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Pacientes recién diagnosticados

Pénfigo y penfigoide no son contagiosas. No por sangre. No por fluidos. No por nada. Pénfigo y penfigoide no son genéticas.

Pénfigo y penfigoide son raras, enfermedades autoinmunes que afectan a un porcentaje muy pequeño de la población. Hay muchas enfermedades autoinmunes diferentes, y cada uno pueden afectar el cuerpo de diferentes maneras. Pénfigo vulgar, el más común de las enfermedades de Pénfigo, afecta a la piel y membranas mucosas.

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Ampollas podrán estar acompañado por dolor severo, prurito, quema, y escozor. If extensive, ampollas pueden conducir a la pérdida de líquido mortal, infección, y desfiguración. PV también puede causar daño significativo a la piel, incluyendo pérdida de uñas y alteración picnometría, lo esencial para la prevención de la discapacidad puntualidad de intervención y tratamiento.

Pénfigo y penfigoide son enfermedades crónicas que, con raras excepciones, no mejoran sin tratamiento activo. Enfoques de tratamiento incluyen una fase de control y, a continuación, una fase de mantenimiento, con la posibilidad de remisión completa o recaída de la enfermedad (FLARE).

Pacientes con Pénfigo y penfigoide son normales, todos los días la gente y puede vivir normal, vida cotidiana. toma tiempo, tratamiento, y perseverancia, pero es posible.

Most Common Types

This information is used courtesy of Dr. Kristine Krafts at the University of Minnesota School of Medicine. http://www.pathologystudent.com/?p=3566.

Pénfigo vulgar

“Pemphigus” is used in a very specific way to describe blistering disorders caused by autoantibodies against some part of the epidermis, which lead to disruption of the intercellular junctions (and hence bullae). Pénfigo vulgar, not surprisingly, is the most common type of pemphigus (“vulgar-” comes from the Latin vulgaris, meaning the general public). It occurs primarily in adults between the ages of 30 and 60, and is characterized by big, flaccid bullae that burst easily (in most patients, you’ll see more ruptured, scab-covered bullae than intact ones). Patients often present first with oral bullae and ulcerations, and later develop bullae on the skin.

In this disease, patients have autoantibodies against desmogleins, which disrupt the connections between the squamous cells of the epidermis and cause very superficial, intraepidermal, fragile bullae. If you do immunofluorescence on the skin, you’ll see a kind of outlining of each individual epidermal cell (because there are autoantibodies bound to the junctions between the cells). Treatment consists of immunosuppressive agents; prognosis is variable, but many patients have a higher than normal mortality rate.

Bullous pemphigoid

This disease is called pemphigoid rather than pemphigus. It looks like pemphigus but really isn’t! Pemphigus is characterized by autoantibodies against the connections between epidermal cells. In bullous pemphigoid, patients have autoantibodies – but they are against the basement membrane of the epidermis, not against epidermal cell junctions. This means that the bullae are actually subepidermal, so they are less fragile than those of pemphigus vulgaris (if you see a patient with bullous pemphigoid, you’ll see lots of intact, tense bullae, rather than a bunch of ruptured bullae covered with scabs). The immunofluorescence pattern is correspondingly different – you’ll see just a line at the base of the epidermis (rather than the lace-like outlining of epidermal cells you see in pemphigus vulgaris).

Patients with bullous pemphigoid are generally elderly, and the clinical presentation varies a lot (but usually it doesn’t start in the mouth, like pemphigus vulgaris). It’s a less serious disease, usually, since the bullae often don’t rupture (so there’s less chance of infection and scarring).