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Transient Intraepidermal Bullous Reaction After Skin Graft for Toxic Epidermal Necrolysis: Ultrastructural and Immunohistochemical Features Similar to Those of Inherited Epidermolysis Bullosa Simplex

Transient Intraepidermal Bullous Reaction After Skin Graft for Toxic Epidermal Necrolysis:... Abstract • Blister formation in skin graft donor or recipient sites is uncommon. We describe a 49-year-old female patient with bullae in sites of grafts used in the treatment of toxic epidermal necrolysis. Generalized loss of skin developed 3 weeks after she had ingested phenobarbital. Sixty days after the beginning of the toxic epidermal necrolysis, the reepidermization was only 80% and skin grafts were placed on lower-extremity and abdominal wounds using the first healed sites as donor sites. Several bullae and erosions were noted on grafted areas 3 weeks later. Skin biopsy specimens revealed separation at the dermoepidermal junction, and no autoantibodies were detected by direct and indirect immunofluorescence. Electron microscopy demonstrated that the blister was formed through the basal keratinocytes and that the dermoepidermal junction, including hemidesmosomes and anchoring fibrils, was normal. Immunofluorescence mapping was performed using polyclonal antibodies from the serum of patients with bullous pemphigoid and epidermolysis bullosa acquisita and monoclonal antibodies against GB3 antigen and collagen type VII. All but the bullous pemphigoid serum gave positive results; only faint and focal staining of the dermoepidermal junction was observed with bullous pemphigoid serum. These findings are the same as those encountered in hereditary epidermolysis bullosa simplex. A biopsy performed 1 year later in the same site as the first one revealed that bullous pemphigoid antigen was normally expressed. Keratinocytes autografted in the treatment of toxic epidermal necrolysis may become transiently, functionally abnormal because of the alteration of recipient sites. (Arch Dermatol. 1991;127:1369-1374) References 1. Barker DJ, Cotterill JA. Development of subepidermal bullae in the split-skin graft donor site of a psoriatic . Dermatologica. 1980;160:311-314.Crossref 2. Baran R, Juhlin L, Brun P. Bullae in skin grafts . Br J Dermatol. 1984;111:221-225.Crossref 3. Berman A. Bullae in the donor site of a split-thickness skin graft . J Dermatol Surg Oncol. 1982;8:291-292.Crossref 4. Epstein A, Hendrick SJ, Sanchez RL, Solomon AR, Fine JD. Persistent subepidermal blistering in split-thickness graft sites: ultrastructural and antigenic features simulating dystrophic or immunofluorescence-negative acquired epidermolysis bullosa . Arch Dermatol. 1988;124:244-249.Crossref 5. Dubertret L, Bertaux B, Fosse M, Boulvin F, Touraine R. A simple method for correlating observations on skin at the light and electron microscopic levels . Br J Dermatol. 1980;102:149-154.Crossref 6. Sakai LY, Keene DR, Morris NP, Burgeson RE. Type VII collagen is a major structural component of anchoring fibrils . J Cell Biol. 1986;103:1577-1586.Crossref 7. Leigh IM, Eady RAJ, Heagerty AHM, Purkis PE, White ME, Burgeson RE. Type VII collagen is a normal component of epidermal basement membrane, which shows altered expression in recessive dystrophic epidermolysis bullosa . J Invest Dermatol. 1988;90:639-642.Crossref 8. Verrando P, Bae-Li HSI, Chang-Jing YEH, Pisani A, Serieys N, Ortonne JP. Monoclonal antibody GB3: a new probe for the study of human basement membranes and hemidesmosomes . Exp Cell Res. 1987;170:116-128.Crossref 9. Heagerty AHM, Eady RAJ, Kennedy AR. Rapid prenatal diagnosis of epidermolysis bullosa letalis using GB3 monoclonal antibody . Br J Dermatol. 1987;117:271-275.Crossref 10. Mutasim DF, Takahashi Y, Labib RS, Anhalt GJ, Patel HP, Diaz LA. A pool of bullous pemphigoid antigen(s) is intracellular and associated with the basal cell cytoskeleton-hemidesmosome complex . J Invest Dermatol. 1985;84:47-53.Crossref 11. Bernard PH, Prost C, Lecerf V, et al. Studies of cicatricial pemphigoid auto-antibodies using direct immunoelectron microscopy and immunoblot analysis . J Invest Dermatol. 1990;94:630-635.Crossref 12. Cooper TW, Bauer EA, Briggaman RA. The mechanobullous diseases (epidermolysis bullosa) . In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine . 3rd ed. New York, NY: McGraw-Hill International Book Co; 1987:610-626. 13. Fine JD. Epidermolysis bullosa: variability of expression of cicatricial pemphigoid, bullous pemphigoid, and epidermolysis bullosa acquisita antigens in clinically uninvolved skin . J Invest Dermatol. 1985;85:47-49.Crossref 14. Thivolet J, Beyvin A, André D. Anticorps `pemphiguslike' et `pemphigoidlike .' Dermatologica. 1970;140:310-317.Crossref 15. Ablin RJ, Milgrom F, Kano K, Rapaport FT, Beutner EH. Pemphigus-like antibodies in patients with skin burns . Vox Sang. 1969;16:73-75.Crossref 16. Quismorio FP, Bland SL, Friou GJ. Autoimmunity in thermal injury: occurrence of rheumatoid factors, antinuclear antibodies and antiepithelial antibodies . Clin Exp Immunol. 1971;8:701-711. 17. Chorzelski T, Jablonska S, Beutner EH, Kowalska M. Can pemphigus be provoked by a burn? Br J Dermatol. 1971;85:320-325.Crossref 18. Head MD. Wound and skin care . In: Fisher SV, Helm PA, eds. Comprehensive Rehabilitation of Burns . Baltimore, Md: Williams & Wilkins; 1984:148-176. 19. Fine JD, Smith LT, Holbrook KA, Katz SI. The appearance of four basement membrane zone antigens in developing human fetal skin . J Invest Dermatol. 1984;83:66-69.Crossref 20. Fine JD, Redmar DA, Goodman AL. Sequence of reconstitution of seven basement-membrane components following split-thickness wound induction in primate skin . Arch Dermatol. 1987;123:1174-1178.Crossref 21. Stanley JR, Alvarez OM, Bere EW Jr, Eaglstein WH, Katz SI. Detection of basement membrane zone antigens during epidermal wound healing in pigs . J Invest Dermatol. 1981;77:240-243.Crossref 22. Demarchez M, Desbas C, Prunieras M. Wound healing of human skin transplanted on to the nude mouse . Br J Dermatol. 1985;113( (suppl 28) ):177-182.Crossref 23. Takamori K, Ikeda S, Naito K, Ogawa H. Proteases are responsible for blister formation in recessive dystrophic epidermolysis bullosa and epidermolysis bullosa simplex . Br J Dermatol. 1985; 112:533-538.Crossref 24. Revuz J, Penso D, Roujeau JC, et al. Toxic epidermal necrolysis . Arch Dermatol. 1987;123:1160-1165.Crossref 25. Saiag P, Coulomb B, Bell E, Lebreton C, Dubertret L. Psoriatic fibroblasts induce hyperproliferation of normal keratinocytes in a skin equivalent model in vitro . Science. 1985;230:669-672.Crossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Dermatology American Medical Association

