Bullous pemphigoid
Bullous pemphigoid tọka si gbogbo iru awọn rudurudu awọ ti o fa awọn akọmalu. "Bullous pemphigoid" jẹ ẹya autoimmune pruritic ara arun preferentially ni agbalagba eniyan, ti ọjọ ori lori 60. Ibiyi ti roro ni awọn aaye laarin awọn epidermal ati dermal ara fẹlẹfẹlẹ ti wa ni woye ni bullous pemphigoid.
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References
Pemphigus ati bullous pemphigoid jẹ awọn arun awọ-ara nibiti awọn roro n dagba nitori awọn ara-ara ti ara ẹni. Ni pemphigus , awọn sẹẹli ti o wa ninu awọ ara ita ati awọn membran mucous padanu agbara wọn lati dapọ pọ, lakoko ti o wa ni pemphigoid , awọn sẹẹli ti o wa ni ipilẹ ti awọ ara padanu asopọ wọn si ipele ti o wa labẹ. Awọn roro ti pemphigus ni o ṣẹlẹ taara nipasẹ awọn autoantibodies, lakoko ti o wa ni pemphigoid , awọn autoantibodies nfa iredodo nipasẹ mimuṣiṣẹpọ. Awọn ọlọjẹ kan pato ti a fojusi nipasẹ awọn autoantibodies wọnyi ni a ti damọ: desmogleins ni pemphigus (eyiti o ni ipa ninu ifaramọ sẹẹli) ati awọn ọlọjẹ ni hemidesmosomes ni pemphigoid (eyiti awọn sẹẹli dakọ si ipele ti o wa labẹ) .
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 jẹ arun bullous autoimmune ti o wọpọ julọ, eyiti o kan awọn agbalagba agbalagba. Ilọsoke ninu awọn ọran ni awọn ewadun aipẹ ti ni asopọ si awọn olugbe ti ogbo, awọn iṣẹlẹ ti o ni ibatan oogun, ati awọn ọna iwadii ilọsiwaju fun awọn fọọmu ti kii ṣe bullous ti ipo naa. O kan aiṣedeede ninu idahun sẹẹli T ati iṣelọpọ ti awọn autoantibodies (IgG ati IgE) ti o fojusi awọn ọlọjẹ kan pato (BP180 ati BP230) , ti o yorisi iredodo ati didenukole eto atilẹyin awọ ara. Awọn aami aisan nigbagbogbo pẹlu roro lori dide, awọn abulẹ yun lori ara ati awọn ẹsẹ, pẹlu ilowosi toje ti awọn membran mucous. Itọju ni akọkọ da lori awọn sitẹriọdu amúṣantóbi ti o lagbara ati eto eto, pẹlu awọn iwadii aipẹ ti n ṣe afihan awọn anfani ati ailewu ti awọn itọju afikun (doxycycline, dapsone, immunosuppressants) , ti a pinnu lati dinku lilo sitẹriọdu.
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.
