Iain Noel Encarnacion, MS

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

Vitiligo is a common autoimmune disorder characterized by cutaneous depigmentation that has a substantial impact on patient quality of life.¹ Vitiligo affects approximately 28.5 million individuals globally, with the highest lifetime prevalence occurring in Central Europe and South Asia.² In the United States, Asian American and Hispanic/Latine populations most commonly are affected.³ The accompanying psychosocial burdens of vitiligo are particularly substantial among individuals with darker skin types, as evidenced by higher rates of concomitant anxiety and depression in these patients.⁴ Despite this, patients with skin of color are underrepresented in vitiligo research.²

Treatment algorithms developed based on worldwide expert consensus recommendations provide valuable insights into the management of segmental and nonsegmental vitiligo.⁵ The mainstay therapeutics include topical and oral corticosteroids, topical calcineurin inhibitors, and phototherapy. While vitiligo pathogenesis is not completely understood, recent advances have focused on the role of the Janus kinase (JAK)/signal transducer and activator of transcription pathway. Interferon gamma drives vitiligo pathogenesis through this pathway, upregulating C-X-C motif chemokine ligand 10 and promoting CD8+ T-cell recruitment, resulting in targeted melanocyte destruction.⁶ The emergence of targeted therapeutics may address equity and inclusion gaps. Herein, we highlight innovations in vitiligo treatment with a focus on oral and topical JAK inhibitors.

Oral JAK Inhibitors for Vitiligo

The therapeutic potential of JAK inhibitors for vitiligo was first reported when patients with alopecia areata and comorbid vitiligo experienced repigmentation of the skin following administration of oral ruxolitinib.⁷ Since this discovery, other oral JAK inhibitors have been investigated for vitiligo treatment. A phase 2b randomized clinical trial (RCT) of 364 patients examined oral ritlecitinib, a JAK3 inhibitor, and found it to be effective in treating active nonsegmental vitiligo.⁸ Patients aged 18 to 65 years with active nonsegmental vitiligo that had been present for 3 months or more as well as 4% to 50% body surface area (BSA) affected excluding acral surfaces and at least 0.25% facial involvement were included. Treatment groups received 50 mg (with or without a 100- or 200- mg loading dose), 30 mg, or 10 mg daily for 24 weeks. The primary endpoint measured the percentage change in Facial Vitiligo Area Scoring Index (F-VASI) score. Significant differences in F-VASI percentage change compared with placebo occurred for those in the 50-mg group who received a loading dose (-21.2 vs 2.1 [P<.001]) and those who did not receive a loading dose (–18.5 vs 2.1 [P<.001]) as well as the 30-mg group (-14.6 vs 2.1 [P=.01]). Continued repigmentation of the skin was observed in the 24-week extension period, indicating that longer treatment periods may be necessary for optimal repigmentation results. Ritlecitinib generally was well tolerated, and the most common treatment-emergent adverse events were nasopharyngitis (15.9%), upper respiratory tract infection (11.5%), and headache (8.8%). Most patients identified as White (67.6%), with 23.6% identifying as Asian and 2.7% identifying as Black. The authors stated that continued improvement was observed in the extension period across all skin types; however, the data were not reported.⁸

Upadacitnib, an oral selective JAK1 inhibitor, also has demonstrated efficacy in nonsegmental vitiligo in a phase 2 RCT.⁹ Adult patients (N=185) with nonsegmental vitiligo were randomized to receive upadacitinib 6 mg, 11 mg, or 22 mg or placebo (the placebo group subsequently was switched to upadacitinib 11 mg or 22 mg after 24 weeks). The primary endpoint measured the percentage change in F-VASI score at 24 weeks. The higher doses of upadacitinib resulted in significant changes in F-VASI scored compared with placebo (6 mg: -7.60 [95% CI, -22.18 to 6.97][P=.30]; 11 mg: -21.27 [95% CI, -36.02 to -6.52][P=.01]; 22 mg: -19.60 [95% CI, -35.04 to –4.16][P=.01]). As with ritlecitinib, continued repigmentation was observed beyond the initial 24-week period. Of the 185 participants, 5.9% identified as Black and 13.5% identified as Asian. The investigators reported that the percentage change in F-VASI score was consistent across skin types.⁹ The results of these phase 2 RCTs are encouraging, and we anticipate the findings of 2 phase 3 RCTs for ritlecitinib and upadacitinib that currently are underway (Clinicaltrials.gov identifiers NCT05583526 and NCT06118411).

