Bullous pemphigoid
Bullous pemphigoid ໝາຍເຖິງຄວາມຜິດປົກກະຕິຂອງຜິວໜັງທຸກປະເພດທີ່ເຮັດໃຫ້ເກີດການເກີດ bullaes. "Bullous pemphigoid" ເປັນພະຍາດຜິວຫນັງ autoimmune pruritic ໂດຍສະເພາະແມ່ນຢູ່ໃນຜູ້ສູງອາຍຸ, ອາຍຸຫຼາຍກວ່າ 60 ປີ.
☆ ໃນປີ 2022 Stiftung Warentest ຜົນໄດ້ຮັບຈາກເຢຍລະມັນ, ຄວາມພໍໃຈຂອງຜູ້ບໍລິໂພກກັບ ModelDerm ແມ່ນຕໍ່າກວ່າການປຶກສາຫາລືທາງດ້ານການປິ່ນປົວທາງໂທລະສັບເລັກນ້ອຍເທົ່ານັ້ນ.
ຮູບທີ່ສະແດງຂາມີຕຸ່ມເປື່ອຍ ເຊິ່ງສາມາດສົ່ງຜົນກະທົບຕໍ່ຮ່າງກາຍທັງໝົດ.
ອາການເບື້ອງຕົ້ນແມ່ນ ບາງຄັ້ງມີອາການເປັນລົມ.
References
Pemphigus ແລະ bullous pemphigoid ແມ່ນພະຍາດຜິວໜັງທີ່ເປັນຕຸ່ມຜື່ນອັນເນື່ອງມາຈາກ autoantibodies. ໃນ pemphigus , ຈຸລັງໃນຊັ້ນຜິວຫນັງຊັ້ນນອກແລະເຍື່ອເມືອກຈະສູນເສຍຄວາມສາມາດໃນການຕິດກັນ, ໃນຂະນະທີ່ຢູ່ໃນ pemphigoid , ຈຸລັງທີ່ຢູ່ໂຄນຂອງຜິວຫນັງຈະສູນເສຍການເຊື່ອມຕໍ່ກັບຊັ້ນໃຕ້ດິນ. ຜື່ນຂອງ pemphigus ແມ່ນເກີດມາຈາກ autoantibodies ໂດຍກົງ, ໃນຂະນະທີ່ຢູ່ໃນ pemphigoid , autoantibodies ເຮັດໃຫ້ເກີດການອັກເສບໂດຍການກະຕຸ້ນການເສີມ. ທາດໂປຼຕີນສະເພາະທີ່ຖືກເປົ້າຫມາຍໂດຍ autoantibodies ເຫຼົ່ານີ້ໄດ້ຖືກລະບຸໄວ້: desmogleins ໃນ pemphigus (ເຊິ່ງມີສ່ວນຮ່ວມໃນການຍຶດຕິດຂອງເຊນ) ແລະໂປຣຕີນໃນ hemidesmosomes ໃນ pemphigoid (ເຊິ່ງຍຶດເອົາຈຸລັງກັບຊັ້ນໃຕ້ດິນ) .
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 ແມ່ນພະຍາດ autoimmune bullous ທີ່ພົບເລື້ອຍທີ່ສຸດ, ໂດຍປົກກະຕິຜົນກະທົບຕໍ່ຜູ້ສູງອາຍຸ. ການເພີ່ມຂຶ້ນຂອງກໍລະນີໃນໄລຍະທົດສະວັດທີ່ຜ່ານມາແມ່ນກ່ຽວຂ້ອງກັບປະຊາກອນຜູ້ສູງອາຍຸ, ເຫດການທີ່ກ່ຽວຂ້ອງກັບຢາເສບຕິດ, ແລະການປັບປຸງວິທີການວິນິດໄສສໍາລັບຮູບແບບທີ່ບໍ່ແມ່ນການຂົ່ມເຫັງຂອງສະພາບ. ມັນກ່ຽວຂ້ອງກັບຄວາມຜິດປົກກະຕິໃນການຕອບສະຫນອງຂອງຈຸລັງ T ແລະການຜະລິດ autoantibodies (IgG ແລະ IgE) ເປົ້າຫມາຍໂປຣຕີນສະເພາະ (BP180 ແລະ BP230) , ເຮັດໃຫ້ເກີດການອັກເສບແລະການທໍາລາຍໂຄງສ້າງສະຫນັບສະຫນູນຂອງຜິວຫນັງ. ອາການຕ່າງໆມັກຈະມີຕຸ່ມຜື່ນຂຶ້ນ, ມີອາການຄັນຕາມຮ່າງກາຍ ແລະ ແຂນຂາ, ໂດຍທີ່ບໍ່ຄ່ອຍມີເຍື່ອເມືອກ. ການປິ່ນປົວຕົ້ນຕໍແມ່ນອີງໃສ່ຢາສະເຕີຣອຍທີ່ມີທ່າແຮງແລະລະບົບ, ດ້ວຍການສຶກສາທີ່ຜ່ານມາໄດ້ຊີ້ໃຫ້ເຫັນຜົນປະໂຫຍດແລະຄວາມປອດໄພຂອງການປິ່ນປົວເພີ່ມເຕີມ (doxycycline, dapsone, immunosuppressants) , ແນໃສ່ຫຼຸດຜ່ອນການໃຊ້ 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.
