S6C36P30-Vesicular, drug

S6C36P30-1: This subepidermal bulla is cell-poor at the dermal-epidermal interface. Dermal papillae are partially preserved along the floor of the bulla. The defect contains fibrin and a few inflammatory cells ( drug eruption, barbiturates).

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S6C36P30-2: At a margin of the bulla, the epidermis shows cytopathic changes with lytic defects at various levels; some of the defects are supra-basilar. Some of the cells in a hyperplastic basal unit (blue arrows define the interface between basal and superficial units) and a few in the overlying superficial unit show ballooning degeneration. Focally, the superficial unit shows coagulation necrosis. Occasional dyskeratotic cells border some of the defects in the basal unit. The dermis is relatively free of inflammatory infiltrates.

S6C36P30-3: Cytopathic changes are also manifested in the epithelium of sweat glands (necrosis of epithelial cells; necrotizing sialadenitis, drug related).

S6C36P30-4: The interface between the basal unit and the superficial unit is defined in part by blue arrows. Centrally, there is a lytic, subepidermal defect; in the roof of the defect, the basal layer is interrupted, or the basal keratinocytes show degenerative changes (ragged cytoplasmic outlines along lower margin of the roof of the defect). At the interface between the superficial unit and the basal unit on the left, keratinocytes are loosely spaced; inter-cellular bridges are not a feature at this magnification.The cells in this area are thin and somewhat flattened; they are dyskeratotic (increased cytoplasmic acidophilia). At the right margin, cells of the superficial unit are represented in ghost outlines (the superficial unit focally is necrotic) (red arrows). The process is cytopathic and cytolytic with no evidence that inflammatory cells have a role in the cytolytic phenomena (drug eruption, barbiturates); keratinocytes apparently have mediated the damage to their own domain.

S6C36P30-5: This lesion, which is late in its evolution, is, in part, a subepidermal defect. The roof of the defect is something more than just a detached epidermis; it is composed of necrotic epidermis and a thin zone of necrotic dermis. The zone of basophilia along the lower margin of the roof of the defect is representative of an infiltrate of degenerating neutrophils. The few inflammatory cells in the perivascular spaces of the underlying dermis are mostly neutrophils. Squamous epithelium has partially re-epithelialized the floor of the defect at both the left and right margins (green arrows). This is the classic pattern of a fully developed “necrotic excoriation” (superficial erosive dermatitis). It is less an excoriation than a limited zone of necrosis involving the epidermis and the dermis (often including a portion of the superficial reticular dermis as well as the papillary dermis). The defect is a sequestration mediated at the level of an infiltrate of neutrophils.The neutrophils collect in a band and the distribution of the infiltrate determines the site in which a separation eventually will occur.

S6C36P30-6: The right margin of the defect is represented. Squamous epithelium has partially re-epithelialized the floor of the defect (and in doing so has made a contribution to the process of sequestration). The roof of the defect is necrotic epithelium and a thin zone of necrotic dermis (this was confirmed by an examination of the section under polarized light). The process is closely related to reactive perforating collagenosis but, in contrast to the neurotic excoriation , the epidermis in reactive perforating collagenosis tends to undergo pseudoepitheliomatous hypreplasia; it invades the dermis, including the reticular dermis, prior to the development of necrosis;  in the process, it entraps connective tissue fibers, including collagen bundles and elastic fibers.

S6C36P30-7: On the left side of the defect, squamous epithelium has regenerated along the floor. Fibrin is present along the interface between the regenerating epithelium and the dermis. This pattern of “inflammation” suggests that the trauma, which originally initiated the sequestration, has been repeated; it has damaged the regenerating epithelium at its interface with the dermis (“neurotic excoriation”). In areas, the epithelium sits upon reticular dermis without an intervening portion of papillary dermis.

 

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