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Practical Dermatology
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Clinical and Dermoscopic Characteristics of Facial Hyperpigmentation Disorders in Skin of Color

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M. Mansilla-Poloa,b, C.J. Díaz-Gómezc, D. Morgado-Carrascod,e,
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morgadodaniel8@gmail.com

Corresponding author.
a Servicio de Dermatología, Hospital Universitario y Politécnico La Fe, Valencia, Spain
b Instituto de Investigación Sanitaria La Fe (IIS La Fe), Valencia, Spain
c Sección de Dermatología, Hospital Universitario del Valle, Cali, Colombia
d Servicio de Dermatología, Hospital Clínic de Barcelona, Universitat de Barcelona, Spain
e Servicio de Dermatología, Hospital de Figueres, Fundació Salut Empordà, Spain
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Table 1. Clinical and dermoscopic characteristics of the main facial hyperpigmentation disorders in darker phototypes.
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Abstract

Facial hyperpigmentation disorders (FHD) are common in dermatology, particularly in people with skin of color (SOC). They include melasma, post-inflammatory hyperpigmentation, and less frequent conditions such as exogenous ochronosis, lichen planus pigmentosus, Riehl's melanosis, acanthosis nigricans, seborrheic melanosis, pigmentary demarcation lines, drug-induced pigmentation, and nevus of Ota, among others. These conditions may significantly affect quality of life. They can present similar clinical and dermoscopic features, making diagnosis challenging. A thorough medical history, physical examination, and careful dermoscopic evaluation are essential to achieve an accurate diagnosis. In this article, we present a narrative review of the clinical and dermoscopic characteristics of FHD in SOC and provide diagnostic clues for the early diagnosis of these conditions.

Keywords:
Melasma
Lichen planus pigmentosus
Riehl's melanosis
Post-inflammatory hyperpigmentation
Drug-induced hyperpigmentation
Dermoscopy
Fitzpatrick phototypes
Ethnic skin
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Introduction

Facial hyperpigmentation disorders (FHD) are a frequent reason for consultation among individuals with skin of color (SOC), with an incidence rate up to seven times higher than in lighter skin types.1 Individuals with SOC include those with Fitzpatrick phototypes IV, V, and VI, whose population proportion has increased in Spain and Europe in recent years.2,3

FHD in SOC may be related to differences in melanosome structure and increased responsiveness to visible light and UVA radiation.4–6 These disorders include very common conditions such as melasma and post-inflammatory hyperpigmentation (PIH), as well as less common entities such as lichen planus pigmentosus, Riehl's melanosis, ochronosis, or nevus of Ota. These dermatoses may significantly affect quality of life, with an impact even greater than that of vitiligo.7 The diagnosis of FHD may be challenging, and dermoscopy can be highly useful.8 Unfortunately, dermoscopic studies in SOC remain relatively scarce.

Below, we review the clinical and dermoscopic presentation of FHD in SOC, providing diagnostic clues to facilitate the clinical approach to these conditions in daily practice.

Material and methods

We conducted a narrative literature review. During September 2024, searches were performed in Spanish and English across Medline and Google Scholar using the following terms (alone or in combination): “dermoscopy,” “dark skin,” “skin of color,” “ethnic skin,” “black skin,” “Fitzpatrick phototypes,” “pigmentary disorders,” “facial,” “pigmentary demarcation lines,” “melasma,” “post-inflammatory hyperpigmentation,” “drug-induced hyperpigmentation,” “acanthosis nigricans,” “frictional melanosis,” “seborrheic melanosis,” “nevus of Ota,” “lichen planus pigmentosus,” “Riehl's melanosis,” “ochronosis,” “maturational hyperpigmentation,” and “erythema dyschromicum perstans.”

Articles were initially screened according to their titles and abstracts and subsequently reviewed in full to determine their relevance. Studies specifically addressing the clinical and dermoscopic description of FHD in SOC were included. Given the limited number of publications, some studies also included patients with lighter skin types or described lesions in other body regions. The search and selection process was performed independently by 2 authors (MMP and DMC), who resolved discrepancies by consensus.

