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Vol. 54. Núm. 7.
Páginas 354-370 (Agosto 2007)
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Vol. 54. Núm. 7.
Páginas 354-370 (Agosto 2007)
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Repercusiones del tratamiento con amiodarona sobre la función tiroidea y su manejo actual
Effects of amiodarone therapy on thryoid function and its current management
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Pedro Iglesias??
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piglesias@hgse.sacyl.es

Correspondencia: Dr. P. Iglesias. Unidad de Endocrinología. Hospital General. Ctra. de Ávila, s/n. 40002 Segovia. España.
Unidad de Endocrinología. Hospital General. Segovia. España
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La amiodarona es un fármaco rico en yodo utilizado como agente antiarrítmico, que puede causar disfunción tiroidea. Sus efectos en la función tiroidea pueden deberse a una acción directa del fármaco y/o del propio yodo. La amiodarona influye sobre la fisiología tiroidea en diferentes áreas: hipofisaria, tiroidea y periférica. Como consecuencia puede causar distintos cambios en las concentraciones séricas de las hormonas tiroideas. Estas modificaciones dependen de varios factores, como dosis y vía de administración del fármaco, duración del tratamiento, enfermedad tiroidea subyacente y aporte habitual de yodo. Aunque la amiodarona puede producir tanto hipotiroidismo como hipertiroidismo, la mayoría de los pacientes permanecen clínicamente eutiroideos. La prevalencia del hipotiroidismo inducido por amiodarona oscila entre el 1-25%. Su aparición no implica la retirada de la amiodarona y, como en otras formas de hipotiroidismo, el tratamiento de elección es la levotiroxina. La prevalencia de la tirotoxicosis inducida por amiodarona (TIA) es del 1-23%. Se han identificado 2 formas clínicas de TIA con implicaciones pronósticas y terapéuticas: la TIA tipo 1 (tirotoxicosis inducida por yodo) y la TIA tipo 2 (tiroiditis destructiva farmacológica). La supresión de la tirotropina (TSH), junto con un aumento de la triyodotironina (T3) y de la tiroxina (T4) libre, y los síntomas de hipertiroidismo son criterios diagnósticos de TIA. La eco-Doppler color de flujo tiroideo es la prueba de elección para establecer el diagnóstico diferencial entre ambos subtipos de TIA. En los casos de TIA, la amiodarona se debería retirar siempre que fuera posible, como en el caso del control de arritmias que no comprometen la vida del paciente. La TIA tipo 1 se controla con tionamidas solas o asociadas a perclorato potásico. La TIA tipo 2 suele responder a esteroides. En las formas mixtas se recomienda la triple terapia con tionamidas, esteroides y perclorato potásico. La tiroidectomía es una buena alternativa terapéutica en los casos de TIA resistente al tratamiento médico.

Palabras clave:
Amiodarona
Disfunción tiroidea
Hipertiroidismo
Hipotiroidismo
Tiroiditis
Tirotoxicosis

Amiodarone is an iodine-rich drug used as an antiarrhythmic agent which can cause thyroid dysfunction. The effects of amiodarone on thyroid function can be due to the intrinsic action of the drug and/or iodine-induced effects. Amiodarone influences thyroid physiology at pituitary, thyroid and peripheral level. Consequently, it can produce several changes in thyroid hormone concentrations. These modifications depend on several factors, such as the dose and route of administration of the drug, length of therapy, underlying thyroid disease, and iodine intake. Although amiodarone can produce both hypo-and hyperthyroidism, most patients remain clinically euthyroid. The prevalence of amiodarone-induced hypothyroidism (AIH) ranges from 1 to 25%. In these patients, amiodarone withdrawal is usually not required and, as in other forms of hypothyroidism, the treatment of choice is levothyroxine (LT4) replacement therapy.

The prevalence of amiodarone-induced thyrotoxicosis (AIT) is between 1 and 23%. Two different clinical forms have been described with therapeutic and prognostic implications: type 1 AIT (iodine-induced thyrotoxicosis) and type 2 AIT (drug-induced destructive thyroiditis). Diagnosis of AIT is established by elevations of free T4 and free T3 with suppression of TSH serum concentrations and clinical symptoms of hyperthyroidism. Color flow Doppler sonography is the most effective procedure to discriminate AIT type 1 from type 2. In patients with AIT, amiodarone therapy should be withdrawn, when feasible, as in the case of non-life-threatening arrhythmias. Type 1 AIT is controlled with antithyroid drugs alone or in combination with potassium perchlorate. Type 2 AIT usually responds to steroids. In mixed forms, triple therapy (antithyroid drugs, steroids and potassium perchlorate) is recommended. Thyroidectomy is an appropriate therapeutic alternative in patients with AIT refractory to medical therapy.

Key words:
Amiodarone
Thyroid dysfunction
Hyperthyroidism
Thyroiditis
Thyrotoxicosis
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