Monthly Archives

July 2026

Psoriasis and Psoriatic Arthritis in Patients With Skin of Color: Diagnostic Insights and Advancements in Treatment

By Sessions

psoriasis in skin of color

At the 2025 Skin of Color Update conference, Mona Shahriari, MD, FAAD, gave a presentation on evaluating and managing psoriasis and psoriatic arthritis (PsA) in patients with skin of color. Through epidemiologic data, clinical pearls, and real-world insights, she underscored the need for a broader diagnostic lens and more equitable treatment strategies.

Epidemiology and Disparities in Psoriasis and Psoriatic Arthritis

Psoriasis affects approximately 3% of the U.S. population (about 7.5 million people), but prevalence and presentation differ by race and ethnicity. Rates are highest among White individuals (3.6%), followed by Asian (2.5%), Hispanic (1.9%) and Black patients (1.5%). Interestingly, while psoriatic arthritis occurs twice as often in Caucasians, Black patients tend to experience greater disease severity.

These statistics, however, only tell part of the story. Dr. Shahriari emphasized that geographic and socioeconomic barriers exacerbate disparities. Many patients of color may struggle to access dermatologic care due to transportation and economic barriers and lack of nearby specialists, often leading them to seek help in urgent care or emergency room settings where access to specialty dermatologic care is limited. Compounding this issue, gaps in healthcare provider education can delay or obscure diagnoses, while a lack of culturally competent care can further postpone timely and effective therapy.

Beyond physical symptoms, the psychosocial toll of psoriasis is greater in skin of color populations. Studies show greater levels of self-consciousness, frustration, helplessness, and anger, even when controlling for disease severity (e.g., similar PASI scores). In addition, patients with PsA and skin of color are more likely to have severe plaque psoriasis and radiographic axial disease.

Diagnostic Challenges in Skin of Color: Rethinking “Red”

One of the biggest hurdles in psoriasis diagnosis among patients with skin of color is recognizing erythema. Dr. Shahriari encouraged the audience to “broaden our color palette.” In darker skin tones, erythema can appear violet, dark brown, or gray rather than bright red. Scale may be less apparent, and induration can be masked by background pigmentation.

Polarized dermoscopy can be a valuable tool, allowing better visualization of subtle erythema and differentiating active inflammation from post-inflammatory hyperpigmentation (PIH).

Scalp and Nail Psoriasis in Skin of Color

Scalp and nail involvement are particularly challenging for patients with skin of color. Scalp psoriasis is more common and more severe in Asian and Black patients, but is often underdiagnosed (or misdiagnosed) and undertreated, especially with systemic therapies. For example, in many patients with tightly coiled or afro-textured hair, haircare and washing/styling practices may limit the use of some topical formulations and daily medicated shampoos. The diagnosis of nail psoriasis in skin of color can be delayed owing to longitudinal melanonychia and darker nail beds obscuring classic features of nail psoriasis. As such, nail disease can be more severe at diagnosis. Beyond the skin, those with scalp psoriasis are at a 3- to 4-fold higher risk of PsA, and nail psoriasis is an independent risk factor for PsA, which is why timely diagnosis and intervention is critical.

Diagnosing Psoriatic Arthritis in Skin of Color

Diagnosing PsA is inherently complex, and even more so in patients with skin of color. Over 80% of PsA presents with skin as the first sign of their joint disease with only 10-15% of patients having joint pain before the psoriasis develops. However, due to challenges in diagnosing psoriasis in skin of color, it is not surprising that PsA goes undiagnosed or misdiagnosed as another inflammatory arthritis in those with skin of color.

Furthermore, lower health literacy and limited disease awareness in our skin of color communities, and the absence of uniform diagnostic or biomarker criteria contribute to diagnostic delay. Early identification through thorough history (including review of systems and a modified PEST questionnaire) and physical exam (joint palpation) remains essential.

Delays in Systemic Therapy in Skin of Color

Even when diagnosed, patients with skin of color are less likely to receive systemic or biologic therapy. Studies show Black patients are less frequently prescribed biologics or cyclosporine and are less likely to receive disease-modifying anti-rheumatologic therapies for newly diagnosed PsA.

