The Effects of Amiodarone on Thyroid Hormone Function: A Review of the Physiology and Clinical Manifestations

Figge, Helen L.; Figge, James

doi:10.1002/j.1552-4604.1990.tb01861.x

Cited by 55 publications

(43 citation statements)

References 38 publications

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“…1,2 Serum thyrotropin (TSH) levels increase in the early phase of treatment (1 to 3 months) and typically return to normal thereafter. 3 These changes are found in euthyroid subjects.…”

mentioning

confidence: 85%

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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“…1,2 Serum thyrotropin (TSH) levels increase in the early phase of treatment (1 to 3 months) and typically return to normal thereafter. 3 These changes are found in euthyroid subjects.…”

mentioning

confidence: 85%

Successful treatment of amiodarone-induced thyrotoxicosis

Osman¹,

Franklyn²,

Sheppard³

et al. 2002

ACC Current Journal Review

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“…Experimental evidence indicates that an imbalance in the production and removal of ROS play a crucial role in gastric mucosal damages due to aspirin and other NSAIGs. As a consequence of this process, oxidative damage occurs 10,11 . Organisms do, however, have enzymatic and non enzymatic defense mechanisms against the toxicity and tissue damage of ROS.…”

Section: Results and Discussion: Peptic Ulcer Disease (Pud)mentioning

confidence: 99%

Untitled

2012

IJPSR

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The present study was designed to evaluate the anti ulcer effect of Basella alba in aspirin induced ulcerated rats. Aspirin induced ulcer was revealed by increased ulcer index, decreased gastric pH, increase in the levels of pepsin, Thio barbituric acid reactive substance (TBARS). Lipid hydroperoxides and decrease in the levels of enzymatic and non enzymatic antioxidants. Treatment with the plant extract brought back the altered parameters to normal.

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“…La amiodarona es metabolizada por desalquilación a desetilAMD (DEA), un metabolito activo (5)(6)(7) .…”

Section: Características De La Amiodaronaunclassified

“…A nivel de tiroides, la AMD puede alterar el metabolismo de las hormonas tiroideas, resultando en alteraciones en las pruebas de función tiroidea en individuos eutirodeos, y puede causar tanto hipotiroidismo como hipertiroidismo, lo que se conoce como disfunción tiroidea inducida por amiodarona (DTIA) (3)(4)(5) .…”

Section: Introductionunclassified

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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The Effects of Amiodarone on Thyroid Hormone Function: A Review of the Physiology and Clinical Manifestations

Cited by 55 publications

References 38 publications

Successful treatment of amiodarone-induced thyrotoxicosis

Successful treatment of amiodarone-induced thyrotoxicosis

Untitled

Disfunción tiroidea inducida por amiodarona en la práctica clínica

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