Persistent subepidermal blistering in split-thickness skin graft sites. Ultrastructural and antigenic features simulating dystrophic or immunofluorescence-negative acquired epidermolysis bullosa.
We describe a child who began developing subepidermal blisters in the recipient sites of split-thickness skin grafts; this process has continued for almost a year and continues to spare nongrafted skin. Routine histologic and immunofluorescence mapping studies demonstrated this disorder to be a relatively noninflammatory one characterized by sub-lamina densa blister formation. Results of direct immunofluorescence were negative. By electron microscopy, anchoring fibrils were sparse in number and in some areas appeared malformed; otherwise, the basement membrane zone was morphologically unremarkable. Bullous pemphigoid antigen, laminin, type IV collagen, epidermolysis bullosa acquisita antigen, and LDA-1 were all normally expressed along the dermoepidermal junction. In contrast, KF-1 antigen was absent. These findings suggest a disease process confined to skin graft recipient sites with features identical to those previously described with recessive dystrophic or immunofluorescence-negative acquired epidermolysis bullosa.
Epstein
A
A
Department of Dermatology, University of Texas Medical Branch, Galveston.
Hendrick
S J
SJ
Sanchez
R L
RL
Solomon
A R
AR
Fine
J D
JD
D000941:Antigens / Q000032:analysis; D001706:Biopsy; D001768:Blister / Q000276:immunology / Q000473:pathology*; D002056:Burns / Q000601:surgery*; D002648:Child; D004820:Epidermolysis Bullosa / Q000276:immunology / Q000473:pathology; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008854:Microscopy, Electron; D011183:Postoperative Complications / Q000473:pathology*; D016038:Skin Transplantation
D000941:Antigens