Dr. Shahriari highlighted some reasons for this, including underestimation of disease severity, limited access to dermatologic care, and lower disease awareness. Another significant contributor is the underrepresentation of skin of color patients in dermatology clinical trials, in particular for psoriasis and PsA.  Encouragingly, emerging data from post-hoc analyses of approved treatments (e.g., etanercept, brodalumab, risankizumab) and the first large-scale prospective study, the VISIBLE trial, assessing the safety and efficacy of guselkumab across diverse skin tones (discussed below) are beginning to bridge this gap.

The VISIBLE Study

The VISIBLE trial aimed to study the safety and efficacy of guselkumab as well as evaluate psoriasis and treatment outcomes in skin of color patients across all skin tones using a combination of objective and patient reported parameters. This study was highly inclusive and included any patient that identified as non-white. As a result, it enrolled a racially and ethnically diverse cohort, encompassing the full spectrum of Fitzpatrick skin types (including Central American, Cuban, and Middle Eastern participants). This underscores the importance of inclusive trial designs that go beyond the basic definitions of certain racial/ethnic groups or Fitzpatrick skin types in a “skin of color” cohort. It also highlighted the power of polarized imaging to help differentiate erythema from hyperpigmentation to appropriately assess disease activity and severity, which ultimately guides treatment decisions. Comorbidities such as hypertension and diabetes were common in this cohort but found to be undiagnosed or poorly controlled in a majority of patients, underscoring the importance of comprehensive care and involvement of primary care for optimal management of psoriatic comorbidities.

In this study, clinically meaningful improvement (PASI 90) was achieved by 75% of patients at 1 year. There was complete scalp clearance in 60% of patients by week 48. PsA was present in 30% of the study patients, with most of these patients being diagnosed during the study itself. Clinically meaningful improvements in joint symptoms and quality of life were seen in about 60% of patients.

Interestingly, pigmentary alteration had a greater impact on quality of life than disease activity (measured by PASI score) in patients with skin of color. Dr. Shahriari emphasized the importance of acknowledging this and counseling patients about post-inflammatory pigment changes, and setting the expectation that this can take months to years to improve despite adequate control of psoriasis and/or PsA. Treatments for this include topical skin lightening agents, chemical peels, and having a low threshold to consider systemic therapy. Prevention is almost always easier than treatment.

Real-World Case

Dr. Shahriari shared the case of a 29-year-old Hispanic man with psoriasis involving 20% body surface area who was previously diagnosed with eczema and tinea. He presented with severe plaque psoriasis, joint pain and dactylitis, and required a cane to walk. After initiating biologic therapy, he achieved significant improvement (PASI90) at 16 weeks and no longer needed his cane after 6 months. His quality of life improved dramatically, and he was able to return to full-time work and lose 40 lbs. in weight. He did experience persistent dyspigmentation and still considered this bothersome: a reminder that PIH, while not captured in PASI scores, significantly impacts patients with skin of color.

Summary and Clinical Pearls

  • Broaden your color palette: Erythema may appear violet, gray, or brown.
  • Assess severity accurately: PIH and scarring can mask activity.
  • Do not undertreat: Topical, oral, biologic, and phototherapy options exist for all skin types.
  • Psoriasis and PsA have many faces and are often underdiagnosed in patients with skin of color.
  • Avoid undertreatment, with a lower threshold for systemic therapy in patients with severe disease or joint symptoms.
  • Skin of color patients are particularly bothered by post-inflammatory pigment alterations. Set realistic expectations about this, initiate early treatment, and consider therapies directly aimed at this.
  • Understanding population-specific practices (e.g., hair care), and treatment preferences and barriers is part of providing culturally competent dermatologic care in patients with skin of color.

This information was presented at the 2025 Skin of Color Update conference by Mona Shahriari, MD, FAAD.  The above highlights from this lecture were written and compiled by Riyad N.H. Seervai, MD, PhD.

