Fibrosis is assumed to be the usual explanation of palpable induration (firmness or hardness) in the breast developing several years post-radiotherapy in the absence of features suggesting tumour recurrence. Fibrosis is a well-recognised late consequence of high dose radiotherapy elsewhere in the body, where it contributes to dose-limiting complications and reduced compliance of organs with important elastic properties. Clinico-pathological studies of induration in the early years following breast radiotherapy suggest that fat necrosis is sometimes a contributory factor (Clarke et al. 1983; RostoM and el-Sayed 1987; Boyages et al. 1988). However, in a recent report, Padhani et al. (2002) showed that radiotherapy-induced induration in the breast many years after treatment is seldom caused by fat necrosis but that there was a close correspondence between breast oedema demonstrated on MRI and the severity of clinical induration (Padhani et al. 2002). They suggested that the parenchymal oedema might be a manifestation of a persistent vascular leak related to radiation induced vascular injury. In another publication, the same authors showed that increased parenchymal oedema contributing to palpable induration was associated with an increased extravascular-extracellular leakage space demonstrated on DCE-MRI (Padhani et al. 2003). They did not demonstrate an increase in transfer constant but did observe increased enhancement of irradiated breasts compared to contralateral non-irradiated breast tissue. They hypothesised that increased enhancement was due to increased number of microvessels with normal permeability and that impaired drainage may be a further con tributing factor for hardness of the breasts following radiotherapy.
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