Cazzadori A, Braggio P, Barbieri E, Ganassini A
Respiration. 1986;49(2):157-60. doi: 10.1159/000194874.
A patient with atrial premature depolarizations developed pulmonary toxicity during long-term treatment with amiodarone. The clinical features were cough and dyspnea. Pulmonary function tests showed a restrictive defect and severe impairment of gas transfer. Diffuse interstitial and intra-alveolar shadows were noted on chest X-ray. Lung specimens obtained by transbronchial biopsy showed hyperplasia of pneumocytes and widening of the alveolar septa. After discontinuation of amiodarone and institution of steroid therapy the patient improved symptomatically, and after 3 weeks the chest X-ray showed clearing of the bilateral infiltrates. The patient was never given any other antiarrhythmic drugs, had no important heart disease, and received the lowest daily dose of amiodarone reported in the literature of cases of pulmonary injury.
一名患有房性早搏的患者在长期使用胺碘酮治疗期间出现了肺部毒性。临床特征为咳嗽和呼吸困难。肺功能测试显示为限制性缺陷和严重的气体交换受损。胸部X线检查发现弥漫性间质和肺泡内阴影。经支气管活检获取的肺标本显示肺细胞增生和肺泡间隔增宽。停用胺碘酮并开始使用类固醇治疗后,患者症状有所改善,3周后胸部X线显示双侧浸润影消退。该患者从未使用过任何其他抗心律失常药物,没有重要的心脏病,并且接受了文献报道的导致肺损伤病例中最低的胺碘酮每日剂量。