Diagnosis and management of amiodarone‐induced thyrotoxicosis: similarities and differences between North American and European thyroidologists*

Tanda, Maria Laura; Piantanida, Eliana; Lai, Adriana; Liparulo, Luigi; Sassi, Lorenza; Bogazzi, Fausto; Wiersinga, Wilmar M.; Braverman, Lewis E.; Martino, Enio; Bartalena, Luigi

doi:10.1111/j.1365-2265.2008.03268.x

Cited by 72 publications

(65 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Indukowane jodem zapalenie tarczycy z rozpadem może wystąpić również u pacjentów z wolem, co czyni różnicowanie typu 1 od mieszanego/nieokreślonego bardzo trudnym. W tych przypadkach wielu ekspertów zaleca leczenie chorych z użyciem ATD i glukokortykoidów od samego początku [60].…”

Section: Typ 1 Aitunclassified

“…Amiodarone-induced destructive thyroiditis may occur in patients with goitre, making differentiation of type 1 and mixed/indefinite forms very difficult. In these cases, many experts treat these patients with a combination of ATDs and glucocorticoids from the beginning [60]. Some experts are concerned about the fact that glucocorticoids may not be easy to handle in patients with cardiac diseases; accordingly, it has been suggested by some to start medical therapy of indefinite forms with thioamides for at least a month and to associate steroids only if response is poor or absent [61].…”

Section: Mixed/indefinite Type Aitmentioning

confidence: 99%

See 1 more Smart Citation

Amiodaron i tarczyca

Jabrocka‐Hybel

Bednarczuk

Bartalena

et al. 2015

Endokrynologia Polska

Self Cite

View full text Add to dashboard Cite

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...

show abstract

Section: Typ 1 Aitunclassified

Section: Mixed/indefinite Type Aitmentioning

confidence: 99%

Amiodaron i tarczyca

Jabrocka‐Hybel

Bednarczuk

Bartalena

et al. 2015

Endokrynologia Polska

Self Cite

View full text Add to dashboard Cite

show abstract

“…260,261 Amiodarone-induced hyperthyroidism occurs in 14% to 21% of treated patients with ACHD, [260][261][262] which is higher than the 2% to 10% incidence in unselected populations. [263][264][265] Risk factors for amiodarone-induced hyperthyroidism in CHD include female sex, low body mass index (BMI), complex cyanotic CHD, Fontan palliation, lower age, goiter, heart failure, and dose >200 mg/d. 260,261,266 There is a small but important incidence of thyrotoxicosis in patients receiving prostacyclin therapy for pulmonary hypertension, and this is a consideration in an otherwise stable patient presenting with acute decompensation on this therapy.…”

Section: Clinical Statements and Guidelinesmentioning

confidence: 99%

Diagnosis and Management of Noncardiac Complications in Adults With Congenital Heart Disease: A Scientific Statement From the American Heart Association

Lui¹,

Saïdi²,

Bhatt³

et al. 2017

Circulation

180

136

View full text Add to dashboard Cite

ABSTRACT:Life expectancy and quality of life for those born with congenital heart disease (CHD) have greatly improved over the past 3 decades. While representing a great advance for these patients, who have been able to move from childhood to successful adult lives in increasing numbers, this development has resulted in an epidemiological shift and a generation of patients who are at risk of developing chronic multisystem disease in adulthood. Noncardiac complications significantly contribute to the morbidity and mortality of adults with CHD. Reduced survival has been documented in patients with CHD with renal dysfunction, restrictive lung disease, anemia, and cirrhosis. Furthermore, as this population ages, atherosclerotic cardiovascular disease and its risk factors are becoming increasingly prevalent. Disorders of psychosocial and cognitive development are key factors affecting the quality of life of these individuals. It is incumbent on physicians who care for patients with CHD to be mindful of the effects that disease of organs other than the heart may have on the well-being of adults with CHD. Further research is needed to understand how these noncardiac complications may affect the long-term outcome in these patients and what modifiable factors can be targeted for preventive intervention.

show abstract

“…Treatment of these forms is based on the concomitant use of thionamides (with or without potassium perchlorate) and glucocorticoids. The diagnostic uncertainty surrounding these forms of AIT is well reflected by recent questionnaire-based surveys carried out among expert thyroidologist members of the European Thyroid Association (9), Latin American Thyroid Society (10), and American Thyroid Association (11). In general, measurement of thyroidal radioactive iodine uptake (RAIU) and assessment by color flow Doppler sonography (CFDS) are considered the best tools to differentiate type 1 and type 2 AIT (12)(13)(14).…”

mentioning

confidence: 99%