Pemphigus e pemphigoid non sono contagiosi. Non da sangue. Non da fluidi. Non per nulla. Pemphigus e pemphigoid non sono genetiche.

Pemphigus e pemphigoid sono rari, malattie autoimmuni che colpiscono una percentuale molto piccola della popolazione. Ci sono molti differenti malattie autoimmuni, e possibile ognuno influenzano il corpo in modi diversi. Pemfigo volgare, la più comune delle malattie pemfigo, colpisce la pelle e le mucose.

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Vesciche può essere accompagnata da dolore severo, prurito, masterizzazione, e pungente. If extensive, vesciche può portare alla perdita di liquidi letali, infezione, e deturpazione. PV può anche causare gravi danni alla pelle, tra cui la perdita del chiodo e l'alterazione della pigmentazione, rendendo la tempestività di intervento e trattamento essenziale per la prevenzione della disabilità.

Pemphigus e pemphigoid sono malattie croniche che, con rara eccezione, non migliorano senza trattamento attivo. Approcci terapeutici includono una fase di controllo e quindi una fase di manutenzione, con la possibilità di remissione completa o recidiva di malattia (Flare).

Pemphigus e pemphigoid pazienti sono normali, tutti i giorni le persone e può vivere normale, vita quotidiana. ci vuole tempo, trattamento, e la perseveranza, ma è possibile.

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.

Pemfigo volgare

“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). Pemfigo volgare, 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).