Transient Intraepidermal Bullous Reaction After Skin Graft for Toxic Epidermal Necrolysis: Ultrastructural and Immunohistochemical Features Similar to Those of Inherited Epidermolysis Bullosa Simplex

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References (27)

Publisher
American Medical Association
Copyright
Copyright © 1991 American Medical Association. All Rights Reserved.
ISSN
0003-987X
eISSN
1538-3652
DOI
10.1001/archderm.1991.01680080105012
Publisher site
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Abstract

Abstract • Blister formation in skin graft donor or recipient sites is uncommon. We describe a 49-year-old female patient with bullae in sites of grafts used in the treatment of toxic epidermal necrolysis. Generalized loss of skin developed 3 weeks after she had ingested phenobarbital. Sixty days after the beginning of the toxic epidermal necrolysis, the reepidermization was only 80% and skin grafts were placed on lower-extremity and abdominal wounds using the first healed sites as donor sites. Several bullae and erosions were noted on grafted areas 3 weeks later. Skin biopsy specimens revealed separation at the dermoepidermal junction, and no autoantibodies were detected by direct and indirect immunofluorescence. Electron microscopy demonstrated that the blister was formed through the basal keratinocytes and that the dermoepidermal junction, including hemidesmosomes and anchoring fibrils, was normal. Immunofluorescence mapping was performed using polyclonal antibodies from the serum of patients with bullous pemphigoid and epidermolysis bullosa acquisita and monoclonal antibodies against GB3 antigen and collagen type VII. All but the bullous pemphigoid serum gave positive results; only faint and focal staining of the dermoepidermal junction was observed with bullous pemphigoid serum. These findings are the same as those encountered in hereditary epidermolysis bullosa simplex. A biopsy performed 1 year later in the same site as the first one revealed that bullous pemphigoid antigen was normally expressed. Keratinocytes autografted in the treatment of toxic epidermal necrolysis may become transiently, functionally abnormal because of the alteration of recipient sites. (Arch Dermatol. 1991;127:1369-1374) References 1. Barker DJ, Cotterill JA. Development of subepidermal bullae in the split-skin graft donor site of a psoriatic . Dermatologica. 1980;160:311-314.Crossref 2. Baran R, Juhlin L, Brun P. Bullae in skin grafts . Br J Dermatol. 1984;111:221-225.Crossref 3. Berman A. Bullae in the donor site of a split-thickness skin graft . J Dermatol Surg Oncol. 1982;8:291-292.Crossref 4. Epstein A, Hendrick SJ, Sanchez RL, Solomon AR, Fine JD. Persistent subepidermal blistering in split-thickness graft sites: ultrastructural and antigenic features simulating dystrophic or immunofluorescence-negative acquired epidermolysis bullosa . Arch Dermatol. 1988;124:244-249.Crossref 5. Dubertret L, Bertaux B, Fosse M, Boulvin F, Touraine R. A simple method for correlating observations on skin at the light and electron microscopic levels . Br J Dermatol. 1980;102:149-154.Crossref 6. Sakai LY, Keene DR, Morris NP, Burgeson RE. Type VII collagen is a major structural component of anchoring fibrils . J Cell Biol. 1986;103:1577-1586.Crossref 7. Leigh IM, Eady RAJ, Heagerty AHM, Purkis PE, White ME, Burgeson RE. Type VII collagen is a normal component of epidermal basement membrane, which shows altered expression in recessive dystrophic epidermolysis bullosa . J Invest Dermatol. 