Bullous pemphigoid
Bullous pemphigoid e bolela mefuta eohle ea mafu a letlalo a bakang li-bulla. "Bullous pemphigoid" ke lefu la letlalo la "autoimmune pruritic" ka ho khetheha ho batho ba baholo, ba lilemo li fetang 60. Ho thehoa ha marako sebakeng se pakeng tsa letlalo la epidermal le dermal ho hlokomeloa ka pemphigoid ea bullous.
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References
Pemphigus le bullous pemphigoid ke mafu a letlalo moo marotholi a hlahang ka lebaka la li-autoantibodies. Ho pemphigus , lisele tse karolong e ka ntle ea letlalo le lera la mucous li lahleheloa ke bokhoni ba tsona ba ho khomarelana, ha ho pemphigoid , lisele tse botlaaseng ba letlalo li lahleheloa ke khokahano ea tsona le lera le ka tlase. Mahlaseli a pemphigus a bakoa ka kotloloho ke li-autoantibodies, ha ho pemphigoid , li-autoantibodies li baka ho ruruha ka ho kenya tšebetsong tlatsetso. Liprotheine tse khethehileng tse tobisitsoeng ke li-autoantibodies tsena li khethiloe: li-desmogleins ho pemphigus (tse amehang ho khomaretseng lisele) le liprotheine tse ho hemidesmosomes ho pemphigoid (e leng lisele tse ankora ho lera le ka tlaase) .
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 ke lefu le atileng haholo la autoimmune bullous, hangata le ama batho ba baholo. Ho eketseha ha linyeoe lilemong tse mashome tsa morao tjena ho amahanngoa le batho ba tsofetseng, liketsahalo tse amanang le lithethefatsi, le mekhoa e ntlafetseng ea ho hlahloba mafu bakeng sa mefuta e sa tsitsang ea boemo boo. E kenyelletsa ho se sebetse hantle ha karabelo ea T cell le tlhahiso ea li-autoantibodies (IgG le IgE) tse shebileng liprotheine tse itseng (BP180 le BP230) , ho baka ho ruruha le ho senyeha ha sebopeho se tšehetsang letlalo. Matšoao hangata a kenyelletsa makhopho a makhopho a phahamisitsoeng, a hlohlona 'meleng le maotong le maotong, ka ho ameha ka seoelo lera la mucous. Kalafo haholo-holo e itšetlehile ka li-steroid tse matla tsa lihlooho le tsa tsamaiso, 'me liphuputso tsa morao-rao li totobatsa melemo le polokeho ea liphekolo tse eketsehileng (doxycycline, dapsone, immunosuppressants) , tse reretsoeng ho fokotsa tšebeliso ea li-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.
