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Psoriasiform Dermatitis (parent chapter for 6 pictorial pages)
(erythrodermas)
The erythrodermas are expressed in patterns that have psoriasiform qualities; some examples are sufficiently psoriasiform to suggest that the erythroderma is symptomatic of psoriasis.
For other examples, there is basal unit hyperplasia and alternating hyperkeratosis and parakeratosis, but rete patterns are not accentuated (S2C14P8-1-3). In the category of the erythrodermas, careful attention must be paid to the cytologic features of the lymphoid
infiltrates, particularly cells in the epidermis; an erythrodermic Tcell dysplasia should be ruled out.
Guttate psoriasis deviates somewhat from classic psoriasis; the rete patterns are not as regularly, or as prominently, accentuated. The papillary dermis is edematous and some of the vessels of the dermal papillae are
tortuous and dilated. The most characteristic changes are to be found in the keratin layer; in this layer, zones of parakeratosis often are stratified both horizonally and vertically (S2C14P8-4 & 5 & S2C14P8-8 & 9).
The patterns of psoriasis often are complicated, if a lower extremity is selected as the site for biopsy. Inflammatory disorders affecting the lower extremities are commonly
complicated by angiodermatitis; the effects of this complication may significantly alter histologic patterns. For lesions of the lower extremities, patterns of psoriasis may be altered to the extent that the changes
are psoriasiform, but not diagnostic of psoriasis (S2C14P8-6).
Flexoral (inverse) psoriasis (S2C14P8-7) is a variant with prominent involvement of the
flexoral sites. This variant may be complicated by associated disorders that are common in flexor sites, such as seborrheic dermatitis, or flexor infections (i.e., fungus infections).
Pityriasis rubra pilaris has been discussed in this section in CHAPTER 13. The keratin layer is compact and orthokeratotic; there may be focal areas of parakeratosis. The basal unit of the epidermis is hyperplastic
and shows mild inter-cellular edema. Intra-epidermal lymphoid infiltrates are spotty and mild (S2C15P9-1-4).
Necrolytic migratory erythema is a manifestation of pancreatic neuro-endocrine carcinoma (S2C16P10-6-7). It has
distorted “psoriasiform” qualities. The basal unit may be thin, or slightly hyperplastic with elongated rete ridges. Its cells have lavender cytoplasm and enlarged, hyperchromatic nuclei; the patterns are in keeping
with regenerative changes in the basal unit. Dyskeratotic cells may be found among the keratinocytes of the basal unit. The boundary between the basal unit and the superficial unit often is sharply defined; the
distinctions between the two units are accentuated by the tinctorial qualities of the cells of each unit. The cells of the superficial unit ( the superficial unit is thin) show a pale, cytoplasmic acidophilia.
Often, the cells of the superficial unit show perinuclear vacuoles. The cells of the superficial unit do not properly keratinize. Instead, the cells are converted to parakeratotic debris in which the pyknotic nuclei
are plump. A cleft may be found at the interface between the superficial unit and the keratin layer; the cleft may be outlined by necrotic keratinocytes (S2C16P10-1-5). Similar changes may be seen in lesions of acrodermatitis enteropathica.
Kasper K, Mc Murray K: Necrolytic migratory erythema without glucagonoma versus canine superficial necrolytic dermatitis: is hepatic impairment a clue to pathogenesis? J Am Acad Dermatol 1991;25: 534-41.
Marinkovich MP, et al: Necrolytic migratory erythema without glucagonoma in patients with liver disease. J Am Acad Dermatol J Am Acad Dermatol 1995;32: 604-9.
Lesions of the Hay-Well syndrome (S2C17P11-1-3) show features similar to those of necrolytic migratory erythema.
Acrodermatitis enteropathica is an inherited disorder characterized by vesiculobullous lesions; it is a disorder of zinc metabolism. Zinc levels are low and the disease is responsive to zinc therapy. A similar
clinical picture may be seen in association with low levels of zinc, but outside the setting of an inherited disorder. The inherited disease is usually manifested in the first year of life, often following weaning,
if the infant has been breast-fed (S2C17P11-4-6, & S2C18P12-1-3).
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