The body develops white macules and patches due to the acquired pigmentary skin disorder known as vitiligo, which is caused by the absence of pigment-producing cells in the epidermis. Thyroid problems are the most frequent autoimmune illness connected with the syndrome. There are numerous theories to explain the pathogenesis of vitiligo, despite the fact that its etiology is unknown.
Clinically, vitiligo manifests as symmetrically distributed white spots on the body, which are more noticeable in those with a dark complexion. Well-defined pearly white and depigmented macules and patches that are oval, circular, or linear in shape with convex borders that can vary in size from a few millimeters - centimeters and expand centrifugally are the hallmarks of the lesions.
Vitiligo comes in a variety of clinical forms, including Marginal Inflammatory, Trichrome & Quadrichrome. Another typical clinical symptom is the Koebner phenomenon, which is the emergence of vitiligo in particular trauma-prone areas, such as cuts, burns, and abrasions. Early lesions tend to favor a periocular and perioral spread, occurring most commonly on the feet, hands, forearms, & face.
The most frequent reason for depigmentation is vitiligo. Although it can manifest at any age, from childhood to maturity, the second & third decades are reported to have the highest occurrence.
The onset age often varies by gender. It affects all races equally and has a prevalence of 0.1% – 2% among all persons, including adults and children, globally.
The multifactorial polygenic condition that is vitiligo has complicated pathophysiology. It is frequently linked to both hereditary and non-genetic variables. However, a number of hypotheses regarding its pathogenesis have been put forth, but the precise etiology is still unclear. The melanocytes in the vitiligo dermis are absent, and their loss is caused by their destruction, according to commonly accepted concepts. Persistent melanocyte reductions are the most common effect of the destruction.
Cytotoxic processes, autoimmune processes, structural melanocyte abnormalities, neurological processes, & oxidant-antioxidant processes are some of the theories regarding melanocyte death. According to neural theory, neurochemical mediation often kills the melanocytes and reduces melanin production. Melanocytes are destroyed by oxidative & antioxidative processes as an intermediate and metabolic result of melanin production.
The proliferation & differentiation of melanocytes is hampered by an inherited defect that is part of their intrinsic abnormality. Another theory is that melanocytes are destroyed or become dysfunctional due to an autoimmune and cytotoxic immune response that alters cellular and humoral immunity. According to this view, nonsegmental vitiligo is more frequently linked to autoimmune diseases than the segmental variety.
It is unclear what causes vitiligo specifically. It frequently occurs in conjunction with certain autoimmune disorders. Its pathophysiology is the subject of numerous theories, and its etiology is complex. Multiple susceptibility loci, genetic variability, and imperfect penetrance are its defining traits.
Studies on families and twins have demonstrated that inheritance is complicated and involves both genetic and environmental influences. The age at which vitiligo first appears may also be influenced by genetics, according to another theory.
Genes involved with the control of autoantibodies, melanin production, and oxidative stress response may also be passed down through the vitiligo family. Recent studies have not found any correlations to any particular HLA subtype. Segmental & nonsegmental vitiligo are thought to have different genetic pathways, which could explain the different treatment outcomes.
It is a long-term skin illness with an erratic course of the disease, and some individuals may have sudden repigmentation over the areas that have lost color. The prognosis is based on the disease’s severity and age of occurrence. Early illness start is typically linked to faster disease progression and involvement of a larger area of the body.
Only a few types and a few sites might respond to treatment. Patients under 14 years old who present with segmental vitiligo have been observed to have cases that are resistant to treatment. The majority of individuals receiving treatment typically go through sporadic cycles of pigment decline & condition stabilization.
Vitiligo is treated with a variety of systemic and topical medicines, laser treatment, phototherapy & surgical treatment. The use of calcineurin inhibitors, corticosteroids, & Vit-D analogs is all examples of topical therapy techniques. One option for treatment is phototherapy. In most individuals with early-stage and localized illness, it causes repigmentation. Narrowband UV-B is frequently utilized, typically twice or three times a week, with a wavelength of 311-312nm.
Due to the harmful side effects of psoralen photochemotherapy, it has mainly supplanted it. Vitiligo is treated with the excimer laser in small, stable spots. Tacrolimus & systemic corticosteroids can be paired with one another to treat segmental hyperpigmentation, which is refractory to the majority of therapies. Emerging therapies include JAK inhibitor therapy and afamelanotide. Ruxolitinib used topically was also proven to be quite efficient (in 2019, placebo-controlled, double-blind, randomized, prospective trial).
