Epidermolysis bullosa (EB) is a rare, hereditary, dermatologic disease with onset at birth or early infancy. Pathologically, the disease is characterized by blister formation resembling that of second-degree burns following slight, sometimes innocuous trauma(l). Immediate and long-term complications of epidermolysis bullosa include infectious, nutritional, orthopedic, gastrointestinal, hemolytic, and psychiatric sequelae. EB is heterogeneous, with varying patterns of inheritance and severity, ranging from mild inconvenience to severe debilitating disease, with death at an early age(2). The lesions ooze large amounts of proteinaceous substance rich in electrolyte content that predisposes the skin to local infections. The underlying defect appears to be a lack of the cellular "glue" in squamous epithelium, which is responsible for maintenance of cellular integrity. This lack of "glue" can be from destruction of the skin layers due to release of either a necrotizing agent or a collagen-lytic substance in the dermis(3). Epidemiologically, the disease is worldwide and rare, occurring in between 1:50,000 for the dominant types and 1:300,000 for the recessive dystrophic forms. There does not seem to be any predilection for a particular ethnic group. No relationship has been found to other genetic markers, such as ABO blood type, RH type, or sex(4). Classification is made by histologic location of the level of defect in the skin, biochemical markers, and by hereditary patterns(2). Clinically, the disease can be divided into three groups: Epidermolysis bullosa simplex (EBS). This is the mildest form of the disease and the one most compatible with life. Lesions occur t the basal layer of the epidermis and do not lead to scarring or to hyperkeratosis(l). It usually in-
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