Amiodarone can cause both ... It can cause hypothyroidism by inhibiting deaminase causes decrease active T3 formation .... It can cause hyperthyroidism as amiodarone has iodine in it , and this excess iodine can cause more Thyroid hormone production . So it can do Hypo or Hyper thyroidism ...
When thre is excess Iodine in the circulation it will be entrapped by thyroid follicles and subsequently organized and coupled to be released as T4 & T3 in excess amounts.
With time, build up of greater amounts of Iodine within the gland will lead to inhibition of many steps involved in T. hormone synthesis (transport, coupling and even release of hormones).
This happens in a way somewhat similar to the down-regulation process in receptors; when u give an acetylcholine agonist, e.g. Physostigmine (Cholinestrase inhibitor), in therapeutic dose there will be improvement of muscle contraction while in overdose it will cause flaccid paralysis by accummulation of Ach in synaptic cleft.
Hyper- & Hypothyroidism ----------both r caused by Iodine Contraction & Paralysis -----------both r caused by Ach
Keep in mind that Radiocontrast media contains Iodine and can affect the thyroid by the same mechanism.
I don't know if there is direct effect of Iodine on the TSH or TRH release, anyone knows about that??
Amiodarone inhibits type 1 5'-deiodinase enzyme activity, thereby decreasing the peripheral conversion of T4 to triiodothyronine (T3) and reducing the clearance of both T4 and reverse T3 (rT3). Consequently, the serum levels of T4 and rT3 increase and the serum levels of T3 decrease by 20-25%.
Amiodarone inhibits entry of T4 and T3 into the peripheral tissue. Serum T4 levels increase by an average of 40% above pretreatment levels after 1-4 months of treatment with amiodarone. This, in itself, does not constitute evidence of hyperthyroidism (thyrotoxicosis).
Amiodarone causes inhibition of type 2 5'-deiodinase enzyme activity in the pituitary due to feedback regulation is seen in the first 1-3 months of therapy and leads to an increase in thyroid-stimulating hormone (TSH) levels. This is not an indication for T4 replacement in these patients. Serum TSH levels return to normal in 2-3 months as T4 concentrations rise sufficiently to overcome the partial block in T3 production. The response of TSH to thyroid-releasing hormone (TRH) may be reduced.