1988;90:639-642.Crossref 8. Verrando P, Bae-Li HSI, Chang-Jing YEH, Pisani A, Serieys N, Ortonne JP. Monoclonal antibody GB3: a new probe for the study of human basement membranes and hemidesmosomes . Exp Cell Res. 1987;170:116-128.Crossref 9. Heagerty AHM, Eady RAJ, Kennedy AR. Rapid prenatal diagnosis of epidermolysis bullosa letalis using GB3 monoclonal antibody . Br J Dermatol. 1987;117:271-275.Crossref 10. Mutasim DF, Takahashi Y, Labib RS, Anhalt GJ, Patel HP, Diaz LA. A pool of bullous pemphigoid antigen(s) is intracellular and associated with the basal cell cytoskeleton-hemidesmosome complex . J Invest Dermatol. 1985;84:47-53.Crossref 11. Bernard PH, Prost C, Lecerf V, et al. Studies of cicatricial pemphigoid auto-antibodies using direct immunoelectron microscopy and immunoblot analysis . J Invest Dermatol. 1990;94:630-635.Crossref 12. Cooper TW, Bauer EA, Briggaman RA. The mechanobullous diseases (epidermolysis bullosa) . In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine . 3rd ed. New York, NY: McGraw-Hill International Book Co; 1987:610-626. 13. Fine JD. Epidermolysis bullosa: variability of expression of cicatricial pemphigoid, bullous pemphigoid, and epidermolysis bullosa acquisita antigens in clinically uninvolved skin . J Invest Dermatol. 1985;85:47-49.Crossref 14. Thivolet J, Beyvin A, André D. Anticorps `pemphiguslike' et `pemphigoidlike .' Dermatologica. 1970;140:310-317.Crossref 15. Ablin RJ, Milgrom F, Kano K, Rapaport FT, Beutner EH. Pemphigus-like antibodies in patients with skin burns . Vox Sang. 1969;16:73-75.Crossref 16. Quismorio FP, Bland SL, Friou GJ. Autoimmunity in thermal injury: occurrence of rheumatoid factors, antinuclear antibodies and antiepithelial antibodies . Clin Exp Immunol. 1971;8:701-711. 17. Chorzelski T, Jablonska S, Beutner EH, Kowalska M. Can pemphigus be provoked by a burn? Br J Dermatol. 1971;85:320-325.Crossref 18. Head MD. Wound and skin care . In: Fisher SV, Helm PA, eds. Comprehensive Rehabilitation of Burns . Baltimore, Md: Williams & Wilkins; 1984:148-176. 19. Fine JD, Smith LT, Holbrook KA, Katz SI. The appearance of four basement membrane zone antigens in developing human fetal skin . J Invest Dermatol. 1984;83:66-69.Crossref 20. Fine JD, Redmar DA, Goodman AL. Sequence of reconstitution of seven basement-membrane components following split-thickness wound induction in primate skin . Arch Dermatol. 1987;123:1174-1178.Crossref 21. Stanley JR, Alvarez OM, Bere EW Jr, Eaglstein WH, Katz SI. Detection of basement membrane zone antigens during epidermal wound healing in pigs . J Invest Dermatol. 1981;77:240-243.Crossref 22. Demarchez M, Desbas C, Prunieras M. Wound healing of human skin transplanted on to the nude mouse . Br J Dermatol. 1985;113( (suppl 28) ):177-182.Crossref 23. Takamori K, Ikeda S, Naito K, Ogawa H. Proteases are responsible for blister formation in recessive dystrophic epidermolysis bullosa and epidermolysis bullosa simplex . Br J Dermatol. 1985; 112:533-538.Crossref 24. Revuz J, Penso D, Roujeau JC, et al. Toxic epidermal necrolysis . Arch Dermatol. 1987;123:1160-1165.Crossref 25. Saiag P, Coulomb B, Bell E, Lebreton C, Dubertret L. Psoriatic fibroblasts induce hyperproliferation of normal keratinocytes in a skin equivalent model in vitro . Science. 1985;230:669-672.Crossref

Journal

Archives of Dermatology – American Medical Association

Published: Sep 1, 1991

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