Within the past five years, our understanding of inherited epidermolysis bullosa (EB) has grown tremendously as a result of a combination of favorable conditions. First, recent advances in the fields of cell biology, applied immunology, and molecular biology have led to the development of in vitro models and in vivo markers for specific subtypes of EB. As a result, more refined and selective immunohistochemical reagents, notably polyclonal and monoclonal antibodies, are now available for diagnosis, both postnatal and prenatal, and for more basic studies aimed at elucidation of further mechanistic aspects of blister formation in this disease (J.D.F., R. Eady, MBBS, FRCP, M. Levy, PhD, unpublished observation, 1988).1-12 Eventually, such work should result in definition of the actual causative gene defects in EB. Second, recent laboratory findings have led to the development of new treatments (ie, phenytoin, autologous epidermal cell culture-derived skin grafts) and the initiation of additional
Fine J. Changing Clinical and Laboratory Concepts in Inherited Epidermolysis Bullosa. Arch Dermatol. 1988;124(4):523–526. doi:10.1001/archderm.1988.01670040025015
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