Vitiligo
☆ Liphethong tsa 2022 Stiftung Warentest tse tsoang Jeremane, khotsofalo ea bareki ka ModelDerm e ne e le tlase hanyane ho feta lipuisano tse lefelloang tsa telemedicine.
Vitiligo ea menoana e thata ho phekola ho feta libaka tse ling. Ntle le ho se khahle hantle, vitiligo e tloaelehile ebile ha e tšoaetsane. Ho dermatology, phekolo e sebetsang ka ho fetisisa ke phototherapy kapa phekolo ea laser (excimer) makhetlo a 2-3 ka beke bonyane selemo se le seng. Haeba u sa khone ho ea sepetlele hangata ka mabaka a lichelete kapa hobane u phathahane, u ka leka mochine oa phototherapy o lumelloang ho sebelisoa lapeng.
Eyelid vitiligo
Vitiligo ka letsohong
References
Vitiligo ke boloetse bo tloaelehileng ba letlalo bo bakang maqeba a letlalo le lesoeu ka lebaka la tahlehelo ea melanocyte. Lipatlisiso tsa morao-rao li bontša hore ke lefu la autoimmune. Le hoja hangata e nkoa e le taba ea litlolo, e ka ama bophelo bo botle ba kelello le bophelo ba letsatsi le letsatsi haholo. Ka 2011, litsebi li ile tsa beha mofuta o bitsoang segmental vitiligo ka thoko ho tse ling.
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.
Bakuli ba mafolofolo ba vitiligo ba na le likhetho tse 'maloa tsa kalafo, joalo ka systemic glucocorticoids, phototherapy, le systemic immunosuppressants. Bakuli ba tsitsitseng ba vitiligo ba ka fumana phomolo ho tsoa ho li-topical corticosteroids, topical calcineurin inhibitors, phototherapy, le mekhoa ea transplantation. Khatelo-pele ea morao-rao ea ho utloisisa lits'ebetso tse ka sehloohong tsa vitiligo e lebisitse ho nts'etsopele ea mekhoa ea phekolo e reretsoeng. Hajoale, li-inhibitors tsa JAK ke tsona tse ts'episang ka ho fetesisa, tse fanang ka mamello e ntle le liphetho tse sebetsang, leha ho na le kotsi ea ho ts'oara ts'oaetso e patehileng le litlamorao tsa systemic tse tloaelehileng le li-immunosuppressive tse ling. Patlisiso e tsoelang pele e ikemiselitse ho tseba li-cytokine tsa bohlokoa tse amehang kholong ea vitiligo (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF) . Ho thibela li-cytokine tsena ho bontšitse tšepiso ho mehlala ea liphoofolo le bakuli ba bang. Ho feta moo, lipatlisiso mabapi le miRNA-based therapeutics le adoptive Treg cell therapy li ntse li tsoela pele.
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.
Ha ho na pheko e tsebahalang ea vitiligo. Bakeng sa ba nang le letlalo le khanyang, setlolo se sireletsang letsatsi le litlolo ke tsona feela tse khothalletsoang. Mekhoa e meng ea phekolo e ka kenyelletsa litlolo tsa steroid kapa phototherapy.
○ Kalafo
#Phototherapy
#Excimer laser
#Tacrolimus ointment