large number of skin biopsies and do not provide precise population based frequencies. The calculated prevalence of busulfan associated SKD may be subject to further slight inaccuracy because of thesampling Zoledronate variance of controls and the inclusion of censored individuals such as second transplantation recipients. Nevertheless, the estimated 16% incidence in busulfan treated patients is the most reliable available for this pathological finding. Keratinocyte dysplasia following chemotherapy has been described infrequently but is now well documented to actually occur at high frequencies. It has been variously described as keratinocyte atypia, keratinocyte dysmaturation, or epidermal dysmaturation. The cause of the epidermal dysmaturation has been postulated to be a direct cytotoxic action of chemotherapeutic drugs or radiation given before engraftment, affecting keratinocytes.
In patients who have not undergone transplantation, Imatinib Gleevec these agents have been associated with a specific skin pathology exhibiting an attenuated epidermis, individual keratinocyte necrosis, and cell poor interface dermatitis. The agents include cyclophosphamide, busulfan, cyclosporine, etoposide, docetaxel, thiotepa, cytarabine, bleomycin, hydroxyurea, methotrexate, and others. Etoposide and busulfan have been associated with specific pathologic abnormalities. The specific keratinocyte pathology associated with busulfan has been described as,busulfan, cells that are abnormally large keratinocytes with extremely large nuclei.
demonstrate irregular nuclear contours, bizarre chromatin patterns, and prominent keratohyaline granules, This description is similar to, but generally Aprepitant 170729-80-3 more marked than, our independently determined criteria defining severe keratinocyte dysplasia. The severe form of keratinocyte dysplasia has been described in posttransplantation patients as a common lesion, more frequent early posttransplantation. Castano et al. reported a 44% incidence of severe keratinocyte dysplasia in the post marrow or liver transplantation recipients inthe period less than 60 days posttransplantation. They found an independent association with cyclophosphamide and not busulfan. Hymes et al. found the incidence of severe keratinocyte dysplasia to be 92% in busulfan treated marrow transplantation recipients in the interval 15 to 45 days posttransplantation.
Because the Idarubicin 57852-57-0 dose of busulfan was similar to ours, one possible explanation of the markedly higher incidence is the earlier procurement of the skin brain biopsies.With weekly biopsies, virtually all of their cases would have been biopsied twice in the 15 to 27 day period, during which they could have found SKD. Our patients were biopsied on day 28 at the earliest. The interval difference is reflected in their median day posttransplantation of 35, versus our mean of 61. They further separated out slight dysplasia present early posttransplantation, median 13 days, and ascribed it to the cyclophosphamide in a TBI cyclophosphamide regimen, as had Sale et al. The most likely explanation is that cyclophosphamide is commonly associated with slight keratinocyte dysplasia early posttransplantation, and busulfan is commonly associated with severe keratinocyte dysplasia, lasting in some smaller number of cases, later into the posttransplantation.