Bullous pemphigoid
Bullous pemphigoid refertur ad omnes morbos cutis, quae bullas inducunt. pemphigoides bullosae (Bullous pemphigoid) autoimmune est morbus cutaneus pruriticus potissimum in senioribus supra 60 annos. Formationem bullarum in spatio inter stratas epidermalem et dermalem observatur.
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In anno 2022 Stiftung Warentest ex Germania provenit, satisfactio consumptoria cum ModelDerm paulo minus fuit quam cum consultationibus telemedicinis solutis.
In anno 2022 Stiftung Warentest ex Germania provenit, satisfactio consumptoria cum ModelDerm paulo minus fuit quam cum consultationibus telemedicinis solutis.
Photo ostendens crura bullarum obtecta, quae totum corpus afficere possunt.
Signa initiales interdum in forma urticaria sunt.
relevance score : -100.0%
ReferencesPemphigus et bullous pemphigoid sunt morbi cutis ubi pusulae ex autoanticorpore formant. In pemphigus, cellulae in strato pellis externae et membranae mucosae amittunt adhesionem inter se, dum in pemphigoid, cellulae ad basim cutis amittunt nexum cum strato substrato. Papulae pemphigus ab autoanticorporibus directe causantur, dum in pemphigoid, autoanticorpora inflammationes per complementum activum provocant. Proprie servo iaculi ab his autoanticorporibus notati sunt: desmogleins in pemphigus (quae in adhaesione cellae versantur) et antigena in hemidesmosomibus in pemphigoid (quae ancorae cellae ad stratum substratum).
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 est morbus autoimmune bullosus, qui typice afficit adultos maiores. Incrementum incidentiarum in decenniis recentibus iungitur cum senescentia populationis, casibus medicamentis inductus et melioratione methodorum diagnosticorum pro formis non‑bullosis morbi. Involvit dysregulationem responsionis cellulae T et productionem auto‑anticorporum (IgG et IgE) contra hemidesmosomales proteina (BP180 et BP230), ducens ad chemotaxis neutrophilorum et degradationem zonae membranae basalis cutis. Symptomata plerumque manifestantur per bullae tensas super plaques urticariae in trunco et extremitatibus, cum rara implicatio mucosae. Tractatio imprimis nititur steroidibus topicae potentiae altae et steroidibus systemicis, cum recentibus studiis quae beneficium et salutem therapiae adjuvantis (doxycycline, dapsone, immunosuppressantia) demonstraverunt, quae ad reductionem usus steroidorum 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.
