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要旨
患者は46歳,男性.37歳時に拡張相肥大型心筋症と診断された.2000年8月より低心拍出を伴う両心不全症状の増悪のため当院に入院中であった.低心機能かつ持続性心室頻拍も認めていたが,アミオダロン200mg/day内服下にてコントロール良好であった.心不全に対してはドブタミンおよびミルリノン持続点滴投与をして安定,漸減段階にあった.入院より4カ月目に前兆のない突然の呼吸困難を訴えた.胸部X線写真上,右下肺野を中心に新たな網状影を認めた.左心不全増悪や感染徴候を認めず,アミオダロン内服継続中であったことからアミオダロン肺障害と診断した.アミオダロン内服を中止し,ステロイド投与を行うことにより呼吸症状および胸部X線写真上の改善を認めた.肺障害はアミオダロン使用に際して重大な副作用である.本例はステロイド療法に良好に反応した例であり,様々な機序があるとされる同症の病態を理解するうえで貴重な症例と考えられる.
A 46-year-old man, who was diagnosed as hypertrophic cardiomyopathy in the dilated phase at 37 years of age, was admitted because of worsening symptoms of heart failure. He had been given amiodarone (200mg/day, orally) for sustained ventricular tachicardia. After the admission, he was treated with dobutamine and milrinone for heart failure, which was followed by symptomatic improvement, Thus, we intended to wean him off this treatment. However, on morning four monthes after admission, he suddenly and without any warning complained of dyspnea. Although there was no evidence of cardiac decomposition or pulmonary infection. A roentgenogram of the chest disclosed a reticulous shadow in the inferior lobe of the right lung, leading to a diagnosis of amiodarone-induced pulmonary toxicity. Amiodarone was discontinued and he was treated with corticosteroid therapy over a one month period, and clinical improvement followed. Amiodarone has been known to cause critical pulmonary complications. In this case, corticosteroid therapy was very effective for amiodarone-induced pulmonary toxicity. This case is important for understanding of the pathoplysiology of this kind of texicity.
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