Marchlinski F E, Gansler T S, Waxman H L, Josephson M E
Ann Intern Med. 1982 Dec;97(6):839-45. doi: 10.7326/0003-4819-97-6-839.
Pulmonary toxicity may occur in association with amiodarone hydrochloride therapy. The clinical features of the pulmonary involvement are mild dyspnea, leukocytosis, hypoxemia, elevation in the erythrocyte sedimentation rate, and restrictive changes on pulmonary function testing. Diffuse interstitial and patchy peripheral alveolar infiltrates, which may frequently involve the upper lobes, characterize the radiologic findings. Accumulation of foamy macrophages in alveolar spaces, hyperplasia of type II pneumocytes, and widening of alveolar septae are noted histologically. Ultrastructural examination shows granular and lamellar membranous structures within distended lysosomes. With cessation of amiodarone therapy and treatment with corticosteroids, clinical symptoms and radiographic abnormalities resolve. The time interval for resolution of radiographic changes appears to be greater than 2 months. The precise role of corticosteroid therapy remains unknown in light of pathologic findings suggesting a metabolic rather than immunologic basis for the toxicity.
盐酸胺碘酮治疗可能会引发肺部毒性。肺部受累的临床特征包括轻度呼吸困难、白细胞增多、低氧血症、红细胞沉降率升高以及肺功能测试显示的限制性改变。放射学表现的特征为弥漫性间质和散在的外周肺泡浸润，常累及上叶。组织学检查可见肺泡腔内泡沫状巨噬细胞积聚、II型肺泡上皮细胞增生以及肺泡间隔增宽。超微结构检查显示扩张的溶酶体内有颗粒状和板层状膜结构。随着胺碘酮治疗的停止以及使用皮质类固醇进行治疗，临床症状和放射学异常会消失。放射学改变消失的时间间隔似乎大于2个月。鉴于病理结果提示毒性的基础是代谢性而非免疫性，皮质类固醇治疗的确切作用仍不明确。