Only segmental and localized vitiligo that affects a small region can be treated surgically. Non-cultured epidermis suspensions, suction epidermal grafts, punch grafting, thin dermo-epidermal implants & cultured epidermal with melanocytes are the five fundamental techniques for repigmentation.
The patients listed below make excellent candidates for surgery:
Localize vitiligo in a small region
Segmental vitiligo
The condition needs to be steady
Areas with vitiligo that typically do not re-pigment well (dorsal fingers, forehead, hairline, ankles)
Apply a thin application to affected regions of up to 10% body surface area twice a day; do not exceed >60 g/week or one 100-gram tube/2 weeks
A satisfactory patient response may necessitate therapy for more than 24 weeks
The patient should be re-evaluated if no significant repigmentation is noticed after 24 weeks
orally
20 mg with food or milk two-four hours before exposure to UV
UV exposure: initially 15-25 minutes (based on the skin color); later, add 5 minutes on each subsequent exposure (every other day) till tenderness tolerance or erythema Topical
To affected area, apply 1% lotion 2 hours before the UV exposure every 3-7 days
Indicated for topical treatment of nonsegmental vitiligo:
<12 years: Safety and efficacy not established
≥12 years: Apply a thin coating, up to 10% of the body's surface area, twice daily; do not use more than 60 g per week or one 100-gram tube every two weeks
Therapy may go longer than 24 weeks, depending on the patient's reaction
At 24 weeks, reassess the patient if there has been no appreciable repigmentation
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https://www.ncbi.nlm.nih.gov/books/NBK559149/
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The body develops white macules and patches due to the acquired pigmentary skin disorder known as vitiligo, which is caused by the absence of pigment-producing cells in the epidermis. Thyroid problems are the most frequent autoimmune illness connected with the syndrome. There are numerous theories to explain the pathogenesis of vitiligo, despite the fact that its etiology is unknown.
Clinically, vitiligo manifests as symmetrically distributed white spots on the body, which are more noticeable in those with a dark complexion. Well-defined pearly white and depigmented macules and patches that are oval, circular, or linear in shape with convex borders that can vary in size from a few millimeters - centimeters and expand centrifugally are the hallmarks of the lesions.
Vitiligo comes in a variety of clinical forms, including Marginal Inflammatory, Trichrome & Quadrichrome. Another typical clinical symptom is the Koebner phenomenon, which is the emergence of vitiligo in particular trauma-prone areas, such as cuts, burns, and abrasions. Early lesions tend to favor a periocular and perioral spread, occurring most commonly on the feet, hands, forearms, & face.
The most frequent reason for depigmentation is vitiligo. Although it can manifest at any age, from childhood to maturity, the second & third decades are reported to have the highest occurrence.
The onset age often varies by gender. It affects all races equally and has a prevalence of 0.1% – 2% among all persons, including adults and children, globally.
The multifactorial polygenic condition that is vitiligo has complicated pathophysiology. It is frequently linked to both hereditary and non-genetic variables. However, a number of hypotheses regarding its pathogenesis have been put forth, but the precise etiology is still unclear. The melanocytes in the vitiligo dermis are absent, and their loss is caused by their destruction, according to commonly accepted concepts. Persistent melanocyte reductions are the most common effect of the destruction.
Cytotoxic processes, autoimmune processes, structural melanocyte abnormalities, neurological processes, & oxidant-antioxidant processes are some of the theories regarding melanocyte death. According to neural theory, neurochemical mediation often kills the melanocytes and reduces melanin production. Melanocytes are destroyed by oxidative & antioxidative processes as an intermediate and metabolic result of melanin production.
The proliferation & differentiation of melanocytes is hampered by an inherited defect that is part of their intrinsic abnormality. Another theory is that melanocytes are destroyed or become dysfunctional due to an autoimmune and cytotoxic immune response that alters cellular and humoral immunity. According to this view, nonsegmental vitiligo is more frequently linked to autoimmune diseases than the segmental variety.
It is unclear what causes vitiligo specifically. It frequently occurs in conjunction with certain autoimmune disorders. Its pathophysiology is the subject of numerous theories, and its etiology is complex. Multiple susceptibility loci, genetic variability, and imperfect penetrance are its defining traits.
