Management of amiodarone-related thyroid problems

Narayana, Shashithej K.; Woods, David R.; Boos, Christopher J.

doi:10.1177/2042018811398516

Cited by 78 publications

(54 citation statements)

References 71 publications

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“…Amiodaron jest pochodną benzofuranu, zawiera około 37% jodu, zaś strukturalnie wykazuje duże podobień-stwo do hormonów tarczycowych [4,5]. Pacjent, który otrzymuje dziennie standardową dawkę leku (200 mg) dostaje 75 mg jodu organicznego na dobę, co znacznie przewyższa zalecaną dobową podaż jodu (150-200 ug).…”

Section: Nadmiar Joduunclassified

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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Section: Nadmiar Joduunclassified

Amiodaron i tarczyca

Jabrocka‐Hybel

Bednarczuk

Bartalena

et al. 2015

Endokrynologia Polska

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“…This is seen especially in patients with underlying hashimoto's disease or grave disease. 4 The above case had one recorded episode of raised TSH and Anti TPO antibodies and was on amiodarone therapy, which may have predisposed him to development of sub clinical hypothyroidism as was evident with the increase in TSH levels and normal T3,T4 levels.…”

Section: Discussionmentioning

confidence: 92%

Amiodarone Toxicity: A Case Report

Lal¹,

Singh²,

Kumar³

et al. 2019

IHRJ

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Amiodarone is one of the commonly used drug in arrhythmias. It is first line of treatment for ventricular tachycardia particularly in treatment of supraventicular tachycardia like atrial fibrillation. Amiodarone has a wide range of adverse effects ranging from endocrine to cardiac system. A case of raised thyroid stimulating Hormone (TSH) with amiodarone was reported in our Adverse drug monitoring centre (AMC), in which several other adverse events such as raised raised billirubin and hyponatremia were present. Patient was treated with thyroxine while amiodarone along with atorvastatin and metoprolol were withdrawn. We present a case who developed subclinical hypothyroidism, electrolyte imbalance and liver dysfunction with amiodarone therapy.

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“…It was reported that AM-associated thyrotoxicosis was higher compared to hypothyroidism (17). On the other hand, Narayana et al (18) stated that AM can lead to both hypothyroidism and less commonly hyperthyroidism.…”

Section: Discussionmentioning

confidence: 99%

Relation between Endogenous Stem Cells and Green Tea Extract in Overconsumption and Amiodarone Induced Thyroid Damage in Rat

Zickri¹,

Embaby²

2013

Int J Stem Cells

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Background and Objectives: Amiodarone (AM), one of the most commonly prescribed antiarrhythmics, is frequently associated with thyroid dysfunction. Green tea extract (GTE) supplementation would attenuate oxidative stress and activate progenitor cells. However, the potential toxicity of GTE on various organs when administered at high doses has not been completely investigated. The present study aimed at investigating the possible relation between endogenous stem cells and GTE in overconsumption and AM induced thyroid damage in albino rat. Methods and Results: Twenty four male albino rats were divided into control group, GTE group (rats given 50 mg/kg), Overconsumption group (rats given 1,000 mg/kg GTE), AM group (rats given 30 mg/kg) and combined AM, GTE therapy group. AM and GTE were administered orally 5 days/week for 8 weeks. Serological tests were performed. Thyroid sections were exposed to histological, immunohistochemical and morphometric studies. In overconsumption group, multiple distorted follicles with cellular debris in the lumen and multiple follicles devoid of colloid were found. In AM group, multiple follicles exhibiting crescent of colloid and few follicles devoid of colloid were detected. In combined therapy group, multiple follicles were filled with colloid. Significant decrease in area of colloid and significant increase in the area% of collagen were recorded in overconsumption and AM groups. Area% of CD 105 +ve cells denoted significant increase in combined therapy group. Serological tests were confirmative. Conclusions: Endogenous SCs activation was proved in AM and GTE combined therapy group with regression of AM induced morphological, morphometric and serological changes. However, overconsumption of GTE recruited endogenous SCs suppression.

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Management of amiodarone-related thyroid problems

Cited by 78 publications

References 71 publications

Amiodaron i tarczyca

Amiodaron i tarczyca

Amiodarone Toxicity: A Case Report

Relation between Endogenous Stem Cells and Green Tea Extract in Overconsumption and Amiodarone Induced Thyroid Damage in Rat

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