Clinical Dermatology

Diagnostic Hallmarks

1. Distribution: back and chest
2. Color variation within and among the nevi
3. Red hues
4. Irregular configuration

Clinical Presentation

The subject of dysplastic nevi ( Clark ’s nevus) is probably the most controversial one in dermatology today. Although it is certainly possible to recognize a type of pigmented lesion that is clinically atypical, the histologic presence of a typicality is not regularly correlated, and the meaning of such lesions, with or without microscopic “dysplasia,” is hotly argued.

Pigmented nevi clinically described as dysplastic have two or more of the following features -

(1) Red or red-brown hues

(2) Diameter larger than 7 mm (lead pencil eraser size)

(3) Irregular or jagged margination

(4) Asymmetrical rather than perfectly round shape

(5) Speckled rather than evenly spread pigmentation.

Lesions possessing these clinical features often, but not always, have certain histologic features (see below) that are likewise described as dysplastic.

Dysplastic nevi occur in two major settings -

• Sporadic
• Familial

The clinical appearance of the individual lesions is similar in both. Generally, patients with the sporadic variant have fewer than 50 pigmented nevi, and the percentage of nevi that are clinically dysplastic is small. Patients with the familial form general1y have more than 50 pigmented nevi, and greater than 10% of the nevi present have clinically dysplastic features. Of course, these latter patients will have family members with similar dysplastic nevi, but this fact is often not known by the patient at the time of first examination. Also, light-skinned people, often Celtic in background, make up a disproportionate percentage of those with the familial form.

Course and Prognosis

People with the familial dysplastic nevus syndrome are at a very high risk for the development of one or more melanomas. This risk is almost 100% if in the family background there is a history of melanoma as well as a history of dysplastic nevi. This risk occurs in two ways. First, photographs taken at regular intervals document that dysplastic lesions can evolve into melanomas. Second, there is an increased likelihood that melanomas will arise de novo rather than in a precursor dysplastic nevus. Some authorities believe these people are also at risk for the development of non melanomatous malignancy as part of a “cancer prone family” syndrome. Patients with acquired dysplastic nevi may also be at increased risk for the development of melanoma, but data to support this belief are rather “soft.” In any event, melanomas can evolve or can arise de novo within a pattern of months, and all patients with dysplastic nevi deserve extraordinarily close and careful follow-up.

Pathogenesis

A distinctive histologic pattern is generally found in nevi that are clinically dysplastic. These features include -

(1) Elongation of the epidermal rete ridges

(2) Increased numbers of nevus cell nests along the sides of the rete ridges

(3) Bridging of adjacent rete ridges by horizontally elongated nevus cell nests

( 4) A lymphohistiocytic inflammatory response

(5) Melanin in melanophages

(6) The presence of fibroplasia in the papillary dermis.

Whether or not individual cell atypia must be present before a lesion should be identified as dysplastic is a matter of great controversy. Certainly if cellular atypia is not required, the percentage of the population with one or more dysplastic nevi is very large, probably 10% or more. Some therefore argue that lesions lacking cellular atypicality are really just “active” variants of normal nevi and that such nevi have no real meaning in the absence of a family history of melanoma.

In addition to the genetic and histologic factors, it is apparent that sunlight damage also plays a role. Several studies indicate that both the number and the location of nevi are dependent on ultraviolet light exposure, In fact, the risk for development of melanoma correlates rather well with the total number of nevi present. Those with fewer than 20 nevi are at very low risk, whereas those with 100 or more are at rather high risk.

Note, however, that the role sunlight plays in the development of melanoma is different than that responsible for the development of basal and squamous cell carcinomas. These latter tumors correlate well with the total cumulative dose of sunlight exposure, whereas melanomas correlate better with the number of sunburns experienced in childhood. Nevertheless, sunlight exposure may be neither necessary nor sufficient, as evidenced by the occurrence of dysplastic nevi and melanomas on the buttocks, scalp, genitalia, and female breasts.

Therapy

No consensus exists as to how to care for patients with dysplastic nevi. First, of course, the diagnosis must be established. This requires the biopsy of one or more clinically suspicious lesions. Once a diagnosis has been confirmed, patients should be followed at regular intervals. For those with the familial type of dysplastic nevi, this interval might well be every 6 months, for those with the sporadic form, it might be every year or two. Some authorities believe that all the nevi should be photographed, so that on subsequent visits hose lesions that on comparison show even minor degrees (If change can be surgically removed. Others recommend surgical removal of all lesions demonstrating any clinically suspicious features regardless of whether or not change can be demonstrated. Still others rely on clinical judgment regarding change with isolated removal of only those lesions that have changed grossly. In spite of these differences, nearly all recommend that this be done by total excision rather than by shave technique.

This entry was posted on Sunday, October 14th, 2007 at 6:10 am and is filed under Lesions. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.