Bullous pemphigoid
Bullous pemphigoid ad omnes morbos cutis, qui bullas inducunt, refertur. “Pemphigoidum bullosum” est morbus cutaneus autoimmunis, praesertim pruritosus, qui senioribus, supra sexaginta annos, maxime occurrit. Formatio pustulae in spatio inter stratas epidermalem et dermalem cutis in bulloso pemphigoide observatur.
☆ In anno 2022 Stiftung Warentest ex Germania provenit, satisfactio consumptoria cum ModelDerm paulo minus fuit quam cum consultationibus telemedicinis solutis.
Photo ostendens crura papaveri pusulae obtecta, quae totum corpus afficere possunt.
Signa initiales interdum in forma alvearia funt.
relevance score : -100.0%
ReferencesPemphigus et bullous pemphigoid sunt morbi cutis ubi pustulae ex autoanticorpore formantur. In pemphigso cellulae in strato epidermali et membrana mucosa suam facultatem cohaerent, dum in pemphigoide cellulae ad basim cutis amittunt nexum cum strato substrato. Papulae in pemphigso a autoanticorpora directe causantur, dum in pemphigoide inflammationes a autoanticorpora per complementum activum mediatae sunt. Propriae structurae iaculi a his autoanticorpora notatae sunt: desmogleins in pemphigso (quae in adhesione cellulari versantur) et hemidesmosomes in pemphigoide (quae cellulas ad stratum substratum ancorae).
Pemphigus and bullous pemphigoid are autoantibody-mediated blistering skin diseases. In pemphigus, keratinocytes in epidermis and mucous membranes lose cell-cell adhesion, and in pemphigoid, the basal keratinocytes lose adhesion to the basement membrane. Pemphigus lesions are mediated directly by the autoantibodies, whereas the autoantibodies in pemphigoid fix complement and mediate inflammation. In both diseases, the autoantigens have been cloned and characterized; pemphigus antigens are desmogleins (cell adhesion molecules in desmosomes), and pemphigoid antigens are found in hemidesmosomes (which mediate adhesion to the basement membrane).
Pemphigus and bullous pemphigoid are autoantibody-mediated blistering skin diseases. In pemphigus, keratinocytes in epidermis and mucous membranes lose cell-cell adhesion, and in pemphigoid, the basal keratinocytes lose adhesion to the basement membrane. Pemphigus lesions are mediated directly by the autoantibodies, whereas the autoantibodies in pemphigoid fix complement and mediate inflammation. In both diseases, the autoantigens have been cloned and characterized; pemphigus antigens are desmogleins (cell adhesion molecules in desmosomes), and pemphigoid antigens are found in hemidesmosomes (which mediate adhesion to the basement membrane).
Bullous pemphigoid communis est morbus autoimmune bullosus, qui typice afficit adultos maiores. Exortus in causis recentium decenniis iungitur cum senescente, medicamentis actis, et methodis diagnosticis melioribus pro non‑bullis conditionis formis. Involvit dysfunctio responsionis cellarum T et productionem autoanticorporum (IgG et IgE) contra specificas antigenas (BP180 et BP230), quod ducit ad inflammationem et disruptionem structurae cutis. Symptomata plerumque includunt vesculas duras, eructationes, scabiosum cutis et membranarum commissuras, cum rara implicatione membranarum mucosarum. Tractatio praecipue nititur steroidibus topicis et systemicis potentissimis, cum recentibus studiis illustrantibus beneficia therapiae additae (doxycycline, dapsone, immunosuppressantia), quae ad minuendum usum steroideorum intendunt.
Bullous pemphigoid is the most frequent autoimmune bullous disease and mainly affects elderly individuals. Increase in incidence rates in the past decades has been attributed to population aging, drug-induced cases and improvement in the diagnosis of the nonbullous presentations of the disease. A dysregulated T cell immune response and synthesis of IgG and IgE autoantibodies against hemidesmosomal proteins (BP180 and BP230) lead to neutrophil chemotaxis and degradation of the basement membrane zone. Bullous pemphigoid classically manifests with tense blisters over urticarial plaques on the trunk and extremities accompanied by intense pruritus. Mucosal involvement is rarely reported. High potency topical steroids and systemic steroids are the current mainstay of therapy. Recent randomized controlled studies have demonstrated the benefit and safety of adjuvant treatment with doxycycline, dapsone and immunosuppressants aiming a reduction in the cumulative steroid dose and mortality.
Bullous pemphigoid is the most frequent autoimmune bullous disease and mainly affects elderly individuals. Increase in incidence rates in the past decades has been attributed to population aging, drug-induced cases and improvement in the diagnosis of the nonbullous presentations of the disease. A dysregulated T cell immune response and synthesis of IgG and IgE autoantibodies against hemidesmosomal proteins (BP180 and BP230) lead to neutrophil chemotaxis and degradation of the basement membrane zone. Bullous pemphigoid classically manifests with tense blisters over urticarial plaques on the trunk and extremities accompanied by intense pruritus. Mucosal involvement is rarely reported. High potency topical steroids and systemic steroids are the current mainstay of therapy. Recent randomized controlled studies have demonstrated the benefit and safety of adjuvant treatment with doxycycline, dapsone and immunosuppressants aiming a reduction in the cumulative steroid dose and mortality.
