Vitiligohttps://en.wikipedia.org/wiki/Vitiligo
Vitiligo bụ ọnọdụ akpụkpọ ahụ na-adịte aka nke a na-eji akwa akpụkpọ anụ na-efunahụ pigmenti ha. Ihe mgbochi akpụkpọ ahụ metụtara na-acha ọcha ma na-enwekarị akụkụ dị nkọ. Ntutu si na akpụkpọ ahụ nwekwara ike ịcha ọcha. A na-ahụta ya karịa na ndị nwere akpụkpọ ahụ gbara ọchịchịrị. Ihe ndị dị ize ndụ gụnyere akụkọ ihe mere eme ezinụlọ nke ọnọdụ ahụ ma ọ bụ ọrịa autoimmune ndị ọzọ, dị ka hyperthyroidism, alopecia areata, na anaemia na-emerụ ahụ. Ọ naghị efe efe. N'ụwa niile ihe dị ka 1% nke ndị mmadụ na-emetụta vitiligo. Ihe dị ka ọkara na-egosi ọrịa ahụ tupu afọ 20 ma ọtụtụ na-ebute ya tupu ha eruo afọ 40.

Enweghị ọgwụgwọ a ma ama maka vitiligo. Maka ndị nwere akpụkpọ anụ, ihe mkpuchi anwụ na etemeete bụ ihe a na-atụkarị aro. Nhọrọ ọgwụgwọ ndị ọzọ nwere ike ịgụnye ude steroid ma ọ bụ phototherapy.

Ọgwụgwọ
#Phototherapy
#Excimer laser
#Tacrolimus ointment
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  • Non-segmental vitiligo
  • Vitiligo nwere ike na-esonyere ya na ntutu isi mgbe ụfọdụ.
  • Vitiligo nke mkpịsị aka siri ike ịgwọ karịa ebe ndị ọzọ. Ewezuga ịbụ onye ịchọ mma na-adịghị mma, vitiligo bụ ihe nkịtị na ọ naghị efe efe. Na dermatology, ọgwụgwọ kachasị dị irè bụ phototherapy ma ọ bụ ọgwụgwọ laser (excimer) ugboro 2-3 n'izu ọ dịkarịa ala otu afọ. Ọ bụrụ na ịnweghị ike ịga ụlọ ọgwụ mgbe mgbe maka ihe gbasara ego ma ọ bụ n'ihi na ị na-arụsi ọrụ ike, ị nwere ike ịnwale igwe phototherapy nke akwadoro maka iji ụlọ.
  • vitiligo anya
  • Vitiligo dị n'aka
References Vitiligo: A Review 32155629
Vitiligo bụ ọrịa akpụkpọ anụ nke na-ebute akpụkpọ anụ ọcha n'ihi mfu nke melanocytes. Nnyocha e mere na nso nso a gosiri na ọ bụ ọrịa autoimmune. Ọ bụ ezie na a na-ahụkarị ya dị ka okwu ịchọ mma, ọ nwere ike imetụta ahụike uche na ndụ kwa ụbọchị. N'afọ 2011, ndị ọkachamara kewapụrụ ụdị a na-akpọ segmental vitiligo dị iche na ndị ọzọ.
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
Ndị ọrịa vitiligo na-arụsi ọrụ ike nwere ọtụtụ nhọrọ ọgwụgwọ, dị ka glucocorticoids sistemu, phototherapy, na sistemu immunosuppressants. Ndị ọrịa vitiligo kwụsiri ike nwere ike nweta ahụ efe site na corticosteroids dị n'elu, ihe mgbochi calcineurin n'elu, phototherapy, na usoro ntụgharị. Ọganiihu n'oge na-adịbeghị anya n'ịghọta usoro ndị dị n'okpuru vitiligo ebutela mmepe nke usoro ọgwụgwọ ezubere iche. Ugbu a, ndị na-egbochi JAK bụ ndị na-ekwe nkwa, na-enye ezigbo nnabata na nsonaazụ ọrụ, n'agbanyeghị ihe ize ndụ nke ịgbalite ọrịa latent na mmetụta sistemu nke jikọtara ya na ndị ọrụ immunosuppressive ndị ọzọ. Nchọpụta na-aga n'ihu na-achọ ịchọpụta cytokines bụ isi na-etinye aka na mmepe vitiligo (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF) . Igbochi cytokines ndị a egosila nkwa na ụdị anụmanụ na ụfọdụ ndị ọrịa. Ọzọkwa, a na-eme nyocha n'ime miRNA-based therapeutics na 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.