Blisters

• Pemphigus vulgaris
• Blisters and bullae, rupture→erosions, crusting→post-inflammatory changes
• Nikolsky sign—skin slides off with gentle pressure, separating epidermis from basal layer→blister on skin that was not previously involved
• Usually starts with oral ulcers, progresses to skin blisters. Lesions become bigger, more generalized if left untreated.
• Etiology—autoimmunity to pemphigus vulgaris antigen, member of cadherins (cell adhesion molecules) and normal keratinocyte membranes. Blisters result from loss of integrity of normal intercellular attachments within epidermis and mucosal epithelium.
• Find IgG in intercellular regions of epidermis, rarely IgM, IgA, C3.
• Path—Basal cells lose intercellular bridges but remain attached to dermis, causes “tombstone appearance.” Acantholysis=keratinocytes that lose their attachments to other cells, float freely within the blister cavity.
• Rx—steroids, azathioprine, plasmapharesis
• Bullous pemphigoid
• Subepidermal blisters, also autoimmune
• Tense, pruritic blisters on flexor surfaces (vs. intertriginous areas in PV)
NO positive Nikolsky sign, as skin is tense and not fragile, some post-inflammatory changes but not as marked as in PV.
• 
  
• Starts as “hives,” then blisters appear on urticarial regions
• Does not usually start with oral blisters, but mild and transient if present
• Little epidermal change—because it’s subepidermal. Also eosinophils (remember—eos go with hives and allergies)
• IF—shows IgG, C3 along basement membrane
• Autoab against hemidesmosomes (also cell adhesion molecules)
• Rx—steroids, immunosuppressants

Category: Dermatology Notes