Facial hyperpigmentation disorders (Table 1)Pigmentary demarcation lines

Pigmentary demarcation lines (PDL), also known as Futcher–Voigt lines, are more easily observed in SOC due to the greater contrast with hypopigmented skin. Approximately 6% of patients with PDL present facial involvement (types F, G, and H) (Fig. 1).9

Fig. 1.

Facial pigmentary demarcation lines. (A) Diagram illustrating the location of the lines. (B, C) Asian patient with type G lines (black arrows), forming a “W” shape at the lateral canthus of the right eye. Dermoscopy showed accentuation of the facial pseudoreticular pattern (white arrows) and a granular white pattern (white arrowheads).

Table 1.

Clinical and dermoscopic characteristics of the main facial hyperpigmentation disorders in darker phototypes.

Disorder  Clinical characteristics  Dermoscopic characteristics  Diagnostic clues 
Pigmentary demarcation lines  Well-defined brown lines. Bilateral and symmetrical. Three patterns: F, G, and H.  Light or dark brown color. Exaggeration of the facial pseudoreticular pattern.White dots in a granular pattern.  Congenital.Well-defined, bilateral, symmetrical, and often subtle. 
Melasma  Irregular, well-defined brown macules. Areas of spared skin.  Light or dark brown color. Exaggeration of the facial pseudoreticular pattern.No predominance of dots or globules.Arcuate structures. Preservation of follicular openings.  Most frequent centrofacial distribution (malar area, forehead, upper lip).Islands of spared skin. Young women, often associated with oral contraceptive use. 
Post-inflammatory hyperpigmentation  Well-defined hyperpigmented macules. History of prior inflammation.  Brown structureless areas, sometimes with erythema.  Previous inflammatory process.Well-defined margins similar to those of the preceding dermatosis. 
Drug-induced hyperpigmentation  Variable depending on the drug.Diffuse or localized lesions. Usually involvement of other body areas.  Not clearly defined. In fixed drug eruption: diffuse brown-gray dots and globules.  History of drug intake. Pigmentation in other areas (e.g., melanonychia with minocycline) or generalized pigmentation with antimalarial use. 
Acanthosis nigricans  Dark-brown velvety plaques on cheeks and frontal region.Also present in skin folds (neck, axillae, groin).History of obesity, metabolic syndrome, and acrochordons.  “Sulci and gyri/cristae” pattern (papillomatous appearance). Occasionally dark-brown dots or globules or telangiectasias. “Dirty” background.  Middle-aged adults, obesity, and other signs of insulin resistance.Textural changes of affected skin.“Dirty” appearance in folds, especially neck and axillae. 
Frictional melanosis  Lesions in friction areas.Well-defined hyperpigmented lesions.Typical locations (nasal dorsum in allergic rhinitis; central forehead in Muslim individuals).  Exaggeration of the facial pseudoreticular pattern.Diffuse brown or gray dots and globules.  Friction areas: detailed history-taking is essential. Exogenous-appearing pigmentation. 
Seborrheic melanosis  Seborrheic areas such as the alar groove.Typical involvement of nasal base and perioral region.May be associated with seborrheic dermatitis elsewhere. Pruritus may be present.  Superficial whitish-yellow scales similar to seborrheic dermatitis, but with a hyperpigmented background and exaggerated pseudoreticular pattern.  Almost exclusive to darker skin types.Typical seborrheic areas plus nasal base and perioral region.Superficial scaling clinically and dermoscopically. 
Nevus of Ota  Present during the first years of life.Blue-gray plaques in the V1 and V2 distribution of the trigeminal nerve.Possible ocular involvement (glaucoma, melanoma).  Blue-gray background. Superimposed brown globules.  Appears in early childhood and may progressively enlarge.V1 and V2 involvement. Diffuse blue-gray background. 
Lichen planus pigmentosus  Brown-gray macules, sometimes well defined. Possible association with other lichen planus variants.May involve eyelids.  Exaggerated pseudoreticular pattern with predominance of brown-gray dots or globules. Telangiectasias.Occasionally alopecic plaques.  Poorly defined grayish macules.Possible association with lichen planopilaris or frontal fibrosing alopecia. 
Riehl's melanosis  Brown-gray (sometimes bluish) hyperpigmented plaques. Erythematous background, sometimes with scaling.History of exposure to exogenous substances (e.g., perfumes). Pruritus may be present.  Brown/gray/blue reticular pattern on erythematous background.Fine scaling, follicular keratotic plugs, and perifollicular pigmented halos.  History of perfumes or other exogenous substances (detailed investigation in the clinical history). 
Exogenous ochronosis  Previous use of depigmenting agents.Brownish or blackish macules and patches with superimposed hypopigmented areas.  Very dark brown/black color. Obliteration of follicular openings.Hypopigmented areas within an exaggerated facial pseudoreticular pattern. Curvilinear or amorphous very dark structures.  History of prolonged depigmenting agent use (especially hydroquinone). “Banana bodies” on histology. 
Maturational hyperpigmentation  Brown macules and patches with a central “granular” area. Involves temples, cheeks, and forehead.Often reported in individuals of Indian origin and associated with metabolic syndrome.  Hyperpigmented rings with predominantly follicular distribution.  Indian ethnicity.Cheeks and temples with granular background. 
Ashy dermatosis  Blue-gray macules and patches on trunk, extremities, neck, and less frequently on the face.  Blue-gray dots without vascular structures.  Subtle blue-gray background. Involvement of trunk and limbs in addition to the face.In early stages, lesions may have a palpable border. 

