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Dapsone therapy for oral‐genital ulceration

Although the patient had recieved many other drugs during this period, only the cytotoxics could be linked temporally with the separate attacks of inflammation. Histologically, one of the erythematous lesions showed an atrophic actinic keratosis with a mild superficial and deep lymphohistiocytic perivascular infiltrate. In one area there was a suprabasal cleft associated with acantholytic and dyskeratotic cells in the lower levels of the epidermis. This reaction has been described previously only in association with the systemic administration of 5-fiuorouracil (Falkson & Schulz, 1962) and of deoxycoformycin (Camisa, Grever & Bouroncle, 1985). Which cytotoxic drug or combination of drugs caused the reaction in our patient is not clear. However, it is of interest that both doxorubicin and 5-fluorouracil cause radiation recall reactions (Hood & Haynes, 1983). As actinic keratoses are caused by long-term damage to the skin by UV radiation, their inflammation may be considered a form of radiation recall reaction. It is possible that the dysplastic cells of actinic keratoses bear accumulated UV-induced damage in their DNA which renders them more susceptible to the toxic effects of cytotoxic drugs. Clearly this reaction is different from the development of solar keratoses and cutaneous malignancies in chronically immunosuppressed transplant recipients. In these cases the lesions appear to develop as a result of impaired immunosurveillance, and the clinical course is different. The recognition of this reaction is of clinical importance as it may be misdiagnosed as a drug allergy, resulting in the unnecessary withholding of drugs. The most important clue to the true nature of the eruption is its restriction to sun-damaged skin.