Amiodarone
	Amiodarone is notorious for its effects on the thyroid gland and on thyroid hormone metabolism. It may induce hypothyroidism, hyperthyroidism, and also thyroid cell destruction. Martino et al., Pisa, Italy, distinguished between amiodarone induced thyrotoxicosis type I (AIT-I) and AIT-II i.e. in the presence or absence of an underlying thyroid disorder. AIT-II is probably due to thyroid cell destruction and is accompanied by increased serum IL-6 concentrations, whereas IL-6 levels are only slightly increased in AIT-I. In the present report they further evaluated IL-6 levels in 9 patients with AIT-I and 9 patients with AIT-II. On the basis of their results they conclude the following: 1. IL-6 is a marker of amiodarone-induced thyroid destruction, 2. this destructive process can also occur in AIT-I patients. AIT-II responds to glycocorticoid treatment but poorly to combined methimazole plus perchlorate treatment. Pitsiavas et al., Westmead and Kogarah, Australia, studied the ultrastructure of thyroid follicular cells of rats exposed to amiodarone, and compared the results of exposure to NaI in concentrations equivalent to those delivered by amiodarone. The results showed that amioda rone induces ultrastructural changes which differ markedly from those caused by iodine in equivalent concentrations. In the presence of amiodarone thyroid follicles appeared more distorted and amiodarone caused apoptotic cell death in contrast to iodine. From these results it seems that it is more than iodine alone that causes thyroid cell destruction in the case of amiodarone exposure. Maciel et al., Ribeirao PretoSP, Brasil, studied the effect of amiodarone on the heart of rats as it is known that amiodarone may induce changes in the heart resembling those of hypothyroidism. The results were compared with hypothyroid rats and controls. Both in amiodarone treated rats and in hypothyroid rats, the heart sarcoplasmatic reticulum calcium levels were decreased as were ATPase mRNA levels. The changes in amiodarone treated hearts were reversed by treatment with T3. These results show that amiodarone causes effects on the hearts of rats similar to those in hypothyroidism, which are reversible by T3 treatment. Amiodarone is known to decrease plasma and tissue T3 and increase plasma LDLcholesterol like what happens in hypothyroidism. The increase of LDL-cholesterol is associated with a 50 % decrease of the mRNA encoding for the LDL receptor. Hudig et al., Amsterdam, The Netherlands, found in rat HEPG2 cells that T3 stimulates LDL receptor mRNA expression whereas amiodarone and its metabolite desethylamiodarone (DEA) inhibited this expression.