Forgotten Conditions in Skin of Color: Dissecting Cellulitis, Acne Keloidalis Nuchae, and More

By Sessions

acne keloidalis nuchae

At the 2025 Skin of Color Update, Prince Adotama, MD, FAAD, started his lecture with a discussion on acne keloidalis nuchae (AKN), a chronic inflammatory condition that leads to fibrotic papules, plaques and potentially keloidal nodules and plaques. This occurs most commonly in African Americans with a reported prevalence up to 13.6%. The pathogenesis of AKN is poorly understood but is thought to be initiated by a mechanically induced folliculitis that becomes extensive enough to result in scar formation. Similarly to pseudofolliculitis barbae (PFB), trauma and mechanical irritation could lead to a primary cicatricial alopecia.

Dr. Adotama also highlighted the role of metabolic syndrome in patients with AKN, citing multiple studies demonstrating a strong association between AKN and metabolic syndrome. It is important that physicians are aware of this possible comorbidity, and similar studies have shown increased risk of hypertension and hypothyroidism in patients with AKN.

Treatment for AKN includes topical and/or oral antimicrobials/antibiotics, as well as topical retinoids, topical steroids, and steroid injections. Laser hair removal (LHR) using diode and Nd:YAG and Alexandrite lasers can be helpful in the early papular stages. Surgical excision is recommended for keloidal plaques that are greater than 3 cm.

Additionally, unlike PFB, patients with AKN can utilize higher potency topical steroids. Dr. Adotama discussed that two weeks on and two weeks off for 8 weeks of topical clobetasol can be used, followed by betamethasone valerate for 4 weeks. This regimen did not yield any side effects of skin atrophy and showed a significant decrease in symptoms at 12 weeks. For patients that can tolerate intralesional steroids, using a strength as high as 40 mg/mL can be used in some cases if there is a keloidal component.

Dr. Adotama focused on an improved injection technique for AKN, where the clinician takes 5-10 mg/mL of triamcinolone and injects 0.1 mL aliquots into the deep dermis in 1 cm intervals until the entire area of involvement is completely treated (in contrast to injecting each individual lesion). This technique was published in the Journal of Dermatologic Surgery in July 2023, where Dr. Adotama presented a case of a 24-year-old man with Fitzpatrick skin type VI who had a six-year history of AKN. The patient had no prior treatments and after one round of deep dermal injections with triamcinolone 5 mg/mL (total volume of 1.4 mL) with topical clindamycin, the patient demonstrated significant improvement.

Dr. Adotama also reviewed the use of topical diclofenac sodium gel in the treatment of both AKN and dissecting cellulitis of the scalp (DCS). Although the mechanism of diclofenac sodium gel for either of these conditions is not fully described, the authors hypothesized that the diclofenac-related effects might result in an overall decrease in the neutrophilic and mixed-lymphocytic infiltrate in hair follicles of patients with DCS and AKN. Four patients were followed (3 with DCS and 1 with AKN) in this study. All 3 patients with DCS showed substantial improvement with diclofenac gel monotherapy, with most lesions resolving within a 3-month treatment period. A similar response was observed in the patient with AKN after 1-month of therapy.

For patients with a papular component, use of the long-pulsed Nd:YAG laser in conjunction with topical steroids has shown promising results in the treatment of AKN. Dr. Adotama highlighted a decrease in global assessment score on the treated side as compared to the control side, which although not statistically significant, did show clinical improvement. In a sub analysis that excluded patients with nodules and plaques, there was a statistically significant change between the treatment and control side, highlighting the importance of early treatment at the papular stage.

In patients who have more extensive disease, AKN lesions can be removed via a horizontal ellipse that includes the posterior hairline. Dr. Adotama highlighted the importance of this technique, as two of the six patients had a nonelliptic excision of the posterior aspect of the scalp that spared the posterior hairline and resulted in an inferior cosmetic outcome. A review from 2025 of surgical complications from AKN removal highlighted the low rate of complications, with an approximate 19% incidence of AKN recurrence after excision, an 11% incidence of hypertrophic scarring, and 3% incidence of infection.

