Bullous pemphigoid
Bullous pemphigoid na-ezo aka n'ụdị ọrịa akpụkpọ anụ nke na-ebute bulla. “Bullous pemphigoid” bụ ọrịa akpụkpọ anụ autoimmune nke na-emekarị n’ọtụtụ ndị agadi, karịsịa ndị gafere afọ 60. A na-ahụ blisters n’etiti epidermis na dermis na bullous pemphigoid.
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Foto a na-egosi blisters n'úkwụ, nke nwere ike imetụta ahụ dum.
Mgbaàmà mbụ na-apụta mgbe ụfọdụ n'ụdị hives.
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ReferencesPemphigus na bullous pemphigoid bụ ọrịa akpụkpọ ebe ọnya na-etolite n'ihi autoantibodies. Na pemphigus, sel ndị dị n'èzí akpụkpọ anụ na akpụkpọ mucous na-efunahụ ikike ijikọta ọnụ, ebe na pemphigoid, sel ndị dị n'okpuru akpụkpọ ahụ na-akwụsị njikọ ha na oyi akwa dị n'okpuru. Ọnya pemphigus na-ebute site na autoantibodies ozugbo, ebe pemphigoid, autoantibodies na-ebute mbufụt site n'ịgbalite mmeju. A chọpụtara protein ndị a kapịrị ọnụ nke autoantibodies: 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).
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 bụ ọrịa na-efe efe nke na-ebute ọrịa autoimmune, na-emetụta ndị okenye. N’ịbụrịrị nke a na-ahụ n’ime iri afọ gara aga, e nwere mmụba nke ikpe, nke jikọtara ọnụ ọgụgụ ndị merela agadi, ihe omume metụtara ọgwụ, yana usoro nyocha ka mma maka ụdị ọnọdụ a na-abụghị nke mkparị. Ọ na-agụnye mmeghachi omume na-adịghị mma nke sel T na mmepụta nke autoantibodies (IgG na IgE) nke na-ezo aka na protein ndị dị iche (BP180 na BP230), nke na-ebute mbufụt na nkwụsị nke nhazi nkwado akpụkpọ ahụ. Mgbaàmà na-agụnyekarị ọnya n'elu akpụkpọ, ihe nfụkasị n'ahụ na n'akụkụ aka, yana mmetụ na akpụkpọ anụ mucous. Ọgwụgwọ na-adabere na steroid dị elu na sistemụ, yana ọmụmụ ihe na-adịbeghị anya egosipụtara 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.
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.
