Treatment of amiodarone induced hyperthyroidism with potassium perchlorate and methimazole during amiodarone treatment.

Reichert, L.J.M.; Rooy, H. A. M. De

doi:10.1136/bmj.298.6687.1547

Cited by 60 publications

(22 citation statements)

References 3 publications

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“…This is in keeping with other data suggesting that thionamides are effective while amiodarone is continued. 9,12 We suggest that the decision to discontinue amiodarone should be made on cardiological grounds because successful antithyroid treatment does not depend on stopping amiodarone.…”

Section: Discussionmentioning

confidence: 99%

Successful treatment of amiodarone-induced thyrotoxicosis

Osman¹,

Franklyn²,

Sheppard³

et al. 2002

ACC Current Journal Review

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Background-Amiodarone-induced thyrotoxicosis (AIT) is a difficult management problem about which there are little published data. We examined whether continuing amiodarone or differentiating AIT into 2 subtypes affected outcome. Methods and Results-The type and duration of antithyroid treatment and response were recorded in a consecutive series of 28 cases. Comparisons were made between those in whom amiodarone either was continued or stopped and between those with either possible type 1 or type 2 AIT. Of the 28 cases, 5 had spontaneous resolution of AIT; 23 received carbimazole (CBZ) alone as first-line therapy. Eleven achieved long-term euthyroidism off CBZ or on a maintenance dose. Five became hypothyroid and required long-term thyroxine. Five relapsed after stopping CBZ treatment and were rendered euthyroid with either long-term CBZ (nϭ3) or radioiodine (nϭ2). Four were intolerant of CBZ and received propylthiouracil (PTU), with good effect in 3. One was resistant to thionamide alone (CBZ then PTU) and responded to adjunctive steroids. No difference in presentation or outcome was noted between those in whom amiodarone was continued or stopped or between possible type 1 or type 2 AIT. Conclusions-Continuing

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Section: Discussionmentioning

confidence: 99%

Successful treatment of amiodarone-induced thyrotoxicosis

Osman¹,

Franklyn²,

Sheppard³

et al. 2002

ACC Current Journal Review

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“…9,16,17 Other therapeutic options are glucocorticosteroids 14,16,17 and iopanoic acid. 18 Thyroidectomy may be also indicated. 19,20 AIT constitutes a significant clinical challenge.…”

Section: Sonography Radioiodine Uptake and Scintigraphymentioning

confidence: 99%

“…AIT was defined on the basis of the following criteria: a history of AM treatment for at least 1 month; signs and symptoms of hyperthyroidism confirmed by increased free thyroxine (FT 4 ), free thriiodothyronine (FT 3 ) and reduced thyroid-stimulating hormone (TSH) levels observed during therapy or within 2 years after AM withdrawal; a negative titer of circulating thyroid autoantibodies (antithyroglobulin [Tg-Abs], antithyroid peroxidase [TPO-Abs], anti-TSH receptor [TSHR-Abs] autoantibodies) 10,17,18 ; and a thyroid of normal or slightly increased volume without relevant nodules (>1 cm) on conventional ultrasonography. Patients were differentiated according to type I and II AIT.…”

mentioning

confidence: 99%

Radioiodine therapy in patients with type II amiodarone‑induced thyrotoxicosis

Czarnywojtek¹,

Warmuz-Stangierska²,

Woliński³

et al. 2014

Polish Archives of Internal Medicine

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“…La dosis va desde 200 a 1000 mg/día, por algunas semanas a meses; se ha reportado de ser efectivo en normalizar la función tiroidea (26) . Perclorato de potasio (KClO4) ha sido asociado con anemia aplásica, pero ningún caso ha sido informado cuando se ha usado para tratar TIA 1.…”

Section: Perclorato De Potasiounclassified

Disfunción tiroidea inducida por amiodarona en la práctica clínica

Paz-Ibarra

2013

An Fac med

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ResumenLa amiodarona (AMD) es una droga antiarrítmica potente (clase III) usada en la práctica clínica para la profilaxis y el tratamiento de muchos disturbios del ritmo cardiaco, desde la fibrilación auricular paroxística hasta las taquiarritmias ventriculares que amenazan la vida. Frecuentemente causa cambios en las pruebas de función tiroidea principalmente relacionados a la inhibición de la actividad de la 5'-deiodinasa, resultando en una disminución de la generación de T3 desde T4 y el consecuente incremento en la producción de T3 reversa y una disminución de su aclaramiento. En 14 a 18% de pacientes tratados con AMD hay una disfunción tiroidea manifiesta, ya sea tirotoxicosis inducida por amiodarona (TIA) o hipotiroidismo inducido por amiodarona (HIA). Tanto TIA como HIA pueden desarrollarse en glándulas aparentemente normales o en glándulas con anormalidades preexistentes clínicamente silentes. La TIA está primariamente relacionada a la síntesis de hormonas tiroideas inducida por el exceso de yodo en una glándula tiroidea anormal (TIA tipo 1) o a una tiroiditis destructiva relacionada a la amiodarona (TIA tipo 2), aunque frecuentemente ocurren formas mixtas. La tiroiditis de Hashimoto preexistente es un factor de riesgo definido para la ocurrencia de HIA. La patogenia del HIA es la falla para escapar del efecto agudo de Wolff-Chaikoff inducido por el yodo, debido a los defectos en la hormonogénesis tiroidea y, en pacientes con pruebas de autoanticuerpos tiroideos positivos, para tiroiditis de Hashimoto concomitante. La TIA es más común en zonas deficientes de yodo mientras que el HIA es usualmente visto en zonas suficientes en yodo. En contraste al HIA, la TIA es una condición difícil de diagnosticar y tratar, y usualmente se recomienda la descontinuación de la amiodarona. En esta revisión se analiza, de acuerdo a los datos actuales, las alteraciones en las pruebas de función tiroidea vistas en pacientes eutirodeos bajo tratamiento con AMD así como la epidemiología y opciones de tratamiento disponibles para ambos tipo de disfunción tiroidea inducida por amiodarona, TIA e HIA. Palabras clave: Amiodarona, tirotoxicosis inducida por amiodarona, hipotiroidismo inducido por amiodarona. Abstract Amiodarone is a potent class III anti-arrhythmic drug used in clinical practice for the prophylaxis and treatment of many cardiac rhythm disturbances, ranging from paroxismal atrial fibrillation to life threatening ventricular tachyarrhythmias. Amiodarone often causes changes in thyroid function tests mainly related to inhibition of 5'-deiodinase activity resulting in decrease in the generation of T3 from T4 with consequent increase in rT3 production and decrease in its clearance. In 14-18% of amiodarone-treated patients, there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting clinically silent abnormalities. AIT is primarily related to excess iodine...

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Treatment of amiodarone induced hyperthyroidism with potassium perchlorate and methimazole during amiodarone treatment.

Cited by 60 publications

References 3 publications

Successful treatment of amiodarone-induced thyrotoxicosis

Successful treatment of amiodarone-induced thyrotoxicosis

Radioiodine therapy in patients with type II amiodarone‑induced thyrotoxicosis

Disfunción tiroidea inducida por amiodarona en la práctica clínica

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