Overall, Dr. Adotama provided three main topical treatment recommendations for patients with AKN:

  1. Retinoid: Vary strength depending on skin sensitivity and hyperpigmentation
  2. Steroid: Choose a mid-high potency
  3. Antimicrobial or antibiotic: Typically, benzoyl peroxide or clindamycin combination, although patients may require an oral antibiotic

In addition to topical treatments, injections are often necessary and Dr. Adotama recommended using the deep dermis technique with 5-10 mg/mL concentration for the papular variant.

Dissecting Cellulitis (DCS)

DCS is a neutrophilic alopecia with IL-1 playing an important role. Hidradenitis suppurativa (HS) is a comorbidity given its shared pathway, and one study found that more than half of patients with DCS presented with comorbidities related to follicular occlusion tetrad, with HS being the most frequent. Dr. Adotama also highlighted his study on long-term cardiovascular morbidity in DCS and found that DCS is associated with elevated risk of thrombotic and ischemic events similar to those reported in HS and moderate-to-severe psoriasis.

DCS most commonly presents in the second to third decade of life in African American men. It progresses through stages with the first stage marked by isolated nodules/abscesses and separated by normal skin without intercommunicating sinus tracts or scarring alopecia. As the disease progresses from stage II to III, it begins to demonstrate nodules and abscesses with intercommunicating sinus tracts, with the hallmark of stage III being scarring or permanent alopecia.

Treatment Options for Dissecting Cellulitis

Isotretinoin can be considered in refractory cases to topical therapy. Second-line therapy includes biologics, with TNF-alpha inhibitors having the highest efficacy (87% of patients demonstrated a sustained improvement). Additionally, dapsone can be used for stage II or III disease with or without isotretinoin. Surgery is also an option for patients and can be curative with 95% of patients in one study demonstrating sustained improvement.

Dr. Adotama discussed updated cases of patients who were trialed on a variety of biologics with improvement in DCS. One patient, a 26-year-old male with DCS, experienced significant clinical improvement following a short course of upadacitinib. The patient had tried and failed multiple other treatment modalities, however, following the initiation of upadacitinib, the patient had reduced pain and significant improvement in his quality of life. Apremilast was also utilized in a patient who had been recalcitrant to topical and systemic therapy (including isotretinoin, minocycline, Bactrim, and adalimumab). After 6 months of 30 mg twice-daily apremilast, the patient reported dramatic improvement in disease symptoms and reduction in flares with no notable side effects.

Dr. Adotama concluded his presentation with information on the Scarring Alopecia Foundation, a nonprofit organization dedicated to raising awareness, supporting research, and providing education about cicatricial (scarring) alopecias. Its mission includes offering resources to patients, connecting them with specialists, and funding scientific studies aimed at understanding and treating scarring hair loss disorders.

References:

Adotama, P., Grullon, K., Ali, S., & Okoye, G. A. (2023). How we do it: our method for triamcinolone injections of acne keloidalis nuchae. Dermatologic Surgery, 49(7), 713-714.

Alexis, A., Heath, C. R., & Halder, R. M. (2014). Folliculitis keloidalis nuchae and pseudofolliculitis barbae: are prevention and effective treatment within reach?. Dermatologic clinics, 32(2), 183-191.

Badaoui, A., Reygagne, P., Cavelier‐Balloy, B., Pinquier, L., Deschamps, L., Crickx, B., & Descamps, V. (2016). Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. British Journal of Dermatology, 174(2), 421-423.

Bernard, J. W., Reddy, S., & Flowers, R. H. (2023). The successful use of oral apremilast for a case of dissecting cellulitis. JAAD Case Reports, 39, 122-124.

Callender, V. D., Young, C. M., Haverstock, C. L., Carroll, C. L., & Feldman, S. R. (2005). An open label study of clobetasol propionate 0.05% and betamethasone valerate 0.12% foams in the treatment of mild to moderate acne keloidalis. Cutis, 75(6), 317-321.

