Vitiligohttps://en.wikipedia.org/wiki/Vitiligo
Vitiligo se yon kondisyon po alontèm karakterize pa plak nan po a pèdi pigman yo. Plak po ki afekte yo vin blan epi anjeneral gen maj byen file. Cheve ki soti nan po a ka vin tou blan. Li pi aparan nan moun ki gen po nwa. Faktè risk yo enkli yon istwa fanmi nan kondisyon an oswa lòt maladi otoiminitè, tankou ipètiwoyid, alopesi areata, ak anemi danjere. Li pa kontajye. Globalman, apeprè 1% nan moun yo afekte pa vitiligo. Apeprè mwatye montre maladi a anvan laj 20 e pifò devlope li anvan laj 40.

Pa gen okenn gerizon li te ye pou vitiligo. Pou moun ki gen po limyè, krèm pwotèj kont solèy ak makiyaj se tout sa ki tipikman rekòmande. Lòt opsyon tretman ka gen ladan krèm esteroyid oswa fototerapi.

Tretman
#Phototherapy
#Excimer laser
#Tacrolimus ointment
☆ Nan rezilta Stiftung Warentest 2022 ki soti nan Almay, satisfaksyon konsomatè yo ak ModelDerm te sèlman yon ti kras pi ba pase ak konsiltasyon telemedsin peye.
  • Non-segmental vitiligo
  • Vitiligo ka pafwa akonpaye pa cheve blan.
  • Vitiligo nan dwèt yo pi difisil pou trete pase lòt zòn. Akote ke yo te kosmetik disgrasyeu, vitiligo se nòmal epi li pa kontajye. Nan dèrmatoloji, tretman ki pi efikas se fototerapi oswa tretman lazè (excimer) 2-3 fwa pa semèn pou omwen 1 ane. Si ou pa ka ale lopital souvan pou rezon finansye oswa paske ou okipe, ou ka eseye yon machin fototerapi ki apwouve pou itilizasyon lakay ou.
  • Vitiligo po je
  • Vitiligo nan men
References Vitiligo: A Review 32155629
Vitiligo se yon maladi po komen ki lakòz plak nan po blan akòz pèt la nan melanosit. Dènye rechèch montre li se yon maladi otoiminitè. Pandan ke yo souvan wè li kòm yon pwoblèm kosmetik, li ka pwofondman afekte byennèt mantal ak lavi chak jou. An 2011, ekspè yo klase yon kalite ki rele segmental vitiligo separeman de lòt moun.
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.
 Advances in vitiligo: Update on therapeutic targets 36119071 
NIH
Pasyan aktif vitiligo yo gen plizyè opsyon terapi, tankou glikokortikoyid sistemik, fototerapi, ak imunosuppressants sistemik. Pasyan ki estab vitiligo ka jwenn soulajman nan kortikoterapi aktualite, inibitè calcineurin aktualite, fototerapi, ak pwosedi transplantasyon. Avansman ki sot pase yo nan konpreyansyon pwosesis kache vitiligo a te mennen nan devlopman nan terapi vize. Kounye a, inibitè JAK yo se pi pwomèt la, ki ofri bon tolerabilite ak rezilta fonksyonèl, malgre risk pou yo aktive enfeksyon inaktif ak efè segondè sistemik ki komen ak lòt ajan imunosuppressive. Rechèch kontinyèl gen pou objaktif pou idantifye sitokin kle ki enplike nan devlopman vitiligo a (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF) . Bloke cytokines sa yo te montre pwomès nan modèl bèt ak kèk pasyan. Anplis de sa, envestigasyon sou miRNA-based therapeutics ak adoptive Treg cell therapy ap fèt.
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.