Abstract
Conclusions
Since the discovery of amiodarone over 30 years ago, the mechanisms underlying serious adverse effects remain to be resolved and still limit drug usefulness. Morphologic and biochemical studies indicate that amiodarone exerts an adverse effect predominantly on pulmonary tissue. There is a growing body of evidence supporting the role of the metabolite, desethylamioda-rone, in lung toxicity resulting from amiodarone administration. Additionally, there is evidence to indicate that direct cytotoxicity, cellular transport mechanisms, immunologic processes, and oxidant action may play a role in amiodarone-induced pulmonary toxicity. This review demonstrates that further study is necessary for understanding the actions of amiodarone and desethyl-amiodarone on lung tissue.
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