Dyschromia
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Atypical Dyschromia in Skin of Color

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ABSTRACT

Dyschromia is a concern for many patients, especially persons of color. Postinflammatory hypopigmentation and depigmentation can affect all skin types; however, it is more apparent in those with darker skin. Some members of the dermatology community may not comprehensively understand the mechanisms of these reactions and the extent of the psychosocial effect they have on persons of color. Skin of color patients experiencing a decrease or loss of pigmentation are left with few treatment options, with no available evidence-based treatment established from a sufficient sample size. Several diseases may present with hypopigmentation and/or depigmentation despite this not being a major criterion for these conditions, including atopic dermatitis, lichen planus, discoid lupus erythematosus, polymorphous light eruption, and scleroderma. Here, JDD authors Mohammed Moumen, MD and Amy J. McMichael, MD present three cases of atypical dyschromia in skin of color to highlight the underlying hypo- and depigmentation that may present with active disease and persist despite appropriate treatment.

INTRODUCTION

Dyschromia is often the result of an external or internal insult to the skin.1 It is a concern for many patients, especially persons of color.2,3 In black patients, dyschromia is a common diagnosis and substantially affects their quality of life.2-4 Current literature focuses on post-inflammatory hyperpigmentation and treatment options. However, literature on etiologies of secondary hypopigmentation and depigmentation is sparse.1 Hypopigmentation and depigmentation can affect all skin tones; they are more apparent in darker skin.1 Literature suggests several diseases that may present with hypopigmentation and/or depigmentation despite this not being a major criterion for these conditions.5-11 Inflammation associated with atopic dermatitis (AD) may result in hypopigmented change and has been reported in several cases.5-7 There have been three reports of lichen planus (LP) presenting in skin of color as hypopigmented macules.8 Hypopigmentation is unusual for LP as it presents classically with hyperpigmentation.8 Discoid lupus erythematosus (DLE) often presents with erythema, induration, and follicular plugging.9 Presentation of DLE as depigmentation has been reported in seven cases and remains a rarely reported occurrence.9-11 Similarly, scleroderma-associated depigmentation has also been reported.12-15 Here, we present three cases of atypical dyschromia in skin of color to highlight the underlying hypo- and depigmentation that may present with active disease and persist despite appropriate treatment.

Report of a Case of Depigmentation From AD

A 66-year-old African American woman presented to our clinic for a complete body examination of AD. She reports that her AD started around age 52 at menopause, with itching on the legs. Her AD worsened in the past 2-3 years and was particularly bothersome in the summer. She had been treated previously at an outside dermatology office and had tried Dupilumab for a short time; she developed a rash and stopped this medication. She had also tried ultrapotent topical steroids, and topical calcineurin inhibitors, none of which controlled her pruritus or outbreaks.

Pertinent findings on skin exam included lichenified scaling hyperpigmented plaques on the upper arms from the upper arm to the wrists. The anterior shins showed severe lichenification and hypopigmented linear vertical plaques. Her presentation was consistent with severe atopic dermatitis. She was started on Methotrexate systemically which gave her improved control of her pruritus and atopic flares. On subsequent visits, depigmentation was persistent on her shins despite improved control of her disease (Figure 1).
Dyschromia

Report of a Case of Hypopigmentation From Polymorphous Light Eruption (PMLE)

A 52-year-old African American woman presented to our clinic with a new pruritic rash on her forearms. The rash started three months prior to presentation. According to her report, sun exposure and high temperatures seemed to worsen the eruption. She had no relevant past medical history and an unremarkable complete review of systems. On skin examination, there were small hypopigmented 1-2 mm shiny papules on bilateral dorsal forearms extending into dorsal hands (Figure 2). Given the history of worsening with sun exposure, a diagnosis of PMLE was made. On trichoscopy, a hypopigmentary process was observed. The patient was started on midpotency topical steroid cream for her rash in a tapering fashion. Sun protection with sun-protective clothing and inorganic tinted sunscreen was recommended.