Topical JAK Inhibitors for Vitiligo

Tofacitinib cream 2%, a selective JAK3 inhibitor, has shown therapeutic potential for treatment of vitiligo. One of the earliest pilot studies on topical tofacitinib examined the efficacy of tofacitinib cream 2% applied twice daily combined with narrowband UVB therapy 3 times weekly for facial vitiligo. The investigators reported repigmentation of the skin in all 11 patients (which included 4 Asian patients and 1 Hispanic patient), with a mean improvement of 70% in F-VASI score (range, 50%-87%).¹⁰ In a nonrandomized cohort study of 16 patients later that year, twice-daily application of tofacitinib cream 2% on facial and nonfacial vitiligo lesions resulted in partial repigmentation in 81.3% of patients: 4 (25%) achieved greater than 90% improvement, 5 (31.3%) achieved improvement of 25% to 75%, and 4 (25%) achieved 5% to 15% improvement.¹¹ The researchers also found that tofacitinib cream 2% was significantly more effective in facial than nonfacial lesions (P=.02).

While tofacitinib has shown promise in early studies, recent advancements have led to US Food and Drug Administration approval of ruxolitinib cream 1.5%, another topical JAK inhibitor that has undergone robust clinical testing for vitiligo.^12-14 Ruxolitinib, a JAK1, JAK2, and JAK3 inhibitor, is the first and only US Food and Drug Administration–approved topical JAK inhibitor for vitiligo.^14,15 Two phase 3, double-blind, vehicle-controlled trials of identical design conducted across 101 centers in North America and Europe (TRuE-V1 and TRuE-V2) assessed the efficacy of ruxolitinib cream 1.5% in 674 patients aged 12 years and older with nonsegmental vitiligo covering 10% or lower total BSA.¹³ In both trials, twice-daily application of topical ruxolitinib resulted in greater facial repigmentation and improvement in F-VASI75 score (ie, a reduction of at least 75% from baseline) at 24 weeks in 29.9% (66/221) and 30.1% (69/222) of patients in TRuE-V1 and TRuE-V2, respectively. Continued application through 52 weeks resulted in F-VASI75 response in 52.6% (91/173) and 48.0% (85/177) of patients in TRuE-V1 and TRuE-V2, respectively. The most frequently reported adverse events were acne (6.3% [14/221] and 6.6% [15/228]), nasopharyngitis (5.4% [12/221] and 6.1% [14/228]), and pruritus (5.4% [12/221] and 5.3% [12/228]). These findings align with prior subgroup analyses of an earlier phase 2 double- blind RCT of ruxolitinib cream 1.5% that indicated similar improvement in vitiligo among patients with differing skin tones.¹⁷

There are no additional large-scale RCTs examining topical JAK inhibitors with intentional subanalysis of diverse skin tones.^16,17,18 Studies examining topical JAK inhibitors have expanded to be more inclusive, providing hope for the future of topical vitiligo therapeutics for all patients.

Final Thoughts

It is imperative to increase racial/ethnic and skin type diversity in research on JAK inhibitors for vitiligo. While the studies mentioned here are inclusive of an array of races and skin tones, it is crucial that future research continue to expand the number of diverse participants, especially given the increased psychosocial burdens of vitiligo in patients with darker skin types.⁴ Intentional subgroup analyses across skin tones are vital to characterize and unmask potential differences between lighter and darker skin types. This point was exemplified by a 2024 RCT that investigated ritlecitinib efficacy with biomarker analysis across skin types.¹⁹ For patients receiving ritlecitinib 50 mg, IL-9 and IL-22 expression were decreased in darker vs lighter skin tones (P<.05). This intentional and inclusive analysis revealed a potential immunologic mechanism for why darker skin tones respond to JAK inhibitor therapy earlier than lighter skin tones.¹⁹

In the expanding landscape of oral and topical JAK inhibitors for vitiligo, continued efforts to assess these therapies across a range of skin tones and racial/ ethnic groups are critical. The efficacy of JAK inhibitors in other populations, including pediatric patients and patients with refractory segmental disease, have been reported.^20,21 As larger studies are developed based on the success of individual cases, researchers should investigate the efficacy of JAK inhibitors for various vitiligo subtypes (eg, segmental, nonsegmental) and recalcitrant disease and conduct direct comparisons with traditional treatments across diverse skin tones and racial/ethnic subgroup analyses to ensure broad therapeutic applicability.

