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pemphigus vulgaris 562 pemphigus vulgaris
Pemphigus vulgaris; “chickenwire” staining antibody to intercellular
antigen.
form of the disease affects individuals of all ethnic backgrounds,
whereas a second is endemic to certain regions of
Brazil and is known as fogo selvagem. This disease rarely
involves mucosal surfaces. Histologic studies reveal acantholysis
in the subcorneal layers of the epidermis.
Pemphigus vulgaris.
pemphigus vulgaris
A blistering lesion of the skin and mucous membranes produced
by autoantibodies, usually IgG or IgA, that interact
with desmogleins requisite for adhesion between epithelial
cells. This autoimmune disease has a type II hypersensitivity
mechanism. The bullae develop on normal-appearing
skin and rupture easily. The blisters are prominent on both
Pemphigus vulgaris.
Pemphigus vulgaris.
the oral mucosa and anal/genital mucous membranes.
The disorder may have an insidious onset, appearing in
middle-aged individuals, and it tends to be chronic. It may
be associated with autoimmune diseases, thymoma, and
myasthenia gravis. Certain drugs may induce a pemphiguslike
condition. By light microscopy, intraepidermal bullae
are present; suprabasal epidermal acantholysis with only
mild inflammatory reactivity is observed in early pemphigus.
Suprabasal unilocular bullae develop, as do autoantibodies
to intercellular substance with activation of classic
pathway-mediated immunologic injury. Acantholysis results
as the epidermal cells become disengaged from one another
as the bulla develops. Epidermal proteases activated by
autoantibodies may actually cause the loss of intercellular
bridges. Immunofluorescence staining reveals IgG, Clq, and
C3 in the intercellular substance between epidermal cells.
In patients with pemphigus vulgaris, 80 to 90% have circulating
pemphigus antibodies. Their titer usually correlates
positively with clinical manifestations. Corticosteroids and
immunosuppressive therapy, as well as plasmapheresis,
have been used with some success.