Bullous pemphigoid
Bullous pemphigoid yana nufin kowace irin cuta ta fata da ke haifar da bulaes. "Bullous pemphigoid" shine cututtukan fata na autoimmune wanda ya fi dacewa a cikin tsofaffi, masu shekaru sama da 60. Samuwar blisters a cikin sararin samaniya tsakanin epidermal da dermal fata yadudduka ana lura da su a cikin pemphigoid bullous.
☆ A cikin sakamakon Stiftung Warentest na 2022 daga Jamus, gamsuwar mabukaci tare da ModelDerm ya ɗan yi ƙasa kaɗan fiye da biyan shawarwarin telemedicine.
Hoton da ke nuna ƙafafu an rufe su da blisters da suka fito, wanda zai iya shafar jiki duka.
Alamun farko wani lokaci suna cikin sifar amya.
References
Pemphigus da bullous pemphigoid cututtukan fata ne inda blisters ke fitowa saboda autoantibodies. A cikin pemphigus , ƙwayoyin sel a cikin fatar fata na waje da ƙwayoyin mucosa sun rasa ikon mannewa tare, yayin da a cikin pemphigoid , sel a gindin fata sun rasa haɗin su da Layer ɗin da ke ƙasa. Blisters na pemphigus suna haifar da kai tsaye ta hanyar autoantibodies, yayin da a cikin pemphigoid , autoantibodies suna haifar da kumburi ta hanyar kunna haɓakawa. An gano takamaiman sunadaran da waɗannan autoantibodies ke niyya: desmogleins a cikin pemphigus (waɗanda ke da hannu cikin mannewar tantanin halitta) da kuma sunadaran da ke cikin hemidesmosomes a cikin pemphigoid (waɗanda ke ɗaure sel zuwa Layer na ƙasa) .
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 ita ce cuta mai saurin kamuwa da cuta mai saurin kamuwa da cuta, yawanci tana shafar manya. Haɓaka lamura a cikin shekarun baya-bayan nan yana da alaƙa da yawan tsufa, abubuwan da ke da alaƙa da ƙwayoyi, da ingantattun hanyoyin gano yanayin yanayin marasa ƙarfi. Ya haɗa da rashin aiki a cikin amsawar kwayar halitta ta T da kuma samar da autoantibodies (IgG da IgE) da ke niyya takamaiman sunadaran (BP180 da BP230) , wanda ke haifar da kumburi da rushewar tsarin tallafi na fata. Alamomin cutar sun haɗa da kumburin kumburin sama, ƙaiƙayi mai ƙaiƙayi a jiki da gaɓoɓi, tare da saɓanin shigar mucosa. Jiyya da farko ya dogara ne akan magungunan ƙwayoyin cuta masu ƙarfi da na tsarin jiki, tare da nazarin kwanan nan da ke nuna fa'idodi da amincin ƙarin hanyoyin kwantar da hankali (doxycycline, dapsone, immunosuppressants) , da nufin rage amfani da steroid.
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.