Vitiligo is a common autoimmune disorder characterized by cutaneous depigmentation that has a substantial impact on patient quality of life.¹ Vitiligo affects approximately 28.5 million individuals globally, with the highest lifetime prevalence occurring in Central Europe and South Asia.² In the United States, Asian American and Hispanic/Latine populations most commonly are affected.³ The accompanying psychosocial burdens of vitiligo are particularly substantial among individuals with darker skin types, as evidenced by higher rates of concomitant anxiety and depression in these patients.⁴ Despite this, patients with skin of color are underrepresented in vitiligo research.²

Treatment algorithms developed based on worldwide expert consensus recommendations provide valuable insights into the management of segmental and nonsegmental vitiligo.⁵ The mainstay therapeutics include topical and oral corticosteroids, topical calcineurin inhibitors, and phototherapy. While vitiligo pathogenesis is not completely understood, recent advances have focused on the role of the Janus kinase (JAK)/signal transducer and activator of transcription pathway. Interferon gamma drives vitiligo pathogenesis through this pathway, upregulating C-X-C motif chemokine ligand 10 and promoting CD8+ T-cell recruitment, resulting in targeted melanocyte destruction.⁶ The emergence of targeted therapeutics may address equity and inclusion gaps. Herein, we highlight innovations in vitiligo treatment with a focus on oral and topical JAK inhibitors.

Oral JAK Inhibitors for Vitiligo

The therapeutic potential of JAK inhibitors for vitiligo was first reported when patients with alopecia areata and comorbid vitiligo experienced repigmentation of the skin following administration of oral ruxolitinib.⁷ Since this discovery, other oral JAK inhibitors have been investigated for vitiligo treatment. A phase 2b randomized clinical trial (RCT) of 364 patients examined oral ritlecitinib, a JAK3 inhibitor, and found it to be effective in treating active nonsegmental vitiligo.⁸ Patients aged 18 to 65 years with active nonsegmental vitiligo that had been present for 3 months or more as well as 4% to 50% body surface area (BSA) affected excluding acral surfaces and at least 0.25% facial involvement were included. Treatment groups received 50 mg (with or without a 100- or 200- mg loading dose), 30 mg, or 10 mg daily for 24 weeks. The primary endpoint measured the percentage change in Facial Vitiligo Area Scoring Index (F-VASI) score. Significant differences in F-VASI percentage change compared with placebo occurred for those in the 50-mg group who received a loading dose (-21.2 vs 2.1 [P<.001]) and those who did not receive a loading dose (–18.5 vs 2.1 [P<.001]) as well as the 30-mg group (-14.6 vs 2.1 [P=.01]). Continued repigmentation of the skin was observed in the 24-week extension period, indicating that longer treatment periods may be necessary for optimal repigmentation results. Ritlecitinib generally was well tolerated, and the most common treatment-emergent adverse events were nasopharyngitis (15.9%), upper respiratory tract infection (11.5%), and headache (8.8%). Most patients identified as White (67.6%), with 23.6% identifying as Asian and 2.7% identifying as Black. The authors stated that continued improvement was observed in the extension period across all skin types; however, the data were not reported.⁸

Upadacitnib, an oral selective JAK1 inhibitor, also has demonstrated efficacy in nonsegmental vitiligo in a phase 2 RCT.⁹ Adult patients (N=185) with nonsegmental vitiligo were randomized to receive upadacitinib 6 mg, 11 mg, or 22 mg or placebo (the placebo group subsequently was switched to upadacitinib 11 mg or 22 mg after 24 weeks). The primary endpoint measured the percentage change in F-VASI score at 24 weeks. The higher doses of upadacitinib resulted in significant changes in F-VASI scored compared with placebo (6 mg: -7.60 [95% CI, -22.18 to 6.97][P=.30]; 11 mg: -21.27 [95% CI, -36.02 to -6.52][P=.01]; 22 mg: -19.60 [95% CI, -35.04 to –4.16][P=.01]). As with ritlecitinib, continued repigmentation was observed beyond the initial 24-week period. Of the 185 participants, 5.9% identified as Black and 13.5% identified as Asian. The investigators reported that the percentage change in F-VASI score was consistent across skin types.⁹ The results of these phase 2 RCTs are encouraging, and we anticipate the findings of 2 phase 3 RCTs for ritlecitinib and upadacitinib that currently are underway (Clinicaltrials.gov identifiers NCT05583526 and NCT06118411).

