Glucocorticoids Are Preferable to Thionamides as First-Line Treatment for Amiodarone-Induced Thyrotoxicosis due to Destructive Thyroiditis: A Matched Retrospective Cohort Study

Bogazzi, Fausto; Tomisti, Luca; Rossi, Giuseppe; Dell'Unto, Enrica; Pepe, Pasquale; Bartalena, Luigi; Martino, Enio

doi:10.1210/jc.2009-0940

Cited by 49 publications

(39 citation statements)

References 24 publications

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“…Thus, prednisone was considered as the most effective treatment modality for these patients [39]. Although the study was underpowered, these data confirmed an earlier retrospective observation showing that a 6-week treatment of 42 AIT 2 patients with methimazole alone resulted in euthyroidism in 15% of patients compared to 76% of the patients treated with prednisone alone [45]. In a prospective randomized study of 12 patients, prednisone treatment alone was more effective in rapidly restoring euthyroidism compared to treatment with iopanoic acid [46].…”

Section: What Is the Management Of Ait 2?supporting

confidence: 65%

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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195

184

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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: What Is the Management Of Ait 2?supporting

confidence: 65%

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

Bartalena¹,

Bogazzi²,

Chiovato³

et al. 2018

Eur Thyroid J

Self Cite

195

184

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“…Thioamides are not the first-line treatment in type 2 AIT because the underlying pathogenic mechanism is not an enhanced thyroid hormone synthesis. A recent retrospective cohort study of type 2 AIT showed that after about six weeks of therapy more than 85% of patients treated with ATDs were still thyrotoxic, compared to 24% of prednisone-treated patients [57]. Follow-up of these patients is necessary because disease may recur, thus requiring retreatment [14,50].…”

Section: Type 2 Aitmentioning

confidence: 99%

“…Tionamidy nie są lekami pierwszego rzutu w typie 2 AIT, ponieważ mechanizm choroby nie jest zależny od zwiększonej syntezy hormonów. Ostatnie badania retrospektywne wśród chorych z typem 2 AIT pokazują, że po około 6 tygodniach terapii więcej niż 85% pacjentów leczonych ATD było nadczynnych, w porównaniu z jedynie 24% leczonych prednizonem [57]. Dalsza obserwacja tych pacjentów jest konieczna, ponieważ choroba może nawrócić i leczenie będzie ponownie konieczne [14,50].…”

Section: Typ 1 Aitunclassified

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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“…It has to be noted that TPE followed by thyroidectomy is only required in a minority of patients, as the large majority of corticosteroid-treated type 2 AIT patients evolve to euthyroidism within the first weeks of medical therapy. This was demonstrated by Bogazzi et al [15,17] who observed a mean cure time of 21 and 30 days in 2 different cohorts. Eskes et al [16] found a similar median time of 4 weeks to normalize the fT4 level.…”

Section: Discussionmentioning

confidence: 67%

Successful Pretreatment Using Plasma Exchange before Thyroidectomy in a Patient with Amiodarone-Induced Thyrotoxicosis

Tonnelier¹,

Filette²,

Becker³

et al. 2017

Eur Thyroid J

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Introduction: Amiodarone, used for the management of tachyarrhythmias, is associated with both hypothyroidism and thyrotoxicosis. Total thyroidectomy is an effective procedure for promptly reducing circulating thyroid hormone levels. It has been proposed in patients who have severe amiodarone-induced thyrotoxicosis (AIT) or are refractory to medical therapy, or when such therapy is contraindicated. Therapeutic plasma exchange (TPE) may be considered as a pretreatment for restoring a euthyroid state preoperatively, thereby reducing a patient's symptoms and the potential perioperative risk associated with thyrotoxicosis. Case Report: We describe the case of a 62-year-old man with type 2 AIT who presented with severe unremitting thyrotoxicosis after 8 weeks of medical therapy with glucocorticosteroids, thiamazole, and potassium perchlorate. Given the severity of his presentation, a total thyroidectomy was indicated. TPE was performed preoperatively and was successful in rapidly restoring euthyroidism. This dramatically improved the patient's symptoms which had been suggestive of ischemic heart disease. Subsequently, the patient underwent total thyroidectomy under general anesthesia without any major complications. Conclusion: TPE is successful in rapidly restoring a clinical and biochemical euthyroid state, and may be used to decrease the perioperative risks associated with thyroidectomy in patients with life-threatening thyrotoxicosis or in cases refractory to medical treatment.

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Glucocorticoids Are Preferable to Thionamides as First-Line Treatment for Amiodarone-Induced Thyrotoxicosis due to Destructive Thyroiditis: A Matched Retrospective Cohort Study

Abstract: Glucocorticoids are the first-line treatment in type 2 AIT, whereas thionamides play no role in this destructive thyroiditis.

Cited by 49 publications

References 24 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

Amiodaron i tarczyca

Successful Pretreatment Using Plasma Exchange before Thyroidectomy in a Patient with Amiodarone-Induced Thyrotoxicosis

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