Bullous pemphigoid
https://en.wikipedia.org/wiki/Bullous_pemphigoid
☆ Na nsonaazụ Stiftung Warentest nke 2022 sitere na Germany, afọ ojuju ndị ahịa na ModelDerm dị ntakịrị ntakịrị karịa na nyocha telemedicine akwụ ụgwọ. 

Foto na-egosi n'ụkwụ kpuchiri blisters, nke nwere ike imetụta ahụ dum.
relevance score : -100.0%
References
Mechanisms of Disease: Pemphigus and Bullous Pemphigoid 26907530 NIH
Pemphigus na bullous pemphigoid bụ ọrịa akpụkpọ ebe ọnya na-etolite n'ihi autoantibodies. Na pemphigus , sel ndị dị na akpụkpọ anụ dị n'èzí na akpụkpọ anụ mucous na-efunahụ ike ha na-ejikọta ọnụ, ebe na pemphigoid , sel ndị dị n'okpuru akpụkpọ ahụ na-akwụsị njikọ ha na oyi akwa dị n'okpuru. A na-ebute ọnya nke pemphigus site na autoantibodies ozugbo, ebe na pemphigoid , autoantibodies na-ebute mbufụt site na ịgbalite mmeju. Achọpụtara protein ndị a kapịrị ọnụ nke autoantibodies ndị a: desmogleins na pemphigus (nke na-etinye aka na adhesion cell) na protein na hemidesmosomes na pemphigoid (nke na-etinye sel n'ime oyi akwa) .
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 bụ ọrịa na-efe efe na-ebutekarị ọrịa autoimmune, na-emetụta ndị okenye. Mmụba nke ikpe n'ime iri afọ ndị na-adịbeghị anya jikọtara ọnụ ọgụgụ ndị merela agadi, ihe omume metụtara ọgwụ, yana usoro nyocha ka mma maka ụdị ọnọdụ ahụ na-abụghị nke mkparị. Ọ na-agụnye ihe na-adịghị mma na nzaghachi cell T na mmepụta nke autoantibodies (IgG na IgE) na-ezubere maka protein dị iche iche (BP180 na BP230) , na-ebute mbufụt na nkwụsị nke nhazi nkwado akpụkpọ ahụ. Mgbaàmà na-agụnyekarị ọnya n'elu elu, ihe nfụkasị ahụ na ahụ na n'akụkụ aka, na-etinyekarị aka na akpụkpọ anụ mucous. Ọgwụgwọ na-adabere na steroid dị elu na sistemu sistemu, yana ọmụmụ ihe na-adịbeghị anya na-egosipụta uru na nchekwa nke usoro ọgwụgwọ ndị ọzọ (doxycycline, dapsone, immunosuppressants) , iji belata iji 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.