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  • br Discussion EMN is a rare phenomenon

    2018-11-12


    Discussion EMN is a rare phenomenon in which hundreds of melanocytic nevi appear suddenly. The lesions of EMN can include banal nevi, blue nevi, and Spitz nevi. EMN may arise in the setting of blistering skin disease, immunosuppression, cytokine administration, biological agent administration, chemotherapy, Addison disease, paraneoplastic phenomena, pregnancy, and idiopathic causes. The proposed pathogenesis of EMN includes diminished immune surveillance, genetic susceptibility, and drug adverse effects, although the exact pathogenesis is not clearly understood. The chance of potential malignant transformation is assumed to be theoretically higher in patients with EMN. Regular screenings for dysplastic nevi or melanoma have been recommended by many authors. However, to our knowledge, no melanocytic malignancy has been reported following an EMN eruption in the English-language literature. The concept of a MELTUMP was first proposed in 2004 as “borderline” melanocytic lesions that are difficult for dermatopathologists to classify as malignant or benign because of their ambiguous morphology. In the present case, the pathology of the hypopharyngeal lesions exhibited both benign characteristics (well-circumscribed architecture with maturation and no mitotic activity) and also troubling characteristics (a slightly stat 3 inhibitor architecture, confluent cell nests, and frequent pagetoid spread even in the upper half of the epithelium). These lesions could not be classified as merely benign nevi, but they also failed to meet the criteria for melanoma, which is a constellation of multiple atypical findings. Through consultations with dermatopathologists in Taiwan, we concluded that the optimal diagnosis for these lesions is a MELTUMP. Two recent large case series of MELTUMPs have reported a low risk of nodal metastasis (6–15%) and mortality from distant metastasis during follow-up (1%). These results suggest that a MELTUMP is a low-grade malignant melanocytic tumor and should be treated according to the guidelines for invasive melanoma. We performed a careful workup but could not identify any possible underlying diseases or medications related to EMN in this patient. Indeed, most of the cases of EMN have been associated with underlying diseases or medications, of which the disease courses flare and abate in parallel with the activity of the underlying diseases. However, as in the present case, a few cases of EMN have been reported as being idiopathic, of these cases, the documentation of the nature course has generally been incomplete or lacking. These idiopathic cases further highlights the importance of investigating the molecular mechanisms underlying the development of EMN. Sekulic et al proposed that the presence of an activating BRAF mutation may play a role in the genesis of EMN because of the finding that a BRAF V600E mutation was identified in 85% of 20 examined EMN lesions. In another study, however, BRAF V600E mutations were also found in > 80% of benign nevi. This apparent paradox was resolved by the discovery that most nevi display the hallmarks of senescence and stain highly for the tumor suppressor p16. P16 is a tumor suppressor that inhibits the proliferation of cells through the G1 phase of the cell cycle. A normal-functioned p16 may lead to growth arrest in nevi harboring BRAF V600E mutations. Thus, a p16 mutation may lead to bursts of cell proliferation and has been implicated in the melanogenesis of EMN, especially in those harboring BRAF V600E mutations. In previous studies, p16 stains for cutaneous or mucosal benign nevi expressed a consistent pattern of diffuse positivity. Unlike in previous studies, all the cutaneous Spitz nevi and hypopharyngeal MELTUMPs in this case showed considerably decreased percentages of p16 positivity, indicating an underlying aberration of normal senescence pathway.
    Introduction The term “chronic recurrent annular neutrophilic dermatosis (CRAND)” was first used by Christensen et al in 1989 to refer to the skin lesions of two patients who had chronically recurring outbreaks of generalized annular erythematous, edematous cutaneous plaques with histopathological findings suggestive of Sweet syndrome, but without fever or systemic signs and symptoms.