Zhu Y Y, Botvinick E, Dae M, Golden J, Hattner R, Scheinman M
Department of Radiology, University of California, San Francisco.
Chest. 1988 Jun;93(6):1126-31. doi: 10.1378/chest.93.6.1126.
We sought to assess the role of gallium-67 lung scintigrams in the evaluation of amiodarone pulmonary toxicity. Images and laboratory studies were evaluated in 54 patients who had chest radiographs and scintigraphic studies during amiodarone treatment of more than one month's duration among 561 patients receiving the medication for refractory arrhythmias. There were 22 patients with pulmonary symptoms and clinical evidence of amiodarone pulmonary toxicity (group 1); 19 patients had other causes for pulmonary symptoms (group 2); and 21 patients were without symptoms or other clinical evidence of pulmonary toxicity (group 3). There was no difference among groups in treatment duration or total amiodarone dose. Symptomatic presentation could not differentiate between group 1 and group 2 patients. However, radiographic findings of isolated pulmonary congestion or a normal radiograph in the presence of symptoms made amiodarone toxicity unlikely, while the appearance of new, dense radiographic infiltrates--often in a nodular distribution--were more frequent among group 1 patients (p less than 0.01). During symptomatic periods, 18 of 22 group 1 patients had abnormal gallium lung uptake, while four revealed more subtle serial changes but there was only one abnormal scintigram among symptomatic group 2 patients. Nonspecific radiographic abnormalities in patients with pulmonary symptoms on amiodarone therapy were rarely attributed to toxicity in the presence of a normal scintigram. One group 3 patient developed scintigraphic abnormalities early during amiodarone treatment, suggesting toxicity in the presence of a normal chest x-ray examination. Comparison of radiographic and scintigraphic studies performed during symptoms with those performed prior to symptom development best indicated the diagnosis, while comparison with later images assessed the efficacy of treatment. Diffusion capacity testing and transbronchial biopsy were sensitive but not specific for the diagnosis of amiodarone toxicity. Gallium image abnormalities parallel the development of amiodarone pulmonary toxicity and aid this diagnosis, especially when the chest radiograph is abnormal and ambiguous. Serial increments in scintigraphic abnormality appear especially helpful for diagnosis in the population at risk.
我们试图评估镓-67肺闪烁扫描在胺碘酮肺毒性评估中的作用。在561例接受胺碘酮治疗难治性心律失常且治疗时间超过1个月的患者中，对54例患者的影像和实验室检查进行了评估。其中22例有肺部症状且有胺碘酮肺毒性的临床证据（第1组）；19例有肺部症状的其他病因（第2组）；21例无症状或无肺部毒性的其他临床证据（第3组）。三组在治疗时间或胺碘酮总剂量上无差异。症状表现无法区分第1组和第2组患者。然而，孤立性肺充血的影像学表现或有症状时胸片正常则不太可能是胺碘酮毒性，而新出现的、致密的影像学浸润——通常呈结节状分布——在第1组患者中更常见（p<0.01）。在有症状期间，22例第1组患者中有18例镓肺摄取异常，4例显示更细微的系列变化，但有症状的第2组患者中只有1例闪烁扫描异常。胺碘酮治疗有肺部症状的患者中，在闪烁扫描正常的情况下，非特异性影像学异常很少归因于毒性。1例第3组患者在胺碘酮治疗早期出现闪烁扫描异常，提示在胸部X线检查正常的情况下存在毒性。症状期进行的影像学和闪烁扫描检查与症状出现前进行的检查进行比较最有助于诊断，而与后期影像比较可评估治疗效果。弥散功能测试和经支气管活检对胺碘酮毒性诊断敏感但不特异。镓影像异常与胺碘酮肺毒性的发展平行，有助于这一诊断，尤其是当胸片异常且不明确时。闪烁扫描异常的系列增加对高危人群的诊断似乎特别有帮助。
