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HERPES GESTATIONIS
Herpes gestationis (pemphigoid gestationis) (S7C4P1-1) is a subepidermal, bullous dermatitis of pregnancy. It is associated with a basement membrane zone antibody and
linear deposits of C3; deposits of IgG are found in the lamina lucida of the basement membrane zone. Herpes gestationis is an interface disorder with prominent edema in the basal unit of both the epidermis and
the papillary dermis. Vacuolar changes at the dermal-epidermal interface are associated with scattered, small rounded defects in the basal unit. The defects contain a few lymphocytes, histiocytes, and eosinophils (S7C4P1-2-4).
The edematous changes at the dermal-epidermal interface result in the formation of sub-epidermal defects (S7C4aP1a-3); the papillary dermis forming the floor of the defects is compressed by the pressure of fluid within
the cavity of a bulla (S7C4P1-5-6). Eosinophils may be prominent in the defects and in the edematous epidermis bordering the
defects. In areas, the edema irregularly disrupts the basal unit of the epidermis (S7C4P1-7).
In some examples, the dermal-epidermal interface is relatively free of inflammatory cells (S7C4P1-8). In other examples, there are loose infiltrates of lymphocytes, eosinophils, and histiocytes at the dermal-epidermal
interface (S7C4P1-8, & S7C4aP1a-2).
Some examples are associated with prominent perivascular infiltrates of lymphoid cells in the upper portion of
the dermis (S7C4aP1a-1).
LINEAR IgA DERMATITIS
Linear IgA dermatitis is another example of a sub-epidermal bullous dermatitis. Like other sub-epidermal
vesicular or bullous disorders, the process begins with interface changes. In the case of linear IgA dermatitis, the infiltrates are linear in distribution at the dermal-epidermal interface; the preponderant
inflammatory cell at this interface is a neutrophil.
Neutrophils, having collected at the dermal-epidermal interface, release protolytic enzymes; the damage produced
by the release of the enzymes results in a loss of cohesion between the epidermis and the dermis; a sub-epidermal vesicle or bulla is the result (S7C5P2-1). In the region of the defect, neutrophils and histiocytes collect along the floor (S7C5P2-2). Generally, the reaction at the dermal-epidermal interface, beyond the domain of the sub-epidermal defect, shows the
characteristic, linearly distributed infiltrate of neutrophils. The dissection at the stromal-epithelial interface may extend along hair follicles (S7C5P2-4).
Neutrophils and histiocytes collect at the dermal-epidermal interface. In older lesion, the inflammatory cells
may show evidence of karyolysis with distortion of nuclear outlines and a diminution of nuclear basophilia (affinity for hematoxylin) (S7C5P2-3).
Dermatitis herpetiformis must be considered in the differential diagnosis. In the interpretation of the
immunofluorescent findings, strict attention to what is truly a linear pattern is an aid in making distinctions between linear IgA dermatitis and dermatitis herpetiformis (S7C5P2-5 & 6).
At the histologic level, a lesion, in which the epidermis has separated from the dermis, generally will have
lost the features which distinguish IgA linear dermatitis from dermatitis herpetiformis (S7C5P2-7 & 8, & S7C5aP2a-1-4). The IgA disorders, including dermatitis herpetiformis and linear IgA dermatitis, may be
associated with patterns of leukocytoclastic angiitis.
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