dysplastic (Clark's) melanocytic nevus

Introduction

Premalignant lesions.

Etiology

• most dysplastic melanocytic nevi arise in contiguity with a compound melanocytic nevus
• abnormal clones of melanocytes may be activated by exposure to light

Epidemiology

• 5% of white population
• occurs in all patients with familial cutaneous melanoma
• occurs in 30-50% with sporadic nonfamilial melanoma
• white population, no data on blacks, rare in Japanese
• occurs in children & adults
• no sex preference

Pathology

• hyperplasia & proliferation of melanocytes in the basal cell layer either as spindle cells or epithelioid cells
• irregular & dyshesive nests of melanocytes
• melanocytes are atypical
  • larger than normal
  • pleomorphic nuclei & cell bodies
  • hyperchromatic nuclei
• bridging between rete ridges by melanocytic nests
• spindle-cell melanocytes oriented parallel to skin surface
• lamellar fibroplasia & concentric eosinophilic fibrosis may be present
• proliferation of blood vessels may occur
• a sparse to dense lymphocytic infiltrate may occur

Genetics

• sporadic or autosomal dominant dysplastic nevus syndrome
• chromosomal aberrations 1p36 & 9p21

Clinical manifestations

• 5-10 mm or larger macules or papules; commonly > 6 mm (> 5 mm)
• generally on trunk & limbs, may occur in areas not exposed to sunlight
• variegated in color within lesion; pink, tan, brown; lesions may be black
• asymmetric shape with irregular border & surface
• 'fried egg' appearance with darker, elevated central portion & tan, flat edges blending into the surroundings
• lesions 1st appear in late childhood, just before puberty
• new lesions continue to develop over many years
• lesions rarely undergo spontaneous regression
• generally asymptomatic
• imunosuppressed patients with dsyplastic nevi have a higher incidence of melanoma

* images

Laboratory

• Wood's lamp examination will markedly accentuate the epidermal hyperpigmentation of lesions
• epiluminescence microscopy

Complications

• increased risk of melanoma
  • general population - 0.8%
  • familial dysplastic nevi - 100%
  • dysplastic melanocytic nevi - 18%
• most melanomas that arise in patients with dysplastic nevi develop on the intervening 'normal' skin

Differential diagnosis

• congenital melanocytic nevus
• common acquired melanocytic nevus
• superficial spreading malignant melanoma
• melanoma in situ
• lentigo maligna
• Spitz nevus
• pigmented basal cell carcinoma
• seborrheic keratosis

Management

• surgical excision of lesions with minimal margins sent for pathology
  • selection of lesions
    • lesions that are changing in size, shape or color
    • lesions not easily amenable to self-examination by the patient (scalp, genitalia, back)
    • a single, atypical dysplastic nevus
    • symptomatic nevi
    • other lesions should be observed
• lasers or other destructive modalities should not be used because they interfere with histologic diagnosis
• follow-up
  • every 3 months for patients with familial dysplastic nevi
  • every 6 months for patients with sporadic dysplastic nevi
• patient education
  • avoid the sun
  • use sunscreen, clothing
  • self exam
  • illustrative patient informatation depicting dysplastic nevi
• examine family members
• referral to dermatology

More general terms

• melanocytic nevus (mole)
• genetic disease of the skin (genodermatosis)

Additional terms

• basal cell carcinoma (BCC)
• congenital melanocytic nevus
• dysplastic nevus syndrome (inherited familial atypical mole & melanoma syndrome)
• lentigo maligna
• Spitz nevus; spindle cell nevus; epithelioid nevus
• superficial spreading melanoma

Patient information

dysplastic (Clark's) melanocytic nevus patient information