Bullous pemphigoid
https://en.wikipedia.org/wiki/Bullous_pemphigoid
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Chithunzi chosonyeza miyendo yophimbidwa ndi matuza otuluka, omwe amatha kukhudza thupi lonse.
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References
Mechanisms of Disease: Pemphigus and Bullous Pemphigoid 26907530 NIH
Pemphigus ndi bullous pemphigoid ndi matenda apakhungu omwe matuza amapangika chifukwa cha chitetezo cha mthupi. Mu pemphigus , ma cell akunja kwa khungu ndi mucous nembanemba samatha kulumikizana, pomwe mu pemphigoid , ma cell apansi pa khungu amasiya kulumikizana ndi gawo lomwe lili pansi. Matuza a pemphigus amayamba mwachindunji ndi ma autoantibodies, pomwe mu pemphigoid , ma autoantibodies amayambitsa kutupa poyambitsa chothandizira. Mapuloteni enieni omwe amayang'aniridwa ndi ma autoantibodies awa adziwika: desmogleins mu pemphigus (omwe amakhudzidwa ndi ma cell adhesion) ndi mapuloteni mu hemidesmosomes mu pemphigoid (omwe amamanga maselo kumtunda wapansi) .
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 31090818 NIH
Bullous pemphigoid ndi matenda ofala kwambiri a autoimmune bullous, omwe amakhudza okalamba. Kuwonjezeka kwa milandu m'zaka makumi angapo zapitazi kumalumikizidwa ndi ukalamba, zochitika zokhudzana ndi mankhwala osokoneza bongo, komanso njira zodziwira bwino za matenda omwe si ankhanza. Zimakhudza kusagwira bwino ntchito kwa ma T cell kuyankha komanso kupanga ma autoantibodies (IgG ndi IgE) omwe akuloza mapuloteni enieni (BP180 ndi BP230) , zomwe zimapangitsa kutupa ndi kuwonongeka kwa khungu lothandizira. Zizindikiro zake nthawi zambiri zimakhala matuza pamiyendo yokwezeka, kuyabwa m'thupi ndi m'miyendo, zomwe zimachitika kawirikawiri ndi mucous nembanemba. Chithandizo makamaka chimadalira ma topical and systemic steroids, ndipo kafukufuku waposachedwa akuwonetsa zabwino ndi chitetezo chamankhwala owonjezera (doxycycline, dapsone, immunosuppressants) , omwe cholinga chake ndi kuchepetsa kugwiritsa ntchito ma 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.