[A rare cause of thyreotoxicosis].
BACKGROUND
Amiodarone-induced thyrotoxicosis (AIT) should be included in differential diagnoses of thyrotoxicosis in presence of a suggestive drug history. Adequate treatment requires knowledge of the underlying type of AIT.


METHODS
A 68-year-old male was admitted because of progressive dyspnea and tachyarrhythmia. Symptoms of thyrotoxicosis, including agitation, sleep disturbances, and palpitations, had developed 14 days earlier and the patient's condition had worsened despite initiation of antithyroid treatment.


METHODS
Laboratory values showed manifest hyperthyroidism. Thyroid autoantibodies proved negative. C-reactive protein and erythrocyte sedimentation rate were slightly increased. Ultrasound revealed a moderately increased thyroid without nodules and with normal perfusion.


METHODS
Suspecting AIT type 2, treatment with high-dosed glucocorticoids and antithyroid drugs was initiated. Under additional beta-blockade and heart insufficiency therapy the patient's condition significantly improved. After achievement of euthyreosis, thyroidectomy was performed.


CONCLUSIONS
In patients with preexisting thyroid disorders, such as Grave's disease or functional autonomy in multinodular goiter, the high iodine content of amiodarone may cause iodine-induced thyrotoxicosis, also known as AIT type I. Treatment comprises high-dosed antithyroid drugs. In contrast, in patients suffering from AIT type II, toxic effects of amiodarone on a previously healthy thyroid result in destructive thyroiditis. Treatment consists of glucocorticoids in a dosage of 1 mg per kg body weight per day. Antithyroid treatment could be added in cases of equivocal diagnosis. In most cases, thyroidectomy is indicated. Whether amiodarone can be discontinued, should be discussed with the responsible cardiologist. Due to the long half-life time of amiodarone, treatment discontinuation will not result in an immediate improvement.
Sauer-Schulz
Anja
A
Abteilung Endokrinologie, Diabetologie, Nephrologie, Angiologie und Klinische Chemie, Medizinische Klinik, Universitätsklinikum Tübingen, Germany. anja.sauer-schulz@med.uni-tuebingen.de
Müssig
Karsten
K
Kurth
Ralf
R
Fend
Falko
F
Teichmann
Reinhard
R
Schnauder
Günter
G
D000368:Aged; D000638:Amiodarone / Q000009:adverse effects* / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000627:therapeutic use; D013956:Antithyroid Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy; D004417:Dyspnea / Q000188:drug therapy; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D008297:Male; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000188:drug therapy
D000889:Anti-Arrhythmia Agents; D013956:Antithyroid Agents; D005938:Glucocorticoids; D000638:Amiodarone