This disease is described as an autoimmune disorder, in which linear deposits of IgG against a component of hemidesmosomes results in a separation of the dermoepidermal junction.
This disease is characterized by bullae which are formed by an immune reaction. IgG autoantibodies are formed against dystonin, which is a component of hemidesmosomes.
As IgG autoantibodies affect hemidesmosomes (by attacking dystonin), separation along the dermoepidermal junction occurs. It is this separation of the epidermis from its basement membrane which causes stretch bullae.
Separation of the dermoepidermal junction results in stretch bullae, which are tense fluid-filled blisters.
Unlike a similar disease pemphigus vulgaris, bullous pemphigoid is Nikolsky sign negative. This means that on clinical exam, rubbing the skin does not result in exfoliation of the outermost layer.
The tense blisters formed in bullous pemphigoid contain eosinophils.
The tense blisters seen with this disorder rarely affect the oral mucosa, which differentiates this disorder from pemphigus vulgaris.
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