Topical JAK Inhibitors for Vitiligo

Tofacitinib cream 2%, a selective JAK3 inhibitor, has shown therapeutic potential for treatment of vitiligo. One of the earliest pilot studies on topical tofacitinib examined the efficacy of tofacitinib cream 2% applied twice daily combined with narrowband UVB therapy 3 times weekly for facial vitiligo. The investigators reported repigmentation of the skin in all 11 patients (which included 4 Asian patients and 1 Hispanic patient), with a mean improvement of 70% in F-VASI score (range, 50%-87%).¹⁰ In a nonrandomized cohort study of 16 patients later that year, twice-daily application of tofacitinib cream 2% on facial and nonfacial vitiligo lesions resulted in partial repigmentation in 81.3% of patients: 4 (25%) achieved greater than 90% improvement, 5 (31.3%) achieved improvement of 25% to 75%, and 4 (25%) achieved 5% to 15% improvement.¹¹ The researchers also found that tofacitinib cream 2% was significantly more effective in facial than nonfacial lesions (P=.02).

While tofacitinib has shown promise in early studies, recent advancements have led to US Food and Drug Administration approval of ruxolitinib cream 1.5%, another topical JAK inhibitor that has undergone robust clinical testing for vitiligo.^12-14 Ruxolitinib, a JAK1, JAK2, and JAK3 inhibitor, is the first and only US Food and Drug Administration–approved topical JAK inhibitor for vitiligo.^14,15 Two phase 3, double-blind, vehicle-controlled trials of identical design conducted across 101 centers in North America and Europe (TRuE-V1 and TRuE-V2) assessed the efficacy of ruxolitinib cream 1.5% in 674 patients aged 12 years and older with nonsegmental vitiligo covering 10% or lower total BSA.¹³ In both trials, twice-daily application of topical ruxolitinib resulted in greater facial repigmentation and improvement in F-VASI75 score (ie, a reduction of at least 75% from baseline) at 24 weeks in 29.9% (66/221) and 30.1% (69/222) of patients in TRuE-V1 and TRuE-V2, respectively. Continued application through 52 weeks resulted in F-VASI75 response in 52.6% (91/173) and 48.0% (85/177) of patients in TRuE-V1 and TRuE-V2, respectively. The most frequently reported adverse events were acne (6.3% [14/221] and 6.6% [15/228]), nasopharyngitis (5.4% [12/221] and 6.1% [14/228]), and pruritus (5.4% [12/221] and 5.3% [12/228]). These findings align with prior subgroup analyses of an earlier phase 2 double- blind RCT of ruxolitinib cream 1.5% that indicated similar improvement in vitiligo among patients with differing skin tones.¹⁷

There are no additional large-scale RCTs examining topical JAK inhibitors with intentional subanalysis of diverse skin tones.^16,17,18 Studies examining topical JAK inhibitors have expanded to be more inclusive, providing hope for the future of topical vitiligo therapeutics for all patients.

Final Thoughts

It is imperative to increase racial/ethnic and skin type diversity in research on JAK inhibitors for vitiligo. While the studies mentioned here are inclusive of an array of races and skin tones, it is crucial that future research continue to expand the number of diverse participants, especially given the increased psychosocial burdens of vitiligo in patients with darker skin types.⁴ Intentional subgroup analyses across skin tones are vital to characterize and unmask potential differences between lighter and darker skin types. This point was exemplified by a 2024 RCT that investigated ritlecitinib efficacy with biomarker analysis across skin types.¹⁹ For patients receiving ritlecitinib 50 mg, IL-9 and IL-22 expression were decreased in darker vs lighter skin tones (P<.05). This intentional and inclusive analysis revealed a potential immunologic mechanism for why darker skin tones respond to JAK inhibitor therapy earlier than lighter skin tones.¹⁹

In the expanding landscape of oral and topical JAK inhibitors for vitiligo, continued efforts to assess these therapies across a range of skin tones and racial/ ethnic groups are critical. The efficacy of JAK inhibitors in other populations, including pediatric patients and patients with refractory segmental disease, have been reported.^20,21 As larger studies are developed based on the success of individual cases, researchers should investigate the efficacy of JAK inhibitors for various vitiligo subtypes (eg, segmental, nonsegmental) and recalcitrant disease and conduct direct comparisons with traditional treatments across diverse skin tones and racial/ethnic subgroup analyses to ensure broad therapeutic applicability.

