Nature clinical practice. Endocrinology & metabolism · 2007
Treatment of amiodarone-associated thyrotoxicosis.
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Franklyn Jayne A, Gammage Michael D
Аннотация
BACKGROUND: A 75-year-old man had a myocardial infarction complicated by poor left ventricular function and non-sustained ventricular tachycardia. He began treatment with amiodarone and 12 months later developed symptoms of thyrotoxicosis.
INVESTIGATIONS: Thyroid function tests after commencement of amiodarone revealed a high-normal level of free T4 and low-normal level of free T3 with a normal serum TSH. When symptoms of thyrotoxicosis developed, significant rises in T4 and T3 levels and suppression of TSH were observed. Thyroid autoantibodies were detected and thyroid ultrasonography revealed a small multinodular goiter.
DIAGNOSIS: Amiodarone-induced thyrotoxicosis (AIT) with features consistent with both AIT type I (in which thyroid antibodies and nodular goiter are present) and AIT type II (which is not responsive to thionamide therapy and eventually leads to permanent hypothyroidism).
MANAGEMENT: The patient continued to be treated with amiodarone. He commenced thionamide (carbimazole) therapy but failed to improve, even after a dose increase. Glucocorticoid (prednisolone) therapy was therefore added. Combination therapy was associated with gradual clinical and biochemical improvement. The patient became persistently hypothyroid after stopping thionamide and glucocorticoid therapy and was stabilized on long-term thyroxine replacement.
INVESTIGATIONS: Thyroid function tests after commencement of amiodarone revealed a high-normal level of free T4 and low-normal level of free T3 with a normal serum TSH. When symptoms of thyrotoxicosis developed, significant rises in T4 and T3 levels and suppression of TSH were observed. Thyroid autoantibodies were detected and thyroid ultrasonography revealed a small multinodular goiter.
DIAGNOSIS: Amiodarone-induced thyrotoxicosis (AIT) with features consistent with both AIT type I (in which thyroid antibodies and nodular goiter are present) and AIT type II (which is not responsive to thionamide therapy and eventually leads to permanent hypothyroidism).
MANAGEMENT: The patient continued to be treated with amiodarone. He commenced thionamide (carbimazole) therapy but failed to improve, even after a dose increase. Glucocorticoid (prednisolone) therapy was therefore added. Combination therapy was associated with gradual clinical and biochemical improvement. The patient became persistently hypothyroid after stopping thionamide and glucocorticoid therapy and was stabilized on long-term thyroxine replacement.