Congenital Blastoid Nevus
Recently, nodular lesions in congenital-patterned nevi have been examined (J Cutan Pathol 2004; 31: 153-159). The main truth function in the authors’ logic is related to the emergence of nodular components; in their material, both small and giant congenital nevi are included. Generally, the nodules of small congenital nevi differ in histologic characteristics from those of giant congenital nevi.
In giant congenital nevi, the nodules are cellular, cytologically monotonous, and may show mitotic activity. These nodules in my approach to MDM were characterized as MDM of dermal type (congenital nevus variant).
From a different perspective, it is convenient to classify giant congenital nevi as to degree of maturation. This approach is most appropriate for lesions of infancy and childhood. Immature congenital nevi might be characterized as neuromesenchymal hamartomas. In immature variants, cellularity is directly proportional to the degree of development of the fibrous framework of the reticular dermis (figs. c18t3P1-6). Markedly immature lesions are cellular, and the fibrous framework is poorly developed. Relatively mature lesions have a well developed fibrous framework, and cellularity tends to be confined to a band-like zone at the interface between the papillary dermis and the reticular dermis. In mature lesions, cellularity is not a prominent feature.
In immature lesions, nevus cells have scanty cytoplasm and tend to be closely spaced. The patterns have some of the qualities of a small, blue cell neoplasm, but cytologic atypia is not a prominent feature; the patterns are blastoid but not truly blastomatous (figs. c19t3P1-7, and c20t3P1). Often in immature lesions, the immaturity is greatest near the boundary between the reticular dermis and the papillary dermis. In the deeper portion of the reticular dermis in some examples, the nevus cells are somewhat spindle shaped, and a delicate fibrous matrix is associated with the cells (early, partial maturation). Nodular zones are common in these immature lesions; they usually are not significantly atypical; such lesions qualify as blastoid nodules of immature congenital nevi. Such lesions rarely are found to be associated with parenchymal nodal deposits of tumor; these rare nodal “metastases” might be offered as evidence favoring the interpretation that these lesions are of intermediate type. If atypia is prominent and the mitotic rate is high, the lesion is a melanoblastoma.
Cellular nodules in congenital pattern nevi have recently been discussed by Xu X, Belluci KSW, Elenitsas R, and Elder DE (J Cutan Pathol 2004; 31: 153-159). Their figs. 3 & 4 are not blastoid lesions; they are typical of the lesion that I classify as MDM of dermal type or halo nevus-like type. Both share basically similar features; the distinction is based on finding not only a remnant of a common nevus but also associated halo nevus phenomena. I suspect that some of the case which have been reported as Spitz “nevus” with halo nevus reaction are also examples of this distinctive lesion; it take considerable mental molding to accommodate one of these lesions in the category of a Spitz variant. Figs. 2a & b (Belluci, et al) could also be an example of this lesion but the photomicrograph is inadequate. They do not illustrate a convincing blastoid example as seen in congenital giant nevi; I cannot exclude fig. 2f as an example of a blastoid spindle cell variant.
Recurrent nevi present a special pattern. They are basically lentiginous and junctional lesions, and may show mild to moderately severe cytologic atypia. Individual melanocytic cells often migrate upward into the epidermis. For those who subscribe to the concept of melanoma-in-situ, the patterns in the epidermis of a recurrent nevus may be misinterpreted as those of melanoma-in-situ. The epidermal changes in combination with a superficial zone of reactive fibroplasia (the reaction in the biopsy site) are the basic clues to diagnosis (fig. c20t3P2-7). The pattern of fibrosis differs from the fibroplasia which characterized host immune response in the domain of a premalignant melanocytic dysplasia. Often the zone of fibrosis in recurrent nevus is relatively free of inflammation; in some examples, inflammation is a feature. Depending in part on age of the lesion, rounded nests of cells may be a feature of the dermal component. For some examples, the cells are pigmented and spindle shaped; in such lesions, the cells in the dermal component are likely to be arranged in fascicles. A remnant of the preexisting nevus may be represented in the reticular dermis beside, or beneath the recurrent nevus. It is a characteristic of recurrent nevus that the lentiginous and junctional component is confined to the epidermis over the area of fibrosis. If the lentiginous and junctional component extends in the epidermis beyond the area of fibrosis, and if it is associated with some degree of atypia and host immune response, then the lesion should be classified as an atypical recurrent nevus; the original biopsy specimen should be reviewed.
In examples in which rounded nests of atypical cells are loosely, but regularly, spaced in the fibrotic dermis, the patterns may resemble an arrested variant vertical growth component. The patterns then might be misinterpreted as a MDM arising in a premalignant melanocytic dysplasia.
Focal areas of regression are common in melanocytic lesions that are thin (less than 1 mm in vertical dimensions); in these areas of focal regression, the dermal and epidermal patterns of the neoplastic component are interrupted. Occasional lesions may metastasize, and then completely regress in the primary site (figs. c21t3P1 & 2). In the area of regression, there may be no recognizable nest of tumor cells, or there may be a few small nests of tumor cells in a fibrotic dermis. Regressed melanomas commonly are associated with a prominent collection of melanophages in the area of fibrosis. I have not seen a comparable degree of melanoderma in areas in which halo nevi have regressed, but I would not use this observation as a reliable discriminator.
Thin Vertical Growth:
Thin early melanomas may show variant, typical, or migrant vertical growth (figs. c21t3P3-9). Variant, typical, and migrant patterns may be combined in a single lesion.