title: Anticonvulsant-induced toxic epidermal necrolysis: monitoring the immunologic response.
abstract: BACKGROUND
  Toxic epidermal necrolysis is a severe reaction with skin involvement induced by different drugs and other agents. The mechanisms implicated in the induction of the reaction are poorly understood.
  
  
  OBJECTIVE
  Our purpose was to study the involvement of T lymphocytes and other immunocompetent cells in the peripheral blood, blister fluid, and affected skin of 3 patients who had a severe reaction after receiving anticonvulsant medication.
  
  
  METHODS
  Quantification of T lymphocytes expressing the skin-homing receptor (cutaneous lymphocyte-associated antigen ¿CLA) in peripheral blood, skin, and skin blister fluid and assessment of other adhesion molecules, activation markers, and inflammatory interleukins by flow cytometry, immunohistochemistry, and reverse transcription-PCR.
  
  
  RESULTS
  An increase in CD3(+)CLA(+) cells paralleling the severity of the disease was observed in both peripheral blood and skin, tending to normalize as soon as patient's conditions improved. E-selectin was detected in endothelial vessels in parallel with CLA expression on lymphocytes. An overexpression of TNFalpha, IFN-gamma, and IL-2 was also observed in PBMCs. The expression of the different markers changed over the course of the disease.
  
  
  CONCLUSIONS
  These data show an increase in activated T cells expressing the skin-homing receptor in both tissue and peripheral blood accompanying clinical symptoms, with a recruitment of macrophages and an overexpression of cytokines. All these results suggest an important role for T cells in the production of toxic epidermal necrolysis.
authors.affiliation: Research Unit for Allergic Diseases, Carlos Haya Hospital, Malaga, Spain.
authors.forename: L
authors.initials: L
authors.lastname: Leyva
authors.forename: M J
authors.initials: MJ
authors.lastname: Torres
authors.forename: S
authors.initials: S
authors.lastname: Posadas
authors.forename: M
authors.initials: M
authors.lastname: Blanca
authors.forename: G
authors.initials: G
authors.lastname: Besso
authors.forename: F
authors.initials: F
authors.lastname: O'Valle
authors.forename: R G
authors.initials: RG
authors.lastname: del Moral
authors.forename: L F
authors.initials: LF
authors.lastname: Santamaría
authors.forename: C
authors.initials: C
authors.lastname: Juárez
mesh_terms: D000328:Adult; D000917:Antibody Formation; D000927:Anticonvulsants / Q000009:adverse effects*; D001773:Blood Cells / Q000378:metabolism / Q000473:pathology; D017252:CD3 Complex / Q000032:analysis; D002220:Carbamazepine / Q000009:adverse effects; D016207:Cytokines / Q000378:metabolism; D019040:E-Selectin / Q000378:metabolism; D004727:Endothelium / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010672:Phenytoin / Q000009:adverse effects; D016201:Receptors, Lymphocyte Homing / Q000378:metabolism; D012867:Skin / Q000378:metabolism / Q000473:pathology; D013262:Stevens-Johnson Syndrome / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D000927:Anticonvulsants; D017252:CD3 Complex; D016207:Cytokines; D019040:E-Selectin; D016201:Receptors, Lymphocyte Homing; D002220:Carbamazepine; D010672:Phenytoin