Studies on families and twins have demonstrated that inheritance is complicated and involves both genetic and environmental influences. The age at which vitiligo first appears may also be influenced by genetics, according to another theory.
Genes involved with the control of autoantibodies, melanin production, and oxidative stress response may also be passed down through the vitiligo family. Recent studies have not found any correlations to any particular HLA subtype. Segmental & nonsegmental vitiligo are thought to have different genetic pathways, which could explain the different treatment outcomes.
It is a long-term skin illness with an erratic course of the disease, and some individuals may have sudden repigmentation over the areas that have lost color. The prognosis is based on the disease’s severity and age of occurrence. Early illness start is typically linked to faster disease progression and involvement of a larger area of the body.
Only a few types and a few sites might respond to treatment. Patients under 14 years old who present with segmental vitiligo have been observed to have cases that are resistant to treatment. The majority of individuals receiving treatment typically go through sporadic cycles of pigment decline & condition stabilization.
Vitiligo is treated with a variety of systemic and topical medicines, laser treatment, phototherapy & surgical treatment. The use of calcineurin inhibitors, corticosteroids, & Vit-D analogs is all examples of topical therapy techniques. One option for treatment is phototherapy. In most individuals with early-stage and localized illness, it causes repigmentation. Narrowband UV-B is frequently utilized, typically twice or three times a week, with a wavelength of 311-312nm.
Due to the harmful side effects of psoralen photochemotherapy, it has mainly supplanted it. Vitiligo is treated with the excimer laser in small, stable spots. Tacrolimus & systemic corticosteroids can be paired with one another to treat segmental hyperpigmentation, which is refractory to the majority of therapies. Emerging therapies include JAK inhibitor therapy and afamelanotide. Ruxolitinib used topically was also proven to be quite efficient (in 2019, placebo-controlled, double-blind, randomized, prospective trial).
Only segmental and localized vitiligo that affects a small region can be treated surgically. Non-cultured epidermis suspensions, suction epidermal grafts, punch grafting, thin dermo-epidermal implants & cultured epidermal with melanocytes are the five fundamental techniques for repigmentation.
The patients listed below make excellent candidates for surgery:
Localize vitiligo in a small region
Segmental vitiligo
The condition needs to be steady
Areas with vitiligo that typically do not re-pigment well (dorsal fingers, forehead, hairline, ankles)
Apply a thin application to affected regions of up to 10% body surface area twice a day; do not exceed >60 g/week or one 100-gram tube/2 weeks
A satisfactory patient response may necessitate therapy for more than 24 weeks
The patient should be re-evaluated if no significant repigmentation is noticed after 24 weeks
orally
20 mg with food or milk two-four hours before exposure to UV
UV exposure: initially 15-25 minutes (based on the skin color); later, add 5 minutes on each subsequent exposure (every other day) till tenderness tolerance or erythema Topical
To affected area, apply 1% lotion 2 hours before the UV exposure every 3-7 days
Indicated for topical treatment of nonsegmental vitiligo:
<12 years: Safety and efficacy not established
≥12 years: Apply a thin coating, up to 10% of the body's surface area, twice daily; do not use more than 60 g per week or one 100-gram tube every two weeks
Therapy may go longer than 24 weeks, depending on the patient's reaction
At 24 weeks, reassess the patient if there has been no appreciable repigmentation
https://www.ncbi.nlm.nih.gov/books/NBK559149/
medtigo
Vitiligo
Updated :
December 24, 2022
The body develops white macules and patches due to the acquired pigmentary skin disorder known as vitiligo, which is caused by the absence of pigment-producing cells in the epidermis. Thyroid problems are the most frequent autoimmune illness connected with the syndrome. There are numerous theories to explain the pathogenesis of vitiligo, despite the fact that its etiology is unknown.
Clinically, vitiligo manifests as symmetrically distributed white spots on the body, which are more noticeable in those with a dark complexion. Well-defined pearly white and depigmented macules and patches that are oval, circular, or linear in shape with convex borders that can vary in size from a few millimeters - centimeters and expand centrifugally are the hallmarks of the lesions.
