membrane may be decreased, absent, or biochemically altered. Structural and/or functional abnormalities may exist within the epidermis of skin from patients with EB simplex that, in the presence of heat and/or mechanical trauma, lead to intraepidermal blister formation.These abnormalities within both groups suggest that there are several distinct functional and biochemical abnormalities in patients with recessive dystrophic EB and in some patients with EB simplex. In recessive dystro¬ phic EB, these abnormalities may contribute directly to blister formation.Retinoids may be reasonable therapy for certain forms of EB. Recent studies have shown that certain retinoids inhibit collagenase and gelatinase activity in human skin fibroblast cultures, suggesting that retinoids can modulate collagenase in vitro by two mechanisms: by decreasing the synthesis of collagenase and by inducing the synthesis of a fibroblast-derived inhibitor of collagenase activity. A pilot study using low-dose (0.4 mg/kg/d) isotretinoin in three patients with severe recessive dystrophic EB showed a mean reduction of 67% in the number of bullae.4 However, etretinate therapy was found to be ineffective in one patient with recessive dystrophic EB.5Our patient with localized EB simplex had a marked reduction in blistering and acceleration in healing of blisters while receiving low-dose isotretinoin. We conclude that retinoids, in particular isotretinoin, may be a useful therapeutic option in patients with EB simplex.