Gamissans, M., Romaní, J., López‐Llunell, C., Riera‐Martí, N., & Sin, M. (2022). Dissecting cellulitis of the scalp: A review on clinical characteristics and management options in a series of 14 patients. Dermatologic Therapy, 35(8).

Hinson, C., Sink, M., Odobescu, A., Sammer, D. M., & Zhang, A. Y. (2025). Surgical management of acne keloidalis nuchae: A systematic review of outcomes and techniques. Journal of Plastic, Reconstructive & Aesthetic Surgery, 104, 102-112.

Islam, Z., Toker, M., Gandhi, I. M., Sher, A., Campton, K., & Gandhi, I. (2024). Improvement of recalcitrant dissecting cellulitis of the scalp after a trial of upadacitinib. Cureus, 16(1).

Kridin, K., Solomon, A., Tzur-Bitan, D., Damiani, G., Comaneshter, D., & Cohen, A. D. (2020). Acne keloidalis nuchae and the metabolic syndrome: a population-based study. American Journal of Clinical Dermatology, 21(5), 733-739.

Lee, C. N., Chen, W., Hsu, C. K., Weng, T. T., Lee, J. Y. Y., & Yang, C. C. (2018). Dissecting folliculitis (dissecting cellulitis) of the scalp: a 66‐patient case series and proposal of classification. JDDG: Journal der Deutschen Dermatologischen Gesellschaft, 16(10), 1219-1226.

Maranda, E. L., Simmons, B. J., Nguyen, A. H., Lim, V. M., & Keri, J. E. (2016). Treatment of acne keloidalis nuchae: a systematic review of the literature. Dermatology and therapy, 6(3), 363-378.

Melo, D. F., Ramos, P. M., Machado, C. J., Anzai, A., Blanco, A., Mulinari-Brenner, F., … & Doche, I. (2022). Dissecting cellulitis in women: a retrospective multicenter study with 17 patients. International journal of dermatology, 61(11), e427-e430.

Michelen-Gómez, E. A., Chiesa Fuxench, Z. C., Cancel-Artau, K. J., Guerrero, A., Ibrahim, O., Santaliz-Ruiz, L. E., 4th, & Colon-Fontanez, F. (2023). Treatment of acne keloidalis nuchae and dissecting cellulitis of the scalp with diclofenac sodium gel: a case series. JAAD case reports, 42, 113–116. https://doi.org/10.1016/j.jdcr.2023.09.008

Ogunbiyi, A. (2016). Acne keloidalis nuchae: prevalence, impact, and management challenges. Clinical, Cosmetic and Investigational Dermatology, 483-489.

Patel, D., Thakker, S., Olagun-Samuel, C., Wang, D., Mitchell, J., & Adotama, P. (2025). Long-term cardiovascular morbidity in dissecting cellulitis: A propensity-matched TrinetX cohort study. Journal of the American Academy of Dermatology, 93(6), 1614-1616.

Saka, B., Teclessou, J. N., Akakpo, S. A., Pessinaba, S., Gnossike, P., Mahamadou, G., … & Pitché, P. (2020). Acne keloidalis nuchae and hypertension in black subjects: a case–control study. BMC Research Notes, 13(1), 431.

Shah, G. K. (2005). Efficacy of diode laser for treating acne keloidalis nuchae. Indian Journal of Dermatology, Venereology, and Leprology, 71(1), 31.

Sperling, L. C., Homoky, C., Pratt, L., & Sau, P. (2000). Acne keloidalis is a form of primary scarring alopecia. Archives of dermatology, 136(4), 479-484.

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Valdman-Grinshpoun, Y., Kridin, K., Schonmann, Y., & Cohen, A. D. (2021). Acne keloidalis nuchae and thyroid diseases: a population-based cohort study. International journal of dermatology, 60(4), 466–470. https://doi.org/10.1111/ijd.15331 

This summary was prepared by Dr. Courtney Hanna, dermatology resident, who attended the session. The content reflects the resident’s notes and interpretations, may contain errors, and is provided for educational purposes only. It does not constitute official faculty endorsement and should not replace original sources or clinical judgment.