Bullous pemphigoid
Bullous pemphigoid refertur ad omnes morbos cutis, quae bullas inducunt. "Pemphigoidum bulbosum" autoimmune est morbus cutanei pruritici potissimum in senioribus, senibus supra 60. Formatio pusulae in spatio inter epidermalem et dermal stratis cutem 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.
References
Pemphigus et bullous pemphigoid sunt morbi cutis ubi pusulae ex autoanticorpore formant. In pemphigus , cellulae in strato pellis exteriore et membranae mucosae suam facultatem cohaerent, dum in pemphigoid , cellulae ad basin cutis amittunt nexum cum strato substrata. Papulae pemphigus ab autoanticorporibus directe causantur, dum in pemphigoid , autoanticorporum inflammationes felis per complementum activum. Proprie servo iaculi ab his autoanticorporibus notati sunt: desmogleins in pemphigus (quae in adhaesione cellae versantur) et servo in hemidesmosomes 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 Communis est morbus autoimmune bullosus, qui typice afficit adultos maiores. Exortus in causis recentium decenniis iungitur cum senescentis, incidentibus medicamentis actis, et methodis diagnostica melioribus pro non-bullis conditionis formis. Involvit malfunction in T cellam responsionem ac productionem autoanticorporum (IgG et IgE) nisi specificae servo (BP180 et BP230) , ex inflammatione et naufragio structurae adminiculae cutis. Symptomata plerumque duros erectos, scabiosos corporis et membrorum commissuras includunt, cum rara membranarum mucosarum implicatione. Tractatio imprimis nititur steroidibus theologicis et systemicis potentissimis, cum recentibus studiis illustrandis beneficiis et salute additorum therapiarum (doxycycline, dapsone, immunosuppressants) , quae ad usum steroidei minuendum intenderunt.
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.