Vitiligo is a common autoimmune disorder characterized by cutaneous depigmentation that has a substantial impact on patient quality of life.¹ Vitiligo affects approximately 28.5 million individuals globally, with the highest lifetime prevalence occurring in Central Europe and South Asia.² In the United States, Asian American and Hispanic/Latine populations most commonly are affected.³ The accompanying psychosocial burdens of vitiligo are particularly substantial among individuals with darker skin types, as evidenced by higher rates of concomitant anxiety and depression in these patients.⁴ Despite this, patients with skin of color are underrepresented in vitiligo research.²

Treatment algorithms developed based on worldwide expert consensus recommendations provide valuable insights into the management of segmental and nonsegmental vitiligo.⁵ The mainstay therapeutics include topical and oral corticosteroids, topical calcineurin inhibitors, and phototherapy. While vitiligo pathogenesis is not completely understood, recent advances have focused on the role of the Janus kinase (JAK)/signal transducer and activator of transcription pathway. Interferon gamma drives vitiligo pathogenesis through this pathway, upregulating C-X-C motif chemokine ligand 10 and promoting CD8+ T-cell recruitment, resulting in targeted melanocyte destruction.⁶ The emergence of targeted therapeutics may address equity and inclusion gaps. Herein, we highlight innovations in vitiligo treatment with a focus on oral and topical JAK inhibitors.

Oral JAK Inhibitors for Vitiligo

The therapeutic potential of JAK inhibitors for vitiligo was first reported when patients with alopecia areata and comorbid vitiligo experienced repigmentation of the skin following administration of oral ruxolitinib.⁷ Since this discovery, other oral JAK inhibitors have been investigated for vitiligo treatment. A phase 2b randomized clinical trial (RCT) of 364 patients examined oral ritlecitinib, a JAK3 inhibitor, and found it to be effective in treating active nonsegmental vitiligo.⁸ Patients aged 18 to 65 years with active nonsegmental vitiligo that had been present for 3 months or more as well as 4% to 50% body surface area (BSA) affected excluding acral surfaces and at least 0.25% facial involvement were included. Treatment groups received 50 mg (with or without a 100- or 200- mg loading dose), 30 mg, or 10 mg daily for 24 weeks. The primary endpoint measured the percentage change in Facial Vitiligo Area Scoring Index (F-VASI) score. Significant differences in F-VASI percentage change compared with placebo occurred for those in the 50-mg group who received a loading dose (-21.2 vs 2.1 [P<.001]) and those who did not receive a loading dose (–18.5 vs 2.1 [P<.001]) as well as the 30-mg group (-14.6 vs 2.1 [P=.01]). Continued repigmentation of the skin was observed in the 24-week extension period, indicating that longer treatment periods may be necessary for optimal repigmentation results. Ritlecitinib generally was well tolerated, and the most common treatment-emergent adverse events were nasopharyngitis (15.9%), upper respiratory tract infection (11.5%), and headache (8.8%). Most patients identified as White (67.6%), with 23.6% identifying as Asian and 2.7% identifying as Black. The authors stated that continued improvement was observed in the extension period across all skin types; however, the data were not reported.⁸

Upadacitnib, an oral selective JAK1 inhibitor, also has demonstrated efficacy in nonsegmental vitiligo in a phase 2 RCT.⁹ Adult patients (N=185) with nonsegmental vitiligo were randomized to receive upadacitinib 6 mg, 11 mg, or 22 mg or placebo (the placebo group subsequently was switched to upadacitinib 11 mg or 22 mg after 24 weeks). The primary endpoint measured the percentage change in F-VASI score at 24 weeks. The higher doses of upadacitinib resulted in significant changes in F-VASI scored compared with placebo (6 mg: -7.60 [95% CI, -22.18 to 6.97][P=.30]; 11 mg: -21.27 [95% CI, -36.02 to -6.52][P=.01]; 22 mg: -19.60 [95% CI, -35.04 to –4.16][P=.01]). As with ritlecitinib, continued repigmentation was observed beyond the initial 24-week period. Of the 185 participants, 5.9% identified as Black and 13.5% identified as Asian. The investigators reported that the percentage change in F-VASI score was consistent across skin types.⁹ The results of these phase 2 RCTs are encouraging, and we anticipate the findings of 2 phase 3 RCTs for ritlecitinib and upadacitinib that currently are underway (Clinicaltrials.gov identifiers NCT05583526 and NCT06118411).

