Autoinmunidade en distiroidismo secundario a amiodarona: aspectos heredofamiliares / Autoinmunity in amiodarone induced thyroid disease: heredofamilial aspects

El distiroidismo espontáneo autoinmune (DE) tiene agregación familiar positiva. Se ha identificado distiroidismo en pacientes que reciben amiodarona (DIA). Hemos observado que este grupo muestra predisposición genética y ahora se analizó en forma prospoectiva, la presencia de autoanticuerpos y la historia familiar para identificar factores de riesgo en 140 enfermos que reciben amiodarona (A), 40 de estos con DIA y 30 sujetos con DE. Se estudió tambíen un grupo testigo formado por personas sanas, y sin historia familiar de distiroidismo. En todos se investigaron los antecedentes de distiroidismo en familiares de primer grado y se buscaron anticuerpos anti-tiroglobulina, músculo liso mucosa gástrica, miocardio, mitocondrias, sustancia intercelular del epitelio y membrana basal epitelial, así como anticuerpos antinucleo y factores reumatoides. Los anticuerpos anti-tiroglobulina, mucosa gastríca y miocardio se encontraron con mayor frecuencia en los tres grupos de enfermos que entre los testigos (P < 0.05). Los Ac anti tiroglobulina fueron iguales en frecuencia en los individuos que reciben A, tengan o no distiroidismo. La estratificación pronóstica de las dos poblaciones con A indicó que la presencia de este antoanticuerpo es independiente del sexo, edad, dosis o tiempo de tratamiento con la droga. La expresión clínica del padecimiento tiroideo, depende de la predisposición genética individual, los antecedentes familiares de distiroidismo se encontraron con mayor frecuencia en las familias de los pacientes con DE y DIA que en ls sujetos que reciben la droga y no alteraron la función (P < 0.005). El análisis de asociación entre antecedentes familiares y la manifestación clínica de distiroidismo secundario al tratamiento con A indicó riesgo mayor en los pacientes con uno o más familiares distiroideos (riesgo relativo 7.6)

[Autoimmunity in thyroid disease secondary to amiodarone: heredofamilial aspects]. / Autoinmunidad en distiroidismo secundario a amiodarona: aspectos heredofamiliares.

Spontaneous autoimmune thyroid disease (SATD) shows familial aggregation. Some patients receiving amiodarone treatment have been found to develop thyroid dysfunction. Previously, we reported genetic predisposition among this group of patients, now we inform a prospective study which includes the search for autoantibodies and family history to identify risk factors in amiodarone treated patients, 40 of them with amiodarone related thyroid disfunction, and 100 without it; for comparison, 30 patients with SATD and a control group of healthy subjects were also studied. We looked for the presence of autoantibodies against thyroglobulin, smooth muscle, gastric mucosa, myocardium, mitochondria, epithelial intercellular substance, and basal membrane as well as antinuclear antibodies and rheumatoid factors; in addition the history of thyroid disease in first degree relatives was investigated. Organ-specific antibodies anti-thyroglobulin, gastric mucosa and myocardium were found with increased frequency in the three groups of patients compared with controls (p less than 0.05). The frequency of antihydroglobulin antibodies was similar in patients receiving amiodarone with or without thyroid dysfunction. Prognostic stratification revealed that this finding is independent of sex, age, dosage or duration of treatment. A family history of thyroid dysfunction was found more frequently among patients with SATD and amiodarone related dysthyroidism in comparison with patients receiving amiodarone without altered thyroid function (p less than 0.005). The appearance of clinical thyroid disease depends on individual genetical predisposition. In patients with a positive family history, the risk of developing clinical, thyroid disease is 7.6 when treated with amiodarone.

[Thyroid dysfunction induced by amiodarone]. / Disfunción tiroidea inducida por amiodarona.

Amiodarone (2-n-butyl-3,4-diethylaminoethoxy-3',-diiodobenzoyl-benzofurone ) is a drug widely used for the treatment of cardiac arrhythmias. Due to its high iodine content and structural similarity to thyroxine it produces abnormalities in thyroid hormone metabolism and, in some cases, clinical thyroid dysfunction as well. We report 18 patients, 11 females and 7 males, whose thyroid disease developed during treatment with amiodarone (A). Age ranged from 13 to 64 years. A history of thyroid disease in a first-degree relative was present in five, and three patients had goiter prior to A therapy. Fifteen patients had atrial arrhythmias, and 3 had ventricular arrhythmias. Amiodarone was being given in doses of 200 to 800 mg daily. Thyroid function abnormalities appeared between 1 and 29 months after starting A therapy. Nine patients became clinically and chemically thyrotoxic; three patients developed diffuse thyroid enlargement and had total T4 concentration and FI4I increased with normal T3 and no signs of hyperthyroidism; and the six remaining patients became clinically hypothyroid with low values of total T4 and FTI and raised basal TSH. No relationship between dosages of A or duration of treatment and the appearance or severity of thyroid dysfunction was found. Regression of symptoms occurred in all but two patients with simple goiter between 1 and 8 months after amiodarone was discontinued and appropriate treatment was given. Our observations confirm the potential of A to induce thyroid abnormalities in patients with and without preexistent thyroid disease.(ABSTRACT TRUNCATED AT 250 WORDS)