Martin W J
Indiana University School of Medicine, Indianapolis.
Clin Chest Med. 1990 Mar;11(1):131-8.
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.
胺碘酮肺毒性是由非癌症化疗药物引起的药物性肺病的最重要例子之一。目前的观念认为，患者临床上可能表现为提示超敏反应的急性疾病，或表现为类似恶性过程的更慢性的隐匿病程。同样，胺碘酮肺毒性的机制表明至少存在两种不同的毒性途径：（1）一种间接机制，其特征是炎症或免疫效应细胞流入肺部；（2）一种直接毒性机制，导致肺实质细胞损伤并随后发生纤维化反应。显然，在任何给定患者中，所提出的毒性途径之间存在很大的交叉和相互作用可能性。更好地理解胺碘酮肺毒性的机制不仅将改善我们对患有这种严重肺部疾病患者的诊断方法，还将提供机会开发独特的治疗策略，以控制毒性并可能不干扰药物的预期治疗效果。
