Diagnosis: Dysplastic nevus with mild atypia
The dysplastic nevus initially was described in the 1980s as a mole with increased risk of developing melanoma and requiring total removal. However, dermatopathologists now consider dysplastic nevi to be merely one type of benign skin mole, namely the Clark nevus. The chances a dysplastic nevus will become malignant are no greater than those of any other benign nevus, but it can happen, so all moles bear watching.
The common mole is made up of pigmented nevus cells. Most people are born without any moles but will have approximately 40 moles by age 40. Moles often appear to increase in size and number during the years of increased hormonal activity (such as adolescence and pregnancy and when starting oral contraceptives).
In insects, melanin is the primary immune response mechanism. Humans have a more sophisticated defense system, but we retain our primordial immunologic forms as well. Melanocytes manufacture substances with a range of biological functions, including structural strengthening by cross-linking proteins, antimicrobial defense, photon shielding, and chemoprotection. Melanocytes and moles provide several physiologically significant functions, including communication links with several different systems, e.g., the skin, central nervous system, and the immune/inflammatory response.1,2
As they apply to nevi, the words “dysplastic” and “atypia” continue to confuse patients, primary-care physicians, and dermatologists when it comes to definition and significance. The loose use of the term “dysplastic” in our present histologic melanocyte terminology is, at best, misleading. Many dermatologists, including myself, consider dysplastic nevi to be a form of benign acquired melanocytic nevus. In fact, the NIH has, since 1992, recommended eliminating the terms dysplastic and atypia in the discussion of nevi. Instead the terminology should be in line with other pathologic fields in which “dysplastic” indicates abnormal growth or development as well as implying that the lesion is a direct precursor of malignancy.
Some authors believe that all nevi should be considered precursors of melanoma. But if a progressive transformation exists from normal melanocyte to melanoma, the point along the continuum at which a mole should always be excised prophylactically needs to be defined.
Nuclear atypia is not a separate criterion for dysplastic nevi but rather can be seen with any melanocytic nevi. Many additional surgical excisions and repeat excisions continue to be performed unnecessarily because of an improper understanding of dysplastic nevi.
Dysplastic nevi should be considered benign and treated accordingly, with repeated excisions reserved for only those showing clinically significant cytologic atypia (just as with any other type of nevus).3,4 In short, a coherent, sensible classification of melanocytic nevi should be established. Despite pleas for a panel of dermatopathologists to expound the truth about this confusing terminology,5 all they have provided thus far is a survey on the confusion related to this entity.6
According to the patient’s records, two of the moles previously removed were read as dysplastic nevus with mild atypia; one was a compound nevus. The two moles I removed were also read as dysplastic nevus with mild atypia. Although the pathologist stated that the lesion extended beyond the lateral margins of the biopsy, it was benign and did not need further excision. Because the patient has a few other moles of various hues, I will be monitoring her every six months as well as having her continue to inventory her moles at home.