IMMUNOHISTOCHEMICAL FEATURES IN INFLAMMATORY LINEAR VERRUCOUS EPIDERMAL NEVI SUGGEST A DISTINCTIVE PATTERN OF CLONAL DYSREGULATION OF GROWTH

Citation
Ml. Welch et al., IMMUNOHISTOCHEMICAL FEATURES IN INFLAMMATORY LINEAR VERRUCOUS EPIDERMAL NEVI SUGGEST A DISTINCTIVE PATTERN OF CLONAL DYSREGULATION OF GROWTH, Journal of the American Academy of Dermatology, 29(2), 1993, pp. 242-248
Citations number
21
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
01909622
Volume
29
Issue
2
Year of publication
1993
Part
1
Pages
242 - 248
Database
ISI
SICI code
0190-9622(1993)29:2<242:IFIILV>2.0.ZU;2-H
Abstract
Background: We studied biopsy material from four patients with inflamm atory linear verrucous epidermal nevi (ILVEN) that had a psoriasiform appearance histologically and seven cases of linear epidermal nevi (LE N). Of the seven LEN, five showed hyperkeratosis, papillomatosis, and varying degrees of acanthosis; two had features of epidermolytic hyper keratosis. Because these lesions have distinctive histologic patterns, we wanted to determine whether we could also demonstrate a distinctiv e 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 PCN A, factor XIIIa, MAC-38 7, UCHL-1, and OPD-4 was distinctly different in ILVEN and LEN. Staining for ICAM-1 was present on keratinocytes, an d ELAM-1 was present on endothelial cells in two cases of ILVEN. HLA-D R in these same two cases of ILVEN stained mainly dendritic cells in t he epidermis. Conclusion: The different pattern of staining of PCNA, f actor XIIIa, MAC-387, UCHL-1, and OPD-4 in LEN and ILVEN indicates a d ifferent mechanism of growth dysregulation. Stains for ICAM-1, ELAM-1, and HLA-DR in ILVEN suggest that an inability to down-regulate the in flammatory 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 factor s that initiates ILVEN in a susceptible person.