Vitiligo
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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.
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.
Non-segmental vitiligo (vitiligo kāore i te wehewehe)
Ko te Vitiligo o ngā maihao he uaua ake te rongoā i ērā atu wāhi. I tua atu i te āhua kino, he mea noa te Vitiligo, ā, kāore e pā ki te mamae. I roto i te dermatology, ko te maimoatanga tino whai hua ko te phototherapy, te maimoatanga laser rānei (excimer) 2–3 wā i ia wiki mō te iti rawa 1 tau. Mēnā kāore e taea e koe te haere ki te hōhipera i ngā wā katoa mō ngā take pūtea, nā te mea he pukumahi rānei koe, ka taea e koe te whakamātau i tētahi mīhini whakamārama whakaahua kua whakaaetia mō te whakamahi i te kāinga.
He vitiligo kei te ringa.
relevance score : -100.0%
ReferencesKo te Vitiligo he mate kiri noa e pā ana ki te kiri mā te ngaro o ngā melanocytes. Ko ngā rangahau tata nei e whakaatu ana i te mea he mate autoimmune. Ahakoa ka kitea he take whakapaipai, ka tino pā ki te oranga hinengaro me te oranga o ia rā. I te tau 2011, ka whakarōpūtia e ngā tohunga tētahi momo e kīia nei ko segmental vitiligo, wehe atu i ētahi 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 ngā whiringa rongoā mō te vitiligo kaha, pērā i ngā glucocorticoids pūnahanaha, phototherapy, me ngā immunosuppressants pūnahanaha. Ka taea e ngā turoro vitiligo pūmau te awhina i ngā corticosteroids, te aukati calcineurin, te whakamārama whakaahua, me ngā tikanga whakawhiti. Ko ngā ahunga whakamua i mua tata nei i roto i te māramatanga ki ngā tikanga o te vitiligo i ahu mai i te whanaketanga o ngā rongoā kua whakaritea. I tēnei wā, ko ngā aukati JAK te mea tino pai, e tuku ana i te painga o te manawanui me ngā hua mahi, ahakoa te tūpono ki te whakahohe i ngā mate huna me ngā pānga taha nahanaha e pā ana ki ētahi atu o ngā maataki immunosuppressive. Ko te rangahau haere tonu e whai ana ki te tautuhi i ngā cytokine matua e uru ana ki te whanaketanga o te vitiligo (IFN-γ, CXCL10, CXCR3, HSP70i, IL-15, IL-17/23, TNF). Kua whakaatu te aukati i ēnei cytokines te oati i roto i ngā tauira kararehe me ētahi turoro. I tua atu, kei te haere tonu ngā tirotiro mō 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.
Kāore he rongoā mō te vitiligo. Mō te hunga he kiri maramara, ko te whakamarumaru rā me te whakapaipai ko ngā mea katoa e taunaki ana. Ko ētahi atu momo māimoatanga ka uru pea ki te kirīmi pūtaiaki, ki te whakamārama whakaahua rānei.
○ Maimoatanga
#Phototherapy
#Excimer laser
#Tacrolimus ointment