单侧肺放射1个月后双侧放射性肺炎及放射后肺纤维化1例

X. Ying, R. Wozniak, H. Swerdloff, R. Kalil, T. Wong
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引用次数: 0

摘要

放射诱导的肺纤维化通常发生在放射治疗(RT)完成后6-12个月,通常只影响被照射的肺。我们报告了一例罕见的双侧放射引起的肺纤维化病例,仅在单侧放疗完成一个月后发生。病例描述:一位75岁男性胸膜间皮瘤患者接受了5个周期的新辅助卡铂和培美曲塞治疗,随后进行了开胸、胸膜切除术、去皮术和6周的放疗(28个部分,总计50.4灰色)(图1A),在完成放疗后33天出现了5天的呼吸困难和干咳。呼吸室内空气时血氧饱和度可达86%,经鼻插管4升/分钟后可达97%。CT检查显示左侧支气管扩张和基底部磨玻璃衰减代表炎症后的变化(图1B)。RT完成后27天重复CT显示新的双侧弥漫性磨玻璃影伴左上肺叶和下肺叶纤维化(图1C);目前表现的CT显示磨玻璃影增加,双侧纤维化(图1D)。血培养、SARSCoV-2 PCR、呼吸道病原体检测(包括流感A/B和呼吸道合胞病毒)、隐球菌抗原、半乳甘露聚糖和1,3- β -d-葡聚糖均未发现。经胸超声心动图显示肺动脉E/ E比12.6,肺动脉收缩压30 mmHg,血清b型利钠肽48 pg/ml。详细的核对证实他没有服用任何新的药物,包括他汀类药物。超敏性肺炎阴性。他的工作诊断是放射性肺损伤,具有早期肺炎和晚期纤维化的特征。开始使用短效支气管扩张剂和全身性皮质类固醇治疗,临床明显改善;患者在住院第6天出院回家。讨论:放射性肺损伤一般可分为急性期和晚期。前者通常被称为放射性肺炎,在放疗完成后4-12周表现为磨玻璃样混浊,后者在6-12个月后表现为支气管扩张和纤维化。我们的病例是一例罕见的在完成放疗后一个月内出现肺炎和纤维化的病例。此外,该患者在未接受任何放疗的情况下出现右肺肺炎和纤维化,未接受放疗的肺很少有肺炎的报道。免疫介导的淋巴细胞性肺泡炎被认为是放射性纤维化对侧扩散的一种机制。我们的病人在开始使用皮质类固醇后表现出显著的临床改善,并计划根据临床反应进行长期、缓慢的门诊减药。
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A Case of Bilateral Radiation Pneumonitis and Post Radiation Pulmonary Fibrosis One Month After Unilateral Lung Radiation
Introduction: Radiation induced pulmonary fibrosis typically develops between 6-12 months after completion of radiation therapy (RT), and typically affects only the irradiated lung. We present a rare case of bilateral radiation induced pulmonary fibrosis occurring only one month after completion of unilateral RT. Case Presentation: A 75-year-old male with pleural mesothelioma treated with five cycles of neoadjuvant carboplatin and pemetrexed followed by thoracotomy, pleurectomy, decortication and six weeks of RT (28 fractions, total 50.4 Grays) (Figure 1A) presented 33 days after completing RT with five days of dyspnea and dry cough. Vitals were notable for oxygen saturation of 86% on room air with improvement to 97% on 4 L/min via nasal cannula. Review of his pre-RT computed tomography (CT) demonstrated left-sided bronchiectasis and basilar ground glass attenuation representing post-inflammatory changes (Figure 1B). Repeat CT 27 days after completion of RT showed new bilateral diffuse ground-glass opacities with left upper and lower lobe fibrosis (Figure 1C);CT upon current presentation revealed increased ground-glass opacities and bilateral fibrosis (Figure 1D). Blood cultures, SARSCoV-2 PCR, respiratory pathogen panel (including influenza A/B and respiratory syncytial virus), cryptococcal antigen, galactomannan and 1,3-beta-d-glucan were all unrevealing. Transthoracic echocardiogram revealed septal E/e' ratio 12.6 and estimated pulmonary artery systolic pressure 30 mmHg, and serum b-type natriuretic peptide level was 48 pg/ml. Detailed reconciliation confirmed he was not taking any new medications, including statins. Hypersensitivity pneumonitis panel was negative. His working diagnosis was radiation induced lung injury with features of both early pneumonitis and late fibrosis. Therapy with short-acting bronchodilators and systemic corticosteroids was initiated with significant clinical improvement;patient was discharged home on hospital day six off oxygen. Discussion: Radiation induced lung injury can generally be divided into acute and late phases. The former is commonly known as radiation pneumonitis and manifests as ground-glass opacities 4-12 weeks after completion of RT, and the latter presents as bronchiectasis and fibrosis 6-12 months later. Ours is a rare case of pneumonitis and fibrosis that developed within one month of completing RT. Additionally, this patient developed pneumonitis and fibrosis of his right lung, which did not receive any radiation;very few cases of pneumonitis on the nonirradiated lung have been reported. Immunologically mediated lymphocytic alveolitis has been proposed as a mechanism for contralateral spread of radiation fibrosis. Our patient showed significant clinical improvement with initiation of corticosteroids with the plan for a long, slow outpatient taper based on clinical response.
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