Bullous pemphigoid
Bullous pemphigoid inoreva marudzi ese ekukanganiswa kweganda anokonzera mabulla. “Bullous pemphigoid” inonzi autoimmune pruritic skin disease inowanikwa kune vanhu vakwegura, vane makore anopfuura 60. Kuumbwa kwezviputi munzvimbo iri pakati pe epidermal ne dermal ganda layers kunoonekwa mu Bullous pemphigoid.
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ReferencesPemphigus uye bullous pemphigoid izvirwere zveganda zvinokonzerwa nekugadzirwa kwemablister nekuda kweautoantibodies. Mu pemphigus, maseru ekunze kweganda pamwe nemukobvu (mucous membranes) anorasikirwa nekubatana, nepo mu pemphigoid, maseru ari pasi peganda anorasikirwa nekubatana neiyo iri pasi pe layer. Mablister e pemphigus anokonzerwa zvakananga neautoantibodies, nepo mu pemphigoid, masoja ekudzivirira anokonzera kuzvimba uye kuita kuti blisters dzive pasi. Mapuroteni chaiwo anorwiswa neaya autoantibodies anozivikanwa: desmogleins mu pemphigus (iyo inobatanidzwa musero adhesion) uye mapuroteni muhemidesmosomes mu pemphigoid (iyo anchor masero kune iri pasi pe layer).
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 ndicho chirwere chinowanzoitika che autoimmune bullous, chinowanzobata vanhu vakuru. Kukwira kwezviitiko mumakumi emakore achangopfuura kwakabatana nehuwandu hwekuchembera, zviitiko zvine chekuita nezvinodhaka, uye nzira dzakavandudzwa dzekuongorora dzemhando dzisiri dzehutsinye. Zvinosanganisira kusashanda zvakanaka kwekupindura kweT‑cell uye kugadzirwa kweautoantibodies (IgG neIgE) kunanga mapuroteni chaiwo (BP180 neBP230), zvichikonzera kuzvimba uye kuparara kweganda rinotsigira chimiro. Zviratidzo zvinowanzo sanganisira kuputika kweganda, zvigamba zvinokwenya pamuviri nemakumbo, uye kusawanzobatanidzwa kwemucous membranes. Kurapa kunonyanya kutsamira pakushandisa systemic steroids ane simba, uye zvidzidzo zvenguva pfupi yapfuura zvinoratidza mabhenefiti uye kuchengetedzeka kwemamwe marapirwo (doxycycline, dapsone, immunosuppressants), ane chinangwa chekudzikisa kushandiswa kwestersoid.
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.
