Vitiligo
☆ I te 2022 Stiftung Warentest hua mai i Tiamana, he iti noa iho te pai o nga kaihoko ki a ModelDerm i nga korero mo te waea rongoa utu.
Ko te Vitiligo o nga maihao he uaua ake te rongoa i era atu waahi. I tua atu i te ahua kino o te ahua, he mea noa te vitiligo me te kore e pangia. I roto i te dermatology, ko te maimoatanga tino whai hua ko te phototherapy, te maimoatanga laser ranei (excimer) 2-3 wa ia wiki mo te iti rawa 1 tau. Mena kaore e taea e koe te haere ki te hohipera i nga wa katoa mo nga take putea, na te mea he pukumahi ranei koe, ka taea e koe te whakamatau i tetahi miihini whakamaarama whakaahua kua whakaaetia mo te whakamahi i te kainga.
Vitiligo kamo
Vitiligo kei te ringa
References
Ko te Vitiligo he mate kiri noa e pa ana ki te kiri ma na te ngaro o nga melanocytes. Ko nga rangahau tata nei e whakaatu ana he mate autoimmune. Ahakoa ka kitea he take whakapaipai, ka tino pa ki te oranga hinengaro me te oranga o ia ra. I te tau 2011, ka whakarōpūtia e nga tohunga tetahi momo e kiia nei ko segmental vitiligo wehe ke atu i etahi atu.
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.
He maha nga whiringa rongoa a nga turoro vitiligo kaha, penei i te glucocorticoids pūnahanaha, phototherapy, me te immunosuppressants pūnahanaha. Ka taea e nga turoro vitiligo pumau te awhina mai i nga corticosteroids, te aukati calcineurin, te whakamaarama whakaahua, me nga tikanga whakawhiti. Ko nga ahunga whakamua i mua tata nei i roto i te maarama ki nga tikanga o te vitiligo i ahu mai i te whanaketanga o nga rongoa kua whakaritea. I tenei wa, ko te hunga aukati JAK te mea tino pai, e tuku ana i te pai o te manawanui me nga hua mahi, ahakoa te tupono ki te whakahohe i nga mate huna me nga paanga taha nahanaha e pa ana ki etahi atu o nga maataki immunosuppressive. Ko te rangahau haere tonu e whai ana ki te tautuhi i nga cytokine matua e uru ana ki te whanaketanga o te vitiligo (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF) . Ko te aukati i enei cytokines kua whakaatu te oati i roto i nga tauira kararehe me etahi turoro. I tua atu, kei te haere tonu nga tirotirohanga mo miRNA-based therapeutics me 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.
Karekau he rongoa mo te vitiligo. Mo te hunga he kiri maramara, ko te whakamarumaru ra me te whakapaipai ko nga mea katoa e taunaki ana. Ko etahi atu momo maimoatanga ka uru pea ki te kirīmi pūtaiaki, ki te whakamaarama whakaahua ranei.
○ Maimoatanga
#Phototherapy
#Excimer laser
#Tacrolimus ointment