Dyschromia

Report of a Case of Depigmentation From Scleroderma

A 19-year-old African American woman presented for evaluation and treatment of a scleroderma diagnosis made one year prior by rheumatology. She reported dry skin and tried ceramide-containing moisturizer without improvement. She stated that her chest and back were the worst areas. She had not tried prescription medication for this concern at the time of presentation. She was taking hydroxychloroquine for maintenance of her systemic symptoms. She was also treated with systemic corticosteroids and intravenous immunoglobulin for her systemic disease without improvement in her skin complaints. Her physical exam was significant for diffuse hyperpigmented ichthyotic and asteatotic plaques over the back and chest. Tightening of the skin and hypopigmentation in areas of the chest and fingers were also observed (Figure 3). Tapering of the fingertips was noted. Her condition was consistent with scleroderma. The patient was initiated on topical ammonium lactate moisturizers and topical calcineurin inhibitors for the diffuse plaques on the chest and back.

Dyschromia

DISCUSSION

Dyschromia in skin of color is common and one of the most frequent chief complaints in dermatology for persons of color.2,3 Possible mechanisms for secondary hypopigmentation include melanocyte loss and decreased melanin production.1 Ruiz et al proposed a theory, “individual chromatic tendency,” that relates post-inflammatory hypopigmentation to genetic factors, where specific individuals have “weak” melanocytes that are easily affected by inflammation.16 The first case discussed demonstrated hypopigmentation in the setting of AD and progressed to depigmentation, an atypical form of dyschromia from AD. The persistence of the dyschromia despite improvement in activity of disease suggests that the expectation of complete repigmentation, even with appropriate treatment, may not be fulfilled. Hypopigmentation from PMLE is not well documented in the literature; the second case discussed here indicates that the inflammatory process associated with PMLE can lead to a change in pigmentation, as indicated by the physical exam and underscored elegantly by dermoscopy. This description may help to clarify the diagnosis if this pattern of hypopigmentation or depigmentation is observed. Case three discusses an unusual presentation of scleroderma with associated depigmented patches on the chest and hands. Again, recognition of this pattern of depigmentation may help to delineate the scleroderma diagnosis if other diagnoses are being considered.

Research is limited on treatment options for hypopigmentation and depigmentation in skin of color.15 Treatment recommendations focus on the identification and treatment of the primary disease process.15 Cosmetic topical and procedural therapies are also available.15 Two studies reported moderate to excellent repigmentation in skin of color patients treated with topical Psoralen + ultraviolet light A.17,18 Reszko et al reported complete repigmentation in an African American male with postinflammatory hypopigmentation using 17 treatments of Q-switched Ruby Laser.19 However, this has not been reported in a large number of skin of color patients and could lead to worsening of dyschromia in patients with dark skin.

Postinflammatory hypopigmentation and depigmentation remain a challenge faced by patients and providers. The impact of this process is more apparent in those with darker skin. Some members of the dermatology community may not comprehensively understand the mechanisms of these reactions and the extent of the psychosocial effect they have on persons of color. Skin of color patients experiencing a decrease or loss of pigmentation are left with few options for treating this process, with no available evidence-based treatment established from a sufficient sample size.

DISCLOSURES

Dr. McMichael received grants from Procter and Gamble, Galderma, and Incyte. She has received consulting support from Lilly, Janssen, Pfizer, Arcutis, Almirall, Abbvie, Galderma, Bristol Meyers Squibb, Sanofi, UCB, Revian, Johnson & Johnson, L’Oreal, and Nutrafol. Dr. Moumen has no conflicts to disclose.

