ABSTRACT. Erythema occurs in 80-90% of women treated for breast cancer with radiation therapy. There is currently no standard treatment for radiation-induced skin reactions. This study investigates the clinical efficacy of Mepilex Lite dressings in reducing radiation-induced erythema in women with breast cancer. A total of 28 patients were recruited; of these, 24 participants presented with 34 erythematous areas of skin for analysis. When erythema was visible, each affected skin area was randomly divided into two similar halves: one half was treated using Mepilex Lite dressings, the other half with standard aqueous cream. Skin reactions were assessed by the RadiationInduced Skin Reaction Assessment Scale. We also evaluated any potential dose build-up by the dressings using a white water phantom, the dose distribution over the breast via thermoluminescent dosimeters (TLDs) and the surface skin temperature with an infrared thermographic scanner. Mepilex Lite dressings significantly reduced the severity of radiation-induced erythema compared with standard aqueous cream (p ,0.001), did not affect surface skin temperature and caused only a small (0.5 mm) dose build-up. TLD measurements showed that the inframammary fold was exposed to significantly higher doses of radiation than any other breast region (p ,0.0001). Mepilex dressings reduce radiation-induced erythema.

The diagnosis of perineural spread is largely clinical and may be confirmed with imaging findings in the majority of cases. The role of biopsy is usually complementary but may be essential in some cases. In patients with evidence of distant perineural spread, radiotherapy volumes inclusive of potential antegrade and retrograde spread are recommended. Three-dimensional conformal planning or intensity-modulated radiation therapy assists in minimizing damage to adjacent structures. Synchronous chemotherapy should be considered to potentiate the effectiveness of radiation. The place of surgery in the treatment of perineural spread is palliative.

Cyanohydroxybutene (CHB), a glycosinolate breakdown product, causes pancreatic injury when given to animals in large amounts. To determine the course of CHB-induced pancreatopathy, rats were given a single subcutaneous dose of CHB and the pancreas weighed and examined by light and electron microscopy and immunohistochemistry at intervals from 2 h to 28 days. The pancreatic lesion was unusual in that there was marked early oedema with limited inflammatory cell infiltration, rapid synchronous onset of acinar cell apoptosis and early advanced atrophy engendering only a limited regenerative response. Acinar cell apoptosis was atypical in that cell fragmentation was limited and phagocytosis delayed, resulting in extensive secondary necrosis. As ducts were unaffected by CHB, the crowded ducts making up the epithelial component of atrophic lobules could be clearly shown to derive from their condensation and proliferation, not the redifferentiation of pre-existing acinar cells, widely held to produce this lesion. Although the basis of CHB selectivity and toxicity for pancreatic acinar cells remains unknown, the potential therapeutic benefit of such an agent in patients with pancreatitis or pancreatic tumours warrants further investigation.

This study reaffirmed that SRT achieves very good local control and eye retention rates. PIB did not appear to reduce the radiation retinopathy rate in this study, and more studies are required especially Phase II and III trials to determine PIB efficacy in preventing RR.

No abstract