Dörr W
Wolfgang Dörr, Klinik und Poliklinik für Strahlentherapie und Radioonkologie, Medizinische Fakultät Carl Gustav Carus, Fetscherstr. 74, 01307 Dresden.
Nuklearmedizin. 2010;49 Suppl 1:S53-8.
The curative effectivity of external or internal radiotherapy necessitates exposure of normal tissues with significant radiation doses, and hence must be associated with an accepted rate of side effects. These complications can not a priori be considered as an indication of a too aggressive therapy. Based on the time of first diagnosis, early (acute) and late (chronic) radiation sequelae in normal tissues can be distinguished. Early reactions per definition occur within 90 days after onset of the radiation exposure. They are based on impairment of cell production in turnover tissues, which in face of ongoing cell loss results in hypoplasia and eventually a complete loss of functional cells. The latent time is largely independent of dose and is defined by tissue biology (turn-over time). Usually, complete healing of early reactions is observed. Late radiation effects can occur after symptom-free latent times of months to many years, with an inverse dependence of latency on dose. Late normal tissue changes are progressive and usually irreversible. They are based on a complex interaction of damage to various cell populations (organ parenchyma, connective tissue, capillaries), with a contribution from macrophages. Late effects are sensitive for a reduction in dose rate (recovery effects). A number of biologically based strategies for protection of normal tissues or for amelioration of radiation effects was and still is tested in experimental systems, yet, only a small fraction of these approaches has so far been introduced into clinical studies. One advantage of most of the methods is that they may be effective even if the treatment starts way after the end of radiation exposure. For a clinical exploitation, hence, the availability of early indicators for the progression of subclinical damage in the individual patient would be desirable. Moreover, there is need to further investigate the molecular pathogenesis of normal tissue effects in more detail, in order to optimise biology based preventive strategies, as well as to identify the precise mechanisms of already tested approaches (e.g. stem cells).
外照射或内照射放疗的疗效需要对正常组织进行高剂量照射，因此必然会伴随一定比例的副作用。这些并发症不能先验地被视为治疗过于激进的表现。根据首次诊断时间，正常组织中的早期（急性）和晚期（慢性）放射性后遗症可以区分。按照定义，早期反应发生在辐射暴露开始后的90天内。它们是由于更新组织中细胞生成受损所致，面对持续的细胞损失，会导致发育不全，最终功能细胞完全丧失。潜伏期在很大程度上与剂量无关，由组织生物学（更新时间）决定。通常，早期反应可完全愈合。晚期放射性效应可在数月至数年的无症状潜伏期后出现，潜伏期与剂量呈反比。晚期正常组织变化是渐进性的，通常不可逆转。它们基于对各种细胞群体（器官实质、结缔组织、毛细血管）的损伤以及巨噬细胞的作用之间的复杂相互作用。晚期效应对剂量率降低敏感（恢复效应）。过去和现在都在实验系统中测试了许多基于生物学的保护正常组织或减轻辐射效应的策略，但迄今为止，只有一小部分方法被引入临床研究。大多数方法的一个优点是，即使在辐射暴露结束后很久才开始治疗，它们也可能有效。因此，对于临床应用来说，获得个体患者亚临床损伤进展的早期指标将是理想的。此外，需要更详细地进一步研究正常组织效应的分子发病机制，以优化基于生物学的预防策略，并确定已测试方法（如干细胞）的确切机制。
