Dean P J, Groshart K D, Porterfield J G, Iansmith D H, Golden E B
Am J Clin Pathol. 1987 Jan;87(1):7-13. doi: 10.1093/ajcp/87.1.7.
The new anti-arrhythmic agent, amiodarone, is increasingly recognized as a cause of pulmonary toxicity (APT). In the present series, 11 of 171 patients (6.4%) receiving the drug had APT develop. Clinical symptoms varied from mild cough and dyspnea to acute respiratory failure. Chest x-rays demonstrated alveolar and/or interstitial opacities in all 11 patients. The microscopic appearance of APT resembled that seen in lung injury from other drugs. The features were those of diffuse alveolar damage, ranging from the early acute to the organizing phase. Mural and intraalveolar foam cells were a prominent component. The epithelial origin of these cells was confirmed by positive immunoperoxidase staining for carcinoembryonic antigen. They were further identified as type II pneumocytes by electron microscopic examination. These findings support the concept that amiodarone is responsible for a drug-induced phospholipidosis. APT was clinically reversible in all patients; however, five patients (45%) died of arrhythmia shortly after discontinuation of amiodarone.
新型抗心律失常药物胺碘酮日益被认为是肺毒性（胺碘酮所致肺毒性，APT）的一个病因。在本系列研究中，171例接受该药治疗的患者中有11例（6.4%）发生了APT。临床症状从轻度咳嗽和呼吸困难到急性呼吸衰竭不等。胸部X线检查显示所有11例患者均有肺泡和/或间质混浊。APT的显微镜下表现类似于其他药物所致肺损伤的表现。其特征为弥漫性肺泡损伤，范围从早期急性阶段到机化期。壁层和肺泡内泡沫细胞是一个突出成分。通过癌胚抗原免疫过氧化物酶染色阳性证实了这些细胞的上皮来源。通过电子显微镜检查进一步将它们鉴定为II型肺泡上皮细胞。这些发现支持胺碘酮导致药物性磷脂沉着症这一概念。所有患者的APT在临床上均可逆转；然而，5例患者（45%）在停用胺碘酮后不久死于心律失常。
