Irradiation protection from hypersensitivity

Abstract

A 71-year-old man with metastatic carcinoma of the prostate was admitted for investigation of severe lower back pain. Spinal-cord compression at the level of the tenth thoracic vertebra (T10) was suspected clinically and multiple areas of vertebral bone metastases were seen on technetium bone scan. He was treated with bed rest, high-dose dexamethasone (4 mg four times a day) and a course of radiotherapy (5 MeV, 2000 cGy in 5 fractions over one week to his thoracic spine as a single posterior field, 8 15 cm), followed by radiotherapy to the lumbar spine (5 MeV, 2000 cGy in 5 fractions over 5 days as a single posterior field, 8 15 cm) as a site of known bony disease. On completion of radiotherapy, the dose of steroids was reduced and stopped, he was mobilised and started on cyproterone acetate (100 mg three times a day). A widespread maculopopular rash developed 2 weeks after completing radiotherapy. The rash covered most of his body except the areas (on both the front and back of his trunk) which had received a dose of radiotherapy (figure). He was treated with piriton and calamine lotion for the mild itch and discomfort associated with the rash. He had no known drug allergies, his medication before appearance of the rash included cyproterone acetate, goserelin, dexamethasone, subcutaneous heparin, codanthrusate, paracetamol, cimetidine, lactulose, and fybogel. He had recently received a blood transfusion. The rash was thought to be a result of cutaneous hypersensitivity although no cause was found, and it slowly faded. Our hypothesis is that skin within the radiation treatment field received a dose of radiotherapy (2000 cGy posteriorly and 600 cGy anteriorly) sufficient to result in local suppression of an otherwise generalised rash. Although the treatment was given as a single posterior field to both sites, a significant dose (approximately 600 cGy) would exit through the anterior surface of the patient at this energy. There are several possible explanations for this observation. Photon irradiation may have resulted in an altered response to an allergen or internal factors, or a cell population was affected in either a functional way (receptor alterations, cytokine production, intercellular or extracellular signals) or by depopulation. We were unable to take skin biopsies in this case which may have helped to elucideate the mechanism of this observed phenomenon. It is known that Langerhans cells have a role in both contact and atopic dermatitis, and that they exhibit multiple cell-surface receptors (allowing antigen recognition) and secrete a variety of cytokines (providing a mechanism for the observed ‘dermatitis’). Whilst there is no data on the sensitivity of Langerhans cells to megavoltage photon irradiation (as used in this case). Grenz rays (which are much less penetrating) delivered to the skin of people with contact hypersensitivity to nickel resulted in almost total suppression of allergic contact dermatitis in treated skin. Biopsies of skin showed pronounced reduction in numbers of Langerhans cells in the irradiated area as demonstrated by the monoclonal antibody OKT6.