Vitiligo comes in a variety of clinical forms, including Marginal Inflammatory, Trichrome & Quadrichrome. Another typical clinical symptom is the Koebner phenomenon, which is the emergence of vitiligo in particular trauma-prone areas, such as cuts, burns, and abrasions. Early lesions tend to favor a periocular and perioral spread, occurring most commonly on the feet, hands, forearms, & face.
The most frequent reason for depigmentation is vitiligo. Although it can manifest at any age, from childhood to maturity, the second & third decades are reported to have the highest occurrence.
The onset age often varies by gender. It affects all races equally and has a prevalence of 0.1% – 2% among all persons, including adults and children, globally.
The multifactorial polygenic condition that is vitiligo has complicated pathophysiology. It is frequently linked to both hereditary and non-genetic variables. However, a number of hypotheses regarding its pathogenesis have been put forth, but the precise etiology is still unclear. The melanocytes in the vitiligo dermis are absent, and their loss is caused by their destruction, according to commonly accepted concepts. Persistent melanocyte reductions are the most common effect of the destruction.
Cytotoxic processes, autoimmune processes, structural melanocyte abnormalities, neurological processes, & oxidant-antioxidant processes are some of the theories regarding melanocyte death. According to neural theory, neurochemical mediation often kills the melanocytes and reduces melanin production. Melanocytes are destroyed by oxidative & antioxidative processes as an intermediate and metabolic result of melanin production.
The proliferation & differentiation of melanocytes is hampered by an inherited defect that is part of their intrinsic abnormality. Another theory is that melanocytes are destroyed or become dysfunctional due to an autoimmune and cytotoxic immune response that alters cellular and humoral immunity. According to this view, nonsegmental vitiligo is more frequently linked to autoimmune diseases than the segmental variety.
It is unclear what causes vitiligo specifically. It frequently occurs in conjunction with certain autoimmune disorders. Its pathophysiology is the subject of numerous theories, and its etiology is complex. Multiple susceptibility loci, genetic variability, and imperfect penetrance are its defining traits.
Studies on families and twins have demonstrated that inheritance is complicated and involves both genetic and environmental influences. The age at which vitiligo first appears may also be influenced by genetics, according to another theory.
Genes involved with the control of autoantibodies, melanin production, and oxidative stress response may also be passed down through the vitiligo family. Recent studies have not found any correlations to any particular HLA subtype. Segmental & nonsegmental vitiligo are thought to have different genetic pathways, which could explain the different treatment outcomes.
It is a long-term skin illness with an erratic course of the disease, and some individuals may have sudden repigmentation over the areas that have lost color. The prognosis is based on the disease’s severity and age of occurrence. Early illness start is typically linked to faster disease progression and involvement of a larger area of the body.
Only a few types and a few sites might respond to treatment. Patients under 14 years old who present with segmental vitiligo have been observed to have cases that are resistant to treatment. The majority of individuals receiving treatment typically go through sporadic cycles of pigment decline & condition stabilization.
Vitiligo is treated with a variety of systemic and topical medicines, laser treatment, phototherapy & surgical treatment. The use of calcineurin inhibitors, corticosteroids, & Vit-D analogs is all examples of topical therapy techniques. One option for treatment is phototherapy. In most individuals with early-stage and localized illness, it causes repigmentation. Narrowband UV-B is frequently utilized, typically twice or three times a week, with a wavelength of 311-312nm.
Due to the harmful side effects of psoralen photochemotherapy, it has mainly supplanted it. Vitiligo is treated with the excimer laser in small, stable spots. Tacrolimus & systemic corticosteroids can be paired with one another to treat segmental hyperpigmentation, which is refractory to the majority of therapies. Emerging therapies include JAK inhibitor therapy and afamelanotide. Ruxolitinib used topically was also proven to be quite efficient (in 2019, placebo-controlled, double-blind, randomized, prospective trial).
Only segmental and localized vitiligo that affects a small region can be treated surgically. Non-cultured epidermis suspensions, suction epidermal grafts, punch grafting, thin dermo-epidermal implants & cultured epidermal with melanocytes are the five fundamental techniques for repigmentation.
The patients listed below make excellent candidates for surgery:
Localize vitiligo in a small region
Segmental vitiligo
The condition needs to be steady
Areas with vitiligo that typically do not re-pigment well (dorsal fingers, forehead, hairline, ankles)
https://www.ncbi.nlm.nih.gov/books/NBK559149/
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