Bullous pemphigoid
Bullous pemphigoid waxaa loola jeedaa dhammaan noocyada cudurrada maqaarka ee keena bullaacada. "Bullous pemphigoid" waa cudur maqaar cuncun leh oo iskiis u difaaca si gaar ah dadka da'da ah, da'doodu ka weyn tahay 60 sano. Sameynta finanka meelaha bannaan ee u dhexeeya lakabyada maqaarka ee epidermal iyo maqaarka ayaa lagu arkay pemphigoid bullous.
☆ Natiijooyinka Stiftung Warentest ee 2022 ee ka yimid Jarmalka, ku qanacsanaanta macaamilka ee ModelDerm ayaa waxyar uun ka hooseysay la-talinta telemedicine-ka ee lacagta lagu bixiyo.
Sawir muujinaya lugaha oo daboolan finan soo baxay, kuwaas oo saameyn kara jirka oo dhan.
Astaamaha bilawga ah mararka qaarkood waxay u eg yihiin cuncun.
References
Pemphigus iyo bullous pemphigoid waa cuduro maqaarka ah oo ay ka sameysmaan finan ka soo baxa unugyada difaaca jirka. Gudaha pemphigus , unugyada lakabka sare ee maqaarka iyo xuubabka xuubka ayaa lumiyaa awooda ay isku dhejiyaan, halka pemphigoid , unugyada maqaarka maqaarka ay lumiyaan xiriirkooda lakabka hoose. Nabarrada pemphigus waxaa si toos ah u keena autoantibodies-ka, halka pemphigoid , autoantibodies-ku ay kiciyaan caabuq iyaga oo dhaqaajiya dhamaystirka. Barootiinada gaarka ah ee ay bartilmaameedsadaan autoantibodies-yadan ayaa la aqoonsaday: desmogleins oo ku jira pemphigus (kuwaas oo ku lug leh adhesion unug) iyo borotiinada ku jira hemidesmosomes ee pemphigoid (kuwaas oo ku xidha unugyada lakabka hoose) .
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 waa cudurka bullous-ka ah ee ugu badan ee difaaca jirka, sida caadiga ah saameeya dadka waaweyn. Kor u kaca kiisaska tobannaankii sano ee la soo dhaafay waxay la xiriirtaa dadyowga gabowga, dhacdooyinka daroogada la xiriira, iyo hababka ogaanshaha oo la hagaajiyay ee qaababka aan cagajugleyn ee xaaladda. Waxay ku lug leedahay cilladda jawaabta unugyada T-ga iyo soo-saarka autoantibodies (IgG iyo IgE) ee lagu beegsanayo borotiinno gaar ah (BP180 iyo BP230) , taasoo keentay barar iyo burburka qaabdhismeedka taageerada maqaarka. Calaamadaha sida caadiga ah waxaa ka mid ah nabarro kor u kaca, cuncun maqaarka iyo addimada, oo ay ku lug leeyihiin naadirka xuubka xabka. Daaweyntu waxay ugu horreyntii ku tiirsan tahay steroids-ka jirka la mariyo iyo kuwa habaysan, iyada oo daraasadihii ugu dambeeyay ay muujinayaan faa'iidooyinka iyo badbaadada daawaynta dheeraadka ah (doxycycline, dapsone, immunosuppressants) , oo loogu talagalay in lagu yareeyo isticmaalka steroids.
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.
