Molls M, Budach V, Bamberg M
Strahlenther Onkol. 1986 Apr;162(4):226-32.
The pathogenesis of interstitial pneumonitis (IP) after chemoradiotherapy and subsequent bone marrow transplantation is not completely understood. Total body irradiation (TBI) with a dose of about 10 Gy significantly contributes to this very serious complication. The radiation induced morphological alterations especially of the crucial targets, namely the pneumocytes type II and capillaries are described. Investigations in animals and in humans reveal that pneumonitis occurs over a very short range of doses. In humans a single dose of 9.3 Gy given at a high dose rate leads to an incidence of 50%. Reduction of the dose by shielding the lungs, fractionation of irradiation and decreasing the dose rate are considered to be the main possibilities which diminish the risk of pneumonitis after TBI. The role of further factors involved in the development of IP such as cytomegalovirus, age, reduced lung volume, immunological mechanisms and others is discussed. Especially chemotherapeutic agents may increase lung morbidity by interacting with TBI.
放化疗及后续骨髓移植后间质性肺炎(IP)的发病机制尚未完全明确。约10 Gy剂量的全身照射(TBI)是导致这一严重并发症的重要因素。文中描述了辐射引起的形态学改变,尤其是关键靶细胞,即Ⅱ型肺细胞和毛细血管的改变。对动物和人类的研究表明,肺炎在很窄的剂量范围内即可发生。在人类中,单次高剂量率给予9.3 Gy的剂量会导致50%的发病率。通过肺部屏蔽减少剂量、分割照射以及降低剂量率被认为是降低TBI后肺炎风险的主要方法。文中还讨论了其他参与IP发生发展的因素,如巨细胞病毒、年龄、肺容积减小、免疫机制等的作用。特别是化疗药物可能通过与TBI相互作用增加肺部发病率。