Radiation Induced Lung Damage: Mechanisms and Clinical Implications

Y. Oh
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引用次数: 2

Abstract

Radiation therapy is one of most important therapeutic modalities for thoracic malignancies. However, radiation-induced lung damage, such as radiation pneumonitis or fibrosis, is a main dose-limiting factor when irradiating the thorax. The radiation over threshold dose results in damage to pneumocytes and endothelial cells and the inflammatory changes following the damage lead to necrosis of damaged tissue, which are then replaced by fibrotic tissue. There is diffuse lung damage and edema on histopathologic inspection; however, the tissue damage and edema is not specific for radiation injury and we are far from a reliable pathogenic model. Many parameters have been evaluated for predicting radiation pneumonitis and the most consistent predictor is cumulative radiation dose to normal lung tissue. The combination of chemotherapy probably increases the incidence and severity of radiation pneumonitis; however, this is not clear. Efforts to reduce the radiation dose to normal lung tissue using new radiotherapy techniques can reduce the incidence and severity of radiationinduced lung damage. Many biological agents have been tried to prevent and treat radiation pneumonitis; however, more data is needed.
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辐射引起的肺损伤:机制和临床意义
放射治疗是胸部恶性肿瘤最重要的治疗方式之一。然而,辐射引起的肺损伤,如放射性肺炎或纤维化,是照射胸部时的主要剂量限制因素。超过阈值剂量的辐射导致肺细胞和内皮细胞的损伤,损伤后的炎症变化导致受损组织坏死,然后被纤维化组织所取代。组织病理学检查可见弥漫性肺损伤及水肿;然而,组织损伤和水肿并不是辐射损伤所特有的,我们还远没有一个可靠的致病模型。许多参数已被评估用于预测放射性肺炎和最一致的预测是正常肺组织的累积辐射剂量。联合化疗可能增加放射性肺炎的发病率和严重程度;然而,这一点尚不清楚。利用新的放射治疗技术减少对正常肺组织的辐射剂量,可以降低辐射引起的肺损伤的发生率和严重程度。已经尝试了许多生物制剂来预防和治疗放射性肺炎;然而,还需要更多的数据。
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