Abstract
Radiation-induced lung damage presents as a typical “black box” situation. The input, i.e., the dose dependence, and the output, i.e., the clinical, histological and radiographic (including CT) features of disease, are well known. However, the pathogenetic mechanisms which transform the lung tissue, normally filled with air, first into alveoli with thickened alveolar capillary membranes filled with exudate and finally into a fibrotic scar are largely unknown. Recent studies, moreover, demonstrate that interstitial pneumonia developing after total body irradiation and bone marrow transplantation is fundamentally different from radiation pneumonitis after fractionated localized radiotherapy with regard to mechanism and radiobiology. The development of interstitial pneumonia associated with bone marrow transplantation is influenced by a variety of factors which also target the lung, including chemotherapy, viremia and decreased immunological defenses (Varekamp 1990; Molls and van Beuningen 1991). Yet the increasing therapeutic use of total body irradiation and bone marrow transplantation has highlighted the doselimiting complications imposed by the lung. Increased research efforts into the radiobiology of radiation-induced pneumopathy has yielded some fundamental observations, which will be discussed here.
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© 1995 Springer-Verlag Berlin Heidelberg
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Herrmann, T., Schorcht, J., Molls, M. (1995). Radiation Pneumopathy — Experimental and Clinical Data. In: Dunst, J., Sauer, R. (eds) Late Sequelae in Oncology. Medical Radiology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-46794-3_19
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DOI: https://doi.org/10.1007/978-3-642-46794-3_19
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