Vitiligo
☆ Mune 2022 Stiftung Warentest mhedzisiro kubva kuGermany, kugutsikana kwevatengi neModelDerm kwakangodzikira zvishoma pane nekubhadharwa kwe telemedicine kubvunzana.
Vitiligo yeminwe yakaoma kurapa kupfuura dzimwe nzvimbo. Kunze kwekusatarisika zvakanaka, vitiligo yakajairika uye haiparadzirike. Mune dermatology, kurapa kunonyanya kushanda ndeye phototherapy kana laser treatment (excimer) 2-3 nguva pavhiki kweinenge 1 gore. Kana usingakwanise kuenda kuchipatara kazhinji nekuda kwezvikonzero zvemari kana nekuti wakabatikana, unogona kuedza muchina wephototherapy unotenderwa kushandiswa pamba.
Eyelid vitiligo
Vitiligo paruoko
References
Vitiligo chirwere cheganda chinowanzoitika chinokonzera zvigamba zveganda jena nekuda kwekurasikirwa kwema melanocytes. Ongororo yazvino inoratidza kuti chirwere che autoimmune. Kunyangwe ichiwanzoonekwa sechinhu chekushongedza, inogona kukanganisa zvakanyanya hutano hwepfungwa uye hupenyu hwezuva nezuva. Muna 2011, nyanzvi dzakaisa mhando inonzi segmental vitiligo zvakasiyana kubva kune vamwe.
Vitiligo is a common skin disorder that causes patches of white skin due to the loss of melanocytes. Recent research shows it's an autoimmune disease. While it's often seen as a cosmetic issue, it can deeply affect mental well-being and daily life. In 2011, experts classified a type called segmental vitiligo separately from others.
Vitiligo is a common skin disorder that causes patches of white skin due to the loss of melanocytes. Recent research shows it's an autoimmune disease. While it's often seen as a cosmetic issue, it can deeply affect mental well-being and daily life. In 2011, experts classified a type called segmental vitiligo separately from others.
Active vitiligo varwere vane akati wandei ekurapa sarudzo, senge systemic glucocorticoids, phototherapy, uye systemic immunosuppressants. Varwere vakagadzikana vevitiligo vanogona kuwana zororo kubva kune topical corticosteroids, topical calcineurin inhibitors, phototherapy, uye transplantation maitiro. Kufambira mberi kuchangobva kuitika mukunzwisisa maitiro evitiligo kwakatungamira mukugadzirwa kwenzira dzakanangwa dzekurapa. Parizvino, JAK inhibitors ndiyo inonyanya kuvimbisa, inopa kushivirira kwakanaka uye mhedzisiro inoshanda, kunyangwe paine njodzi yekumisa hutachiona hwehutachiona uye systemic mhedzisiro inowanzoitika nemamwe ma immunosuppressive agents. Tsvagiridzo inoenderera mberi ine chinangwa chekuona akakosha macytokines anobatanidzwa mukukura kwevitiligo (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF) . Kuvhara aya macytokines kwakaratidza kuvimbiswa mumhando dzemhuka uye vamwe varwere. Pamusoro pezvo, ongororo dze miRNA-based therapeutics ne adoptive Treg cell therapy dziri kuenderera mberi.
Current models of treatment for vitiligo are often nonspecific and general. Various therapy options are available for active vitiligo patients, including systemic glucocorticoids, phototherapy, and systemic immunosuppressants. While stable vitiligo patients may benefit from topical corticosteroids, topical calcineurin inhibitors, phototherapy, as well as transplantation procedures. Recently, a better understanding of the pathophysiological processes of vitiligo led to the advent of novel targeted therapies. To date, JAK inhibitors are the only category that has been proved to have a good tolerability profile and functional outcomes in vitiligo treatment, even though the risk of activation of latent infection and systemic side effects still existed, like other immunosuppressive agents. Research is in progress to investigate the important cytokines involved in the pathogenesis of vitiligo, including IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, and TNF, the blockade of which has undergone preliminary attempts in animal models and some patients. In addition, studies on miRNA-based therapeutics as well as adoptive Treg cell therapy are still primary, and more studies are necessary.
Current models of treatment for vitiligo are often nonspecific and general. Various therapy options are available for active vitiligo patients, including systemic glucocorticoids, phototherapy, and systemic immunosuppressants. While stable vitiligo patients may benefit from topical corticosteroids, topical calcineurin inhibitors, phototherapy, as well as transplantation procedures. Recently, a better understanding of the pathophysiological processes of vitiligo led to the advent of novel targeted therapies. To date, JAK inhibitors are the only category that has been proved to have a good tolerability profile and functional outcomes in vitiligo treatment, even though the risk of activation of latent infection and systemic side effects still existed, like other immunosuppressive agents. Research is in progress to investigate the important cytokines involved in the pathogenesis of vitiligo, including IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, and TNF, the blockade of which has undergone preliminary attempts in animal models and some patients. In addition, studies on miRNA-based therapeutics as well as adoptive Treg cell therapy are still primary, and more studies are necessary.
Hapana mushonga unozivikanwa wevitiligo. Kune avo vane ganda rakajeka, sunscreen uye makeup ndizvo zvese zvinokurudzirwa. Dzimwe nzira dzokurapa dzinogona kusanganisira steroid creams kana phototherapy.
○ Kurapa
#Phototherapy
#Excimer laser
#Tacrolimus ointment