoxicosis). AIH is treated by L-thyroxin replacement and does not need amiodarone discontinuation. There are two main forms of AIT: type 1, a form of true iodineinduced hyperthyroidism; and type 2, a drug-induced destructive thyroiditis. However, mixed/indefinite forms exist, contributed to by both pathogenic mechanisms. Type 1 AIT usually occurs in diseased thyroid glands, whereas type 2 AIT develops in substantially normal thyroid glands. Thioamides represent the first-line treatment for type 1 AIT, but iodine-replete glands are poorly responsive; sodium/ /potassium perchlorate, by inhibiting thyroidal iodine uptake, may increase the response to thioamides. Type 2 AIT is best treated by oral glucocorticoids. Response depends on thyroid volume and severity of thyrotoxicosis. Mixed/indefinite forms may require a combination of thioamides, potassium perchlorate, and steroids. Radioiodine treatment is usually not feasible because amiodarone-related iodine load decreases thyroidal radioiodine uptake. Thyroidectomy represents an important and helpful option in cases resistant to medical therapy. Surgery performed by a skilled surgeon may represent an emergent treatment in patients who have severe cardiac dysfunction. StreszczenieLek antyarytmiczny -amiodaron, pochodna benzofuranu bogata w jod, wywołuje zaburzenia funkcji tarczycy w 15-20% przypadków. Amiodaron może powodować niedoczynność tarczycy (AIH) oraz nadczynność tarczycy (AIT). AIH jest leczona substytucyjnie lewotyroksyną, w jej przypadku nie jest konieczne odstawienie amiodaronu. Nadczynność tarczycy indukowaną amiodaronem dzielimy na dwa typy: typ 1 -nadczynność tarczycy związana z nadmierną produkcją hormonów tarczycowych, oraz typ 2, w której dominuje proces zapalenia tarczycy związanego z rozpadem gruczołu. Wyróżnia się również typ mieszany/nieokreślony, w którego patomechanizmie udział biorą oba powyżej opisane mechanizmy. Typ 1 AIT występuje zwykle na podłożu wcześniej występującej choroby tarczycy, zaś typ 2 w pierwotnie zdrowym gruczole tarczowym. Tionamidy są lekiem pierwszego rzutu w leczeniu typu 1 AIT, nadchloran sodowy/ /potasowy poprzez hamowanie wychwytu jodu może zwiększać odpowiedź na tionamidy. AIT typu 2 jest leczone głównie z zastosowaniem glikokortykosteroidów. Odpowiedź na leczenie zależy od wielkości gruczołu tarczowego i ciężkości tyreotoksykozy. Postaci mieszane mogą wymagać zastosowania złożonej terapii z użyciem tionamidów, nadchloranu sodowego/potasowego oraz steroidów. Leczenie radiojodem często jest niemożliwe z powodu zmniejszonego wychwytu jodu u pacjentów wcześniej leczonych amiodaronem. Zabieg usunięcia tarczycy jest bardzo pomocną formą leczenia nadczynności tarczycy indukowanej jodem, szczególnie w przypadkach opornych na leczenie farmakologiczne. Tyroidektomia wykonana przez do...

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Amiodarone-Induced Thyrotoxicosis Is a Predictor of Adverse Cardiovascular Outcome

Abstract: In patients prescribed long-term amiodarone therapy, occurrence of AIT is associated with a 2.7-fold increased risk of MACE. Regular and close biochemical surveillance is thus advisable to identify and treat this high-risk group of patients.

Cited by 82 publications

References 15 publications

2018 European Thyroid Association (ETA) Guidelines for the Management of Amiodarone-Associated Thyroid Dysfunction

2018 European Thyroid Association (ETA) Guidelines for the Management of Amiodarone-Associated Thyroid Dysfunction

MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction

Amiodaron i tarczyca

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