Topical JAK Inhibitors for Vitiligo

Tofacitinib cream 2%, a selective JAK3 inhibitor, has shown therapeutic potential for treatment of vitiligo. One of the earliest pilot studies on topical tofacitinib examined the efficacy of tofacitinib cream 2% applied twice daily combined with narrowband UVB therapy 3 times weekly for facial vitiligo. The investigators reported repigmentation of the skin in all 11 patients (which included 4 Asian patients and 1 Hispanic patient), with a mean improvement of 70% in F-VASI score (range, 50%-87%).¹⁰ In a nonrandomized cohort study of 16 patients later that year, twice-daily application of tofacitinib cream 2% on facial and nonfacial vitiligo lesions resulted in partial repigmentation in 81.3% of patients: 4 (25%) achieved greater than 90% improvement, 5 (31.3%) achieved improvement of 25% to 75%, and 4 (25%) achieved 5% to 15% improvement.¹¹ The researchers also found that tofacitinib cream 2% was significantly more effective in facial than nonfacial lesions (P=.02).

While tofacitinib has shown promise in early studies, recent advancements have led to US Food and Drug Administration approval of ruxolitinib cream 1.5%, another topical JAK inhibitor that has undergone robust clinical testing for vitiligo.^12-14 Ruxolitinib, a JAK1, JAK2, and JAK3 inhibitor, is the first and only US Food and Drug Administration–approved topical JAK inhibitor for vitiligo.^14,15 Two phase 3, double-blind, vehicle-controlled trials of identical design conducted across 101 centers in North America and Europe (TRuE-V1 and TRuE-V2) assessed the efficacy of ruxolitinib cream 1.5% in 674 patients aged 12 years and older with nonsegmental vitiligo covering 10% or lower total BSA.¹³ In both trials, twice-daily application of topical ruxolitinib resulted in greater facial repigmentation and improvement in F-VASI75 score (ie, a reduction of at least 75% from baseline) at 24 weeks in 29.9% (66/221) and 30.1% (69/222) of patients in TRuE-V1 and TRuE-V2, respectively. Continued application through 52 weeks resulted in F-VASI75 response in 52.6% (91/173) and 48.0% (85/177) of patients in TRuE-V1 and TRuE-V2, respectively. The most frequently reported adverse events were acne (6.3% [14/221] and 6.6% [15/228]), nasopharyngitis (5.4% [12/221] and 6.1% [14/228]), and pruritus (5.4% [12/221] and 5.3% [12/228]). These findings align with prior subgroup analyses of an earlier phase 2 double- blind RCT of ruxolitinib cream 1.5% that indicated similar improvement in vitiligo among patients with differing skin tones.¹⁷

There are no additional large-scale RCTs examining topical JAK inhibitors with intentional subanalysis of diverse skin tones.^16,17,18 Studies examining topical JAK inhibitors have expanded to be more inclusive, providing hope for the future of topical vitiligo therapeutics for all patients.

Final Thoughts

It is imperative to increase racial/ethnic and skin type diversity in research on JAK inhibitors for vitiligo. While the studies mentioned here are inclusive of an array of races and skin tones, it is crucial that future research continue to expand the number of diverse participants, especially given the increased psychosocial burdens of vitiligo in patients with darker skin types.⁴ Intentional subgroup analyses across skin tones are vital to characterize and unmask potential differences between lighter and darker skin types. This point was exemplified by a 2024 RCT that investigated ritlecitinib efficacy with biomarker analysis across skin types.¹⁹ For patients receiving ritlecitinib 50 mg, IL-9 and IL-22 expression were decreased in darker vs lighter skin tones (P<.05). This intentional and inclusive analysis revealed a potential immunologic mechanism for why darker skin tones respond to JAK inhibitor therapy earlier than lighter skin tones.¹⁹

In the expanding landscape of oral and topical JAK inhibitors for vitiligo, continued efforts to assess these therapies across a range of skin tones and racial/ ethnic groups are critical. The efficacy of JAK inhibitors in other populations, including pediatric patients and patients with refractory segmental disease, have been reported.^20,21 As larger studies are developed based on the success of individual cases, researchers should investigate the efficacy of JAK inhibitors for various vitiligo subtypes (eg, segmental, nonsegmental) and recalcitrant disease and conduct direct comparisons with traditional treatments across diverse skin tones and racial/ethnic subgroup analyses to ensure broad therapeutic applicability.