Keratotic melanocytic nevus: a clinicopathologic and immunohistochemical study.
BACKGROUND
Epidermal hyperplasia in melanocytic nevi is a common but little-investigated phenomenon.


METHODS
We prospectively examined all melanocytic nevi diagnosed in our department over an 8-month period, for the criteria of keratotic melanocytic nevus (KMN), namely the presence of marked epidermal hyperplasia with or without horn pseudocyst formation, hyperkeratosis, and papillomatosis. In addition to routine histologic review, we studied 12 representative cases with immunohistochemistry to examine expression of Ki-67, epidermal growth factor receptor (EGFR), Bcl-2, and Bax.


RESULTS
From a total of 1,527 melanocytic nevi, 95 were KMN (prevalence 6%). The average age was 34 years, with a male:female ratio of 1:2. The predominant location was the trunk (76%), followed by head and neck (20%), and extremities (4%). Clinical diagnoses were atypical nevus (44%), nevus not otherwise specified (43%), and others including seborrheic keratosis, acrochordon, and basal cell carcinoma. Two KMN were junctional, 44 compound, and 49 intradermal. Twenty-three KMN (24%) had histologic features suggesting congenital onset, and 15 (16%) had mild to moderate dysplastic features. Two cases demonstrated induction of sebaceous glands. Significantly increased Ki-67 expression was detected in the hyperplastic epidermis, particularly in deeper areas related to keratinous cysts and hair follicles. Bcl-2 and Bax (anti- and pro-apoptosis proteins, respectively) and EGFR were expressed similarly in both normal and hyperplastic epidermis overlying the KMN.


CONCLUSIONS
KMN are commonly biopsied skin lesions, mostly located on the trunk. Many such lesions are clinically considered atypical, in contrast to their benign histologic appearance. The epidermal hyperplasia on top of KMN demonstrates increased cellular proliferation, in the context of adequately regulated apoptosis and EGFR expression. The cellular proliferation seems to commence in hair follicles.
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA.
M G
MG
Horenstein
V G
VG
Prieto
J L
JL
Burchette
C R
CR
Shea
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis; D002648:Child; D002675:Child, Preschool; D066246:ErbB Receptors / Q000032:analysis; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D015603:Keratinocytes / Q000737:chemistry / Q000473:pathology; D007642:Keratosis / Q000473:pathology; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009508:Nevus, Pigmented / Q000737:chemistry* / Q000473:pathology*; D011518:Proto-Oncogene Proteins / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2; D012878:Skin Neoplasms / Q000737:chemistry* / Q000473:pathology*; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D019394:Ki-67 Antigen; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D066246:ErbB Receptors