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      Management of Amiodarone-Induced Thyrotoxicosis at a Cardiac Transplantation Centre

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          Abstract

          Background: Amiodarone-induced thyrotoxicosis (AIT) is associated with significant morbidity and mortality, particularly in patients with cardiac failure. The aim of the study was to evaluate the management of AIT at a tertiary hospital specialising in cardiac failure and transplantation.

          Methods: Retrospective audit of 66 patients treated for AIT by Endocrinology (2007–2016), classified as type 1 (T1) or type 2 (T2) based on radiological criteria. Main outcome measurements were response rate to initial treatment, time to euthyroidism, and frequency/safety of thyroidectomy.

          Results: Mean age was 60 ± 2 years; 80% were male. Sixty-four patients commenced medical treatment: thionamides (THIO) in 23, glucocorticoids (GC) in 17 and combination (COMB) in 24. Median thyroxine (fT4) was 35.1 (31.2–46.7) in THIO, 43.1 (30.4 –60.7) in GC, and 60.0 (39.0 –>99.9) pmol/L in COMB ( p = 0.01). Initial therapy induced euthyroidism in 52%: 70% THIO, 53% GC, and 33% COMB ( p = 0.045) by 100 (49–167), 47 (35–61), and 53 (45–99) days, respectively ( p = 0.02). A further 11% became euthyroid after transitioning from monotherapy to COMB. Thyroidectomy was undertaken in 33%. Patients who underwent thyroidectomy were younger (54 ± 3 vs. 63 ± 2 years; p = 0.03), with higher prevalence of severely impaired left ventricular function prior to diagnosis of AIT (38 vs. 18%; p = 0.08). Despite median American Society of Anaesthesiologists classification 4, no thyroidectomy patient experienced cardiorespiratory complications/death.

          Conclusions: Patients with AIT had limited response to medical treatment. The poorest response was observed in COMB group, likely related to greater hyperthyroidism severity. Thyroidectomy is safe in patients with severe cardiac failure if performed in a centre with cardiac anaesthetic expertise. There should be low threshold for proceeding to thyroidectomy in patients with severe AIT and/or cardiac failure.

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          Most cited references23

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

          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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            Antiarrhythmics for maintaining sinus rhythm after cardioversion of atrial fibrillation.

            Atrial fibrillation is the most frequent sustained arrhythmia. Atrial fibrillation frequently recurs after restoration of normal sinus rhythm. Antiarrhythmic drugs have been widely used to prevent recurrence, but the effect of these drugs on mortality and other clinical outcomes is unclear. This is an update of a review previously published in 2008 and 2012.
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              Approach to the patient with amiodarone-induced thyrotoxicosis.

              Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15-20% of cases. Although amiodarone-induced hypothyroidism poses no particular problem, amiodarone-induced thyrotoxicosis (AIT) is a diagnostic and therapeutic challenge. There are two main forms of AIT: type 1, a form of iodine-induced hyperthyroidism, and type 2, a drug-induced destructive thyroiditis. However, mixed/indefinite forms exist that may be caused by both pathogenic mechanisms. Type 1 AIT usually occurs in abnormal thyroid glands, whereas type 2 AIT develops in apparently normal thyroid glands (or small goiters). Diagnosis of thyrotoxicosis is easy, based on the finding of increased free thyroid hormone concentrations and suppressed TSH levels. Thyroid radioactive iodine (RAI) uptake values are usually very low/suppressed in type 2 AIT, most commonly low or low-normal, but sometimes normal or increased in type 1 AIT despite the iodine load. Color flow Doppler sonography shows absent hypervascularity in type 2 and increased vascularity in type 1 AIT. Mixed/indefinite forms may have features of both AIT types. Thionamides represent the first-line treatment for type 1 AIT, but the iodine-replete gland is not very responsive; potassium perchlorate, by inhibiting thyroid iodine uptake, may increase the response to thionamides. Type 2 AIT is best treated by oral glucocorticoids. The response very much depends on the thyroid volume and the severity of thyrotoxicosis. Mixed/indefinite forms may require a combination of thionamides, potassium perchlorate, and steroids. RAI is usually not feasible in AIT due to low RAI uptake values. Thyroidectomy represents a valid option in cases resistant to medical therapy.
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                Author and article information

                Contributors
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                22 August 2018
                2018
                : 9
                Affiliations
                [1] 1Department of Endocrinology, St Vincent's Hospital Sydney , Darlinghurst, NSW, Australia
                [2] 2Northern Sydney Endocrine Centre , Sydney, NSW, Australia
                [3] 3Faculty of Medicine, University of Notre Dame , Sydney, NSW, Australia
                [4] 4Faculty of Medicine, University of New South Wales , Sydney, NSW, Australia
                [5] 5Department of Ear Nose and Throat Surgery, St Vincent's Hospital Sydney , Darlinghurst, NSW, Australia
                [6] 6Department of Obstetric Medicine, Royal Brisbane and Women's Hospital , Brisbane, QLD, Australia
                [7] 7Faculty of Medicine, University of Queensland , Brisbane, QLD, Australia
                [8] 8Department of Anaesthetics, St Vincent's Hospital Sydney , Darlinghurst, NSW, Australia
                [9] 9Diabetes and Metabolism Division, Garvan Institute of Medical Research , Sydney, NSW, Australia
                Author notes

                Edited by: Jacqueline Jonklaas, Georgetown University, United States

                Reviewed by: Silvia Martina Ferrari, Università degli Studi di Pisa, Italy; Bijay Vaidya, University of Exeter, United Kingdom; Yevgeniya Kushchayeva, National Institutes of Health (NIH), United States

                *Correspondence: Michelle Isaacs michelle.isaacs@ 123456svha.org.au

                This article was submitted to Thyroid Endocrinology, a section of the journal Frontiers in Endocrinology

                †These authors have contributed equally to this work

                Article
                10.3389/fendo.2018.00482
                6113588
                9fcf3f0c-48e0-47f7-8f40-835a2e57b9fd
                Copyright © 2018 Isaacs, Costin, Bova, Barrett, Heffernan, Samaras and Greenfield.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 1, Tables: 3, Equations: 0, References: 25, Pages: 8, Words: 5895
                Categories
                Endocrinology
                Original Research

                Endocrinology & Diabetes
                amiodarone induced thyrotoxicosis,amiodarone,thyrotoxicosis,hyperthyroidism,thyroidectomy,heart failure

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