Amiodaron i tarczyca

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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“…2) [19,44]. In some circumstances (see above) an emergency or salvage thyroidectomy may be the initial therapeutic choice.…”

Section: What Is the Management Of Ait 1?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

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175

184

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“…One of the most frequent ADR-induced thyroiditis is due to Amiodarone, a common antiarrhythmic drug (Ahmed et al, 2011). In the case of Amiodarone-related thyroid disorders, the mechanisms underlying AMIO thyroid toxicity have been elusive, and no link has been found yet between genetic variants and its thyroid disorders, both hypothyroidism and thyrotoxicosis (Jabrocka-Hybel et al, 2015). Noteworthy, some patients developing thyroid-related amiodarone adverse reactions are already affected by diverse thyroid disorders.…”

Section: Drug Induced Thyroid Diseasesmentioning

confidence: 99%

Role of Pharmacogenetics in Adverse Drug Reactions: An Update towards Personalized Medicine

et al. 2021

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Adverse drug reactions (ADRs) are an important and frequent cause of morbidity and mortality. ADR can be related to a variety of drugs, including anticonvulsants, anaesthetics, antibiotics, antiretroviral, anticancer, and antiarrhythmics, and can involve every organ or apparatus. The causes of ADRs are still poorly understood due to their clinical heterogeneity and complexity. In this scenario, genetic predisposition toward ADRs is an emerging issue, not only in anticancer chemotherapy, but also in many other fields of medicine, including hemolytic anemia due to glucose-6-phosphate dehydrogenase (G6PD) deficiency, aplastic anemia, porphyria, malignant hyperthermia, epidermal tissue necrosis (Lyell’s Syndrome and Stevens-Johnson Syndrome), epilepsy, thyroid diseases, diabetes, Long QT and Brugada Syndromes. The role of genetic mutations in the ADRs pathogenesis has been shown either for dose-dependent or for dose-independent reactions. In this review, we present an update of the genetic background of ADRs, with phenotypic manifestations involving blood, muscles, heart, thyroid, liver, and skin disorders. This review aims to illustrate the growing usefulness of genetics both to prevent ADRs and to optimize the safe therapeutic use of many common drugs. In this prospective, ADRs could become an untoward “stress test,” leading to new diagnosis of genetic-determined diseases. Thus, the wider use of pharmacogenetic testing in the work-up of ADRs will lead to new clinical diagnosis of previously unsuspected diseases and to improved safety and efficacy of therapies. Improving the genotype-phenotype correlation through new lab techniques and implementation of artificial intelligence in the future may lead to personalized medicine, able to predict ADR and consequently to choose the appropriate compound and dosage for each patient.

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“…Może wywoływać zarówno niedoczynność tarczycy (rzadziej), jak i nadczynność tarczycy (częściej). O ile niedoczynność zdarza się zwykle już w trakcie przyjmowania amiodaronu, o tyle czas wystąpienia nadczynności bywa różny; może ona bowiem objawić się nawet po kilku miesiącach od zaprzestania przyjmowania leku [17]. Środki cieniujące i amiodaron mogą wywoływać tyreotoksykozę w przebiegu destrukcyjnego zapalenia tarczycy [18].…”

Section: Leki a Podaż Joduunclassified

Zalecenia dietetyczne dotyczące spożywania jodu — w poszukiwaniu konsensusu między kardiologami a endokrynologami

et al. 2019

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Amiodaron i tarczyca

Cited by 34 publications

References 103 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

Role of Pharmacogenetics in Adverse Drug Reactions: An Update towards Personalized Medicine

Zalecenia dietetyczne dotyczące spożywania jodu — w poszukiwaniu konsensusu między kardiologami a endokrynologami

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