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Definition Return to top
Pemphigus vulgaris is an autoimmune skin disorder characterized by blistering of the skin and mucous membrane.Causes, incidence, and risk factors Return to top
Pemphigus involves blistering of the outer (epidermal) layer of the skin and mucous membranes. It is an autoimmune disorder in which the immune system produces antibodies against specific proteins in the skin and mucous membrane. These antibodies produce a reaction that leads to a separation of epidermal cells (acantholysis). The exact cause of the development of antibodies against the body's own tissues (autoantibodies) is unknown.
Sometimes pemphigus appears in reaction to medications, although this is rare. Pemphigus may be a side effect of ACE inhibitors (such as Elanapril) or chelating agents (such as penicillamine).
Pemphigus is uncommon. It occurs almost exclusively in middle-aged or older people of all races and ethnic groups. About one-half of the cases of pemphigus vulgaris begin with blisters in the mouth, followed by skin blisters. The blisters (bullae) are relatively asymptomatic, but the lesions become widespread and complications develop rapidly and may be debilitating or fatal.
Symptoms Return to top
Signs and tests Return to top
Treatment Return to top
Severe cases of pemphigus are treated similarly to severe burns. Treatment may require hospitalization, including care in a burn unit or intensive care unit. Treatment is aimed at reducing symptoms and preventing complications.Expectations (prognosis) Return to top
If not treated, pemphigus vulgaris is usually fatal. Generalized infection is the most frequent cause of death. Treated, the disorder tends to be chronic in most cases. Side effects of treatment may be severe or disabling.Complications Return to top
Calling your health care provider Return to top
Any unexplained blisters should always be examined by your physician.
Call your health care provider if you have been treated for pemphigus vulgaris and you develop any of the following symptoms:
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Page last updated: 28 October 2004 |