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Amiodarone-induced thyrotoxicosis

German: Amiodaron-induzierte Hyperthyreose

1 Definition

Amiodarone-induced thyrotoxicosis also referred to as amiodarone-induced hyperthyroidism, abbreviated 'AIH' , is a form of thyrotoxicosis, which can arise through treatment involving Class III antiarrhythmic amiodarone.

2 Pathogenesis

Amiodarone is employed in the treatment of cardiac arrhythmia . The compound contains iodine, which makes up as much as 37% of molecular weight. Where the recommended maintenance dose is 200 mg about 7 to 9 g iodine is iodine-free. The German Nutrition Society recommended an iodine intake of 200 micrograms for adults. The administration of amiodarone therefore leads to excessive iodine intake. Iodine levels even after discontinuation of the medication remain elevated for several months because amiodarone in being a lipophilic substance accumulates in fat and has a long half-life of 20-100 days.

Amiodarone and even more its metabolite desethyl amiodarone reduce the conversion of T4 to T3. They are similar structurally to hormones in the thyroid and competitively inhibit the enzyme deiodinase, especially in the liver. In addition they also bind to T3 receptors in the nucleus, thereby affecting the transcription of T3-regulated genes.

3 Prevalence

The prevalence of amiodarone-induced thyrotoxicosis varies depending on region. This is due to the iodine supply present. In iodine deficient regions, prevalence is comparatively low (about 5%), in regions with sufficient iodine supply it is over 20%.

4 Forms

Amiodarone-induced hyperthyroidism exhibits two forms.

4.1 Type 1 AIH

Type 1 occurs with preexisting thyroid disease such as Hashimoto's thyroiditis or Graves'disease and is probably induced by an iodine excess. This leads to an increased synthesis of thyroid hormones.

4.2 Type 2 AIH

Type 2 is expressed as tissue-damaged thyroiditis, probably arises via a direct toxic effect of amiodarone on the epithelial cells of the thyroid. Because thyroid hormones are created and stored here, damage leads to an increased release of hormones from the thyroid gland. This type occurs far more commonly than Type I.

4.3 Differentiation

The two forms can be differentiated by thyroglobulin concentration, which is typically elevated in type I. In Color-coded Doppler sonography an increased vascularisation is characteristic of Type I, and which is absent in type II.

5 Symptomatology

Both Type I and Type II are expressed with variations in thyroid hormone serum concentrations:

  • increase in free T4 by 20-30%
  • decrease in free T3 by up to 30%
  • basal TSH in the low normal range

Without treatment amiodarone-induced hyperthyroidism can develop into overt hyperthyroidism, accompanied by typical symptoms such as restlessness, hyperactivity, increased sweating or arterial hypertonie. Since the effect of amiodarone on the thyroid gland is well known, regular monitoring of the organ or of hormone concentrations is meanwhile carried out under therapy using the medication and an evolving induced hyperthyroidism is treated early.

6 Treatment

With Type I, the use of antithyroid in perchlorate form or thiamazole is indicated, since they act competitively against iodine and thus inhibit the synthesis of SD hormones. In the instance of causal thyroid autonomy a thyroidectomy is potentially necessary. In type II cases glucocorticoids can be used to inhibit inflammation. With both forms, consideration to discontinue amiodarone should be made, in view of the individual patient's medical history. It must be recognised that iodine levels remain elevated for up to 6 months after discontinuation of the medication due to its long half-life.

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