Vitiligo
☆ I le 2022 Stiftung Warentest i'uga mai Siamani, o le fa'amalieina o tagata fa'atau i ModelDerm sa na'o sina maualalo ifo nai lo fa'atalanoaga telemedicine totogi.
Vitiligo o tamatamailima e sili atu ona faigata ona togafitia nai lo isi vaega. E ese mai i le le lelei o foliga, o le vitiligo e masani ma e le pipisi. I dermatology, o le togafitiga sili ona aoga o le phototherapy poʻo le laser togafitiga (excimer) 2-3 taimi i le vaiaso mo le itiiti ifo i le 1 le tausaga. Afai e le mafai ona e alu soo i le falemaʻi ona o mea tau tupe pe ona o loʻo e pisi, e mafai ona e faʻataʻitaʻiina se masini phototherapy e faʻatagaina mo le faʻaoga ile fale.
Vitiligo laumata
Vitiligo i lima
References
Vitiligo ose ma'i masani o le pa'u e mafua ai ni pa'u pa'epa'e ona o le to'esea o melanocytes. O su'esu'ega lata mai o lo'o fa'aalia ai ose ma'i autoimmune. E ui e masani ona vaʻaia o se faʻafitauli teuteu, e mafai ona matua afaina ai le soifua manuia o le mafaufau ma le olaga i aso uma. I le 2011, na fa'avasegaina e le au atamamai se ituaiga e ta'ua o le segmental vitiligo ese'ese mai isi.
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.
O tagata ma'i vitiligo gaioi e tele togafitiga, e pei o glucocorticoids systemic, phototherapy, ma immunosuppressants systemic. O tagata mama'i vitiligo mautu e mafai ona maua le toomaga mai corticosteroids, iniseti calcineurin topical, phototherapy, ma faiga fa'anofo. O le alualu i luma lata mai i le malamalama i faiga faavae o le vitiligo ua mafua ai le atinaʻeina o togafitiga faʻatatau. I le taimi nei, JAK inhibitors e sili ona fa'amoemoeina, e ofoina atu le gafatia lelei ma taunu'uga aoga, e ui lava i le lamatiaga o le fa'agaoioia o fa'ama'i pipisi ma fa'alavelave fa'aletonu e masani ai ma isi vaila'au immunosuppressive. O su'esu'ega fa'aauau e fa'amoemoe e iloa ai cytokines autu o lo'o a'afia ile atina'eina ole vitiligo (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF) . O le polokaina o nei cytokines ua faʻaalia ai le folafolaga i faʻataʻitaʻiga manu ma nisi o gasegase. E le gata i lea, o lo'o fa'agasolo su'esu'ega ile miRNA-based therapeutics ma le adoptive Treg cell therapy.
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.
E leai se fofo ua iloa mo vitiligo. Mo i latou e mama pa'u, puipui o le la ma teuteuga o mea uma ia e masani ona fautuaina. O isi togafitiga e mafai ona aofia ai kulimi steroid po'o phototherapy.
○ Togafitiga
#Phototherapy
#Excimer laser
#Tacrolimus ointment