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Eruptive nevi: Trying to connect the dots


DII small banner By Warren R. Heymann, MD
Sept. 15, 2016


Eruptive nevi are striking — they may appear after a variety of disorders, including Stevens-Johnson/toxic epidermal necrolysis, primary blistering diseases, trauma, immunosuppression (from disease or iatrogenically-induced), PUVA therapy, or idiopathically. There are also several reports in the literature for eruptive Spitz nevi and blue nevi.

Ratushny et al report the case of a 48 year-old woman who developed thousands of pigmented lesions corresponding to areas of eczema on her torso (the etiology of the eczematous dermatitis was not clearly defined). Biopsy results ranged from lentiginous nevi, atypical nevi, melanoma in situ, and invasive melanoma. Testing for activating mutations (BRAF, PTEN, NRAS, KRAS, and HRAS) was negative. The expression of the tumor suppressors p16 and PTEN was normal. There was no expression of mutated BRAF V600E protein. Although the pathogenesis of these lesions in unknown, theories include immune stimulation by the eczematous rash, benign “nevic” metastases, or epidermotropic metastatic melanoma (1).

Although the precise etiology for the vast number of pigmented lesions in this patient is an enigma, the number of reports of eruptive nevi associated with medications is rapidly increasing. Perry et al have classified this with the following scheme (with only one of several drugs as an example for each):

Type Ia: nonbiologic immunosuppressants (azathioprine)
Type Ib: biologic immunosuppressants (infliximab)
Type IIa: nonbiologic chemotherapeutics (capecitabine)
Type IIb: biologic chemotherapeutics (vemurafenib)
Type III: direct melanocyte stimulators (synthetic MSH analogs)
Of all the pathogenic hypotheses, the prevailing theory is that attenuated immune surveillance allows melanocyte growth factors to promote proliferation in predisposed individuals. This mandates continued careful clinical follow-up as the malignant risk for melanoma in these patients is approximately two-to- fourfold (2).

The complexity of deciphering each drug’s potential effect on melanogenesis is overwhelming, but may actually be a source of optimism. If we can learn how each drug is linked to melanocytic proliferation, then each drug theoretically provides an opportunity to determine to how melanocytic growth may be inhibited. Targeted therapeutics has forever changed the landscape of treating melanoma; as we have learned, salvage mutations will lead to resistance. Understanding the pathogenesis of eruptive nevi may lead to novel therapeutic agents to circumvent resistant pathways.

1. Ratushny V, et al. A symmetric eczematous eruption harboring thousands of melanocytic lesions. JAMA Dermatology 2016; 152: 1021-4.
2. Perry BM, et al. Eruptive nevi associated with medications (ENAMs). J Am Acad Dermatol 2016 May 27 [Epub ahead of print]

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