title: Immunohistochemical features in inflammatory linear verrucous epidermal nevi suggest a distinctive pattern of clonal dysregulation of growth. Military Medical Consortium for the Advancement of Retroviral Research.
abstract: BACKGROUND
  We studied biopsy material from four patients with inflammatory linear verrucous epidermal nevi (ILVEN) that had a psoriasiform appearance histologically and seven cases of linear epidermal nevi (LEN). Of the seven LEN, five showed hyperkeratosis, papillomatosis, and varying degrees of acanthosis; two had features of epidermolytic hyperkeratosis. Because these lesions have distinctive histologic patterns, we wanted to determine whether we could also demonstrate a distinctive pattern of immunohistochemical markers.
  
  
  METHODS
  On all 11 cases we performed immunohistochemical stains for PCNA, factor XIIIa, MAC-387, UCHL-1, and OPD-4. In addition, on one case of ILVEN we performed ICAM-1, ELAM-1, and HLA-DR stains.
  
  
  RESULTS
  The pattern of staining of PCNA, factor XIIIa, MAC-387, UCHL-1, and OPD-4 was distinctly different in ILVEN and LEN. Staining for ICAM-1 was present on keratinocytes, and ELAM-1 was present on endothelial cells in two cases of ILVEN. HLA-DR in these same two cases of ILVEN stained mainly dendritic cells in the epidermis.
  
  
  CONCLUSIONS
  The different pattern of staining of PCNA, factor XIIIa, MAC-387, UCHL-1, and OPD-4 in LEN and ILVEN indicates a different mechanism of growth dysregulation. Stains for ICAM-1, ELAM-1, and HLA-DR in ILVEN suggest that an inability to down-regulate the inflammatory infiltrate may be important in the growth dysregulation in ILVEN. In addition, the onset of ILVEN at the time of HIV-1 infection in one patient suggests that HIV-1 infection may be one of many factors that initiates ILVEN in a susceptible person.
authors.affiliation: Walter Reed Army Medical Center, Department of Dermatology, Washington, D.C.
authors.forename: M L
authors.initials: ML
authors.lastname: Welch
authors.forename: K J
authors.initials: KJ
authors.lastname: Smith
authors.forename: H G
authors.initials: HG
authors.lastname: Skelton
authors.forename: D M
authors.initials: DM
authors.lastname: Frisman
authors.forename: J
authors.initials: J
authors.lastname: Yeager
authors.forename: P
authors.initials: P
authors.lastname: Angritt
authors.forename: K F
authors.initials: KF
authors.lastname: Wagner
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D000951:Antigens, Neoplasm / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000032:analysis; D002648:Child; D002675:Child, Preschool; D004817:Epidermis / Q000473:pathology; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1; D007642:Keratosis / Q000473:pathology; D008297:Male; D009506:Nevus / Q000473:pathology*; D009687:Nuclear Proteins / Q000032:analysis; D018809:Proliferating Cell Nuclear Antigen; D012878:Skin Neoplasms / Q000473:pathology*; D011503:Transglutaminases / Q000032:analysis
chemical_list: D015703:Antigens, CD; D000951:Antigens, Neoplasm; D015815:Cell Adhesion Molecules; D006684:HLA-DR Antigens; D009687:Nuclear Proteins; D018809:Proliferating Cell Nuclear Antigen; D018799:Intercellular Adhesion Molecule-1; D011503:Transglutaminases