 

REFERENCES

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    2. Kang SJ, Davis SA, Feldman SR, et al. Dyschromia in skin of color. J Drugs Dermatol. 2014;13(4):401-6. PMID: 24719058. 
    3. Davis SA, Narahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11(4):466-473. 
    4. Grimes PE. Management of hyperpigmentation in darker racial ethnic groups. Semin Cutan Med Surg. 2009;28(2):77-85. 
    5. Eichenfield LF, Stein Gold LF. Practical strategies for the diagnosis and assessment of atopic dermatitis. Semin Cutan Med Surg. 2017;36(2 Suppl 2):S36-S38. doi: 10.12788/j.sder.2017.009. PMID: 28654708. 
    6. Nader-Djalal N, Ansarin K. Hypopigmented skin lesions associated with atopic dermatitis in asthma. J Asthma. 1996;33(4):231-8. doi: 10.3109/02770909609055364. PMID: 8707778. 
    7. Ichimiya M, Ohmura A, Muto M. Numerous hypopigmented patches associated with atopic dermatitis. J Dermatol. 1998 Nov;25(11):759-61. doi: 10.1111/j.1346-8138.1998.tb02498.x. PMID: 9863292. 
    8. Arnold D, Hoffman MB, Onajin O, et al. Hypopigmented Macules as Manifestation of Lichen Planus and Lichen Planopilaris. Am J Dermatopathol. 2019;41(7):514-517. doi: 10.1097/DAD.0000000000001389. PMID: 30946098. 
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    10. Gupta S. Epidermal grafting for depigmentation due to discoid lupus erythematosus. Dermatology. 2001;202(4):320-3. doi: 10.1159/000051665. PMID: 11455144. 
    11. Mulekar SV, Ghwish B, Al Issa A, et al. Melanocyte-keratinocyte transplantation for postdiscoid lupus erythematosus depigmentation. Dermatol Surg. 2008;34(2):261-2. doi: 10.1111/j.1524-4725.2007.34053.x. PMID: 18177409. 
    12. Fujimoto N, Hamaguchi Y, Tanaka T. Vitiligo-like depigmentation with perifollicular pigment retention in systemic sclerosis treated successfully with suplatast tosilate. Eur J Dermatol. 2016;26(1):110-2. doi: 10.1684/ ejd.2015.2687. PMID: 26841835. 
    13. De Villiers WJ, Jordaan HF, Bates W. Systemic sclerosis sine scleroderma presenting with vitiligo-like depigmentation and interstitial pulmonary fibrosis. Clin Exp Dermatol. 1992;17(2):127-31. doi: 10.1111/j.1365-2230.1992. tb00180.x. PMID: 1516238. 
    14. Sanchez JL, Vazquez M, Sánchez NP. Vitiligolike macules in systemic scleroderma. Arch Dermatol. 1983;119(2):129-33. doi: 10.1001/ archderm.1983.01650260037013. PMID: 6337560. 
    15. Carlson JA, Grabowski R, Mu XC, et al. A possible mechanism of hypopigmentation in lichen sclerosus. Am J Dermatopathol. 2002;24(2):97-107. 
    16. Ruiz-Maldonado R, Orozco-Covarrubias ML. Postinflammatory hypopigmentation and hyperpigmentation. Semin Cutan Med Surg. 1997;16(1):36-43. 
    17. Grimes PE, Bhawan J, Kim J, et al. Laser resurfacing-induced hypopigmentation: histologic alterations and repigmentation with topical photochemotherapy. Dermatol Surg. 2001;27(6):515-520. 
    18. Lopez I, Ahmed A, Pandya AG. Topical PUVA for post-inflammatory hypopigmentation. J Eur Acad Dermatol Venereol. 2011;25(6):742-743. 
    19. Reszko A, Sukal SA, Geronemus RG. Reversal of laser-induced hypopigmentation with a narrow-band UV-B light source in a patient with skin type VI. Dermatol Surg. 2008;34(10):1423-1426. 

SOURCE

Moumen, M., & McMichael, A. J. (2024). Atypical Dyschromia in Skin of Color. Journal of Drugs in Dermatology: JDD, 23(2), 100-102.

Content and images published with permission from the Journal of Drugs in Dermatology.

Adapted from original article for length and style.

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