Mechanisms of amiodarone pulmonary toxicity

Abstract

Amiodarone pulmonary toxicity is one of the most important examples of drug-induced lung disease by non-cancer chemotherapeutic agents. Current concepts suggest that patients may clinically present with an acute illness suggestive of a hypersensitivity picture or with a more chronic indolent course mimicking a malignant process. Likewise, the mechanism of amiodarone pulmonary toxicity suggests that at least two different pathways of toxicity exist: (1) an indirect mechanism characterized by influx of inflammatory or immune effector cells to the lung and (2) a direct toxic mechanism that results in lung parenchymal cell injury and a subsequent fibrotic response. Clearly, there is the potential for much crossover and interaction between the proposed pathways of toxicity in any given patient. A better understanding of the mechanism of amiodarone pulmonary toxicity will not only improve our diagnostic approaches to patients with this serious lung disorder, but will also provide the opportunity to develop unique therapeutic strategies that control the toxicity and potentially not interfere with the intended therapeutic efficacy of the drug.