FDE, fixed drug eruption; FHD, facial hyperpigmentation disorders; V1 and V2, 1st and 2nd branches of the trigeminal nerve.

A recent article demonstrated that >80% of women with facial PDL present alterations of the sexual hormonal axis.10 Clinically, they appear as well-defined hyperpigmented lines: type F forms a “V” shape on the lateral face between the temple and malar area; type G forms a “W” shape; and type H extends from the angle of the mouth to the chin.11

Dermoscopic findings include exaggeration of the normal facial pseudoreticular pattern12 and white dots arranged in a granular pattern.13

Melasma

Melasma may reach a prevalence of 10–30% in SOC, or even higher when additional risk factors are present.14 It can be disabling, with depression rates of around 50%.15 It typically develops between 20 and 40 years of age and presents as irregular brown macules with well-defined borders in photoexposed areas, often with areas of “spared” skin. Facial melasma is classified as centrofacial (Fig. 2A–C) or peripheral.14,16 The most common dermoscopic finding is accentuation of the facial pseudoreticular pattern. Brown dots and globules may be observed (although not predominating), along with annular or arcuate structures and telangiectasias.17 A recent study demonstrated that the reticuloglobular pattern was more prominent in epidermal melasma, whereas granular or dotted patterns were observed in dermal melasma.18 Unlike ochronosis, follicular openings are preserved in melasma.12,17

Fig. 2.

(A, B) Melasma in a 42-year-old Latin American man. (A) Irregular brown macules with areas of spared skin, predominantly on the cheeks. (B) Dermoscopy shows a prominent pseudoreticular pattern (black arrows), arcuate structures (black arrowheads), and lighter areas of spared skin (white arrows). Note the preservation of follicular units (white arrowheads). (C) Melasma on the cheek of a Latin American patient. (D) Post-inflammatory hyperpigmentation in a woman of African ancestry, with brown macules on the forehead and eyelids secondary to atopic dermatitis. (E) Post-inflammatory hyperpigmentation in a young man due to beard folliculitis. (F) Frontal post-inflammatory hyperpigmentation secondary to prayer in a Muslim man.

Post-inflammatory hyperpigmentation

Post-inflammatory hyperpigmentation (PIH) represents pigmentation due to a previous inflammatory process.19 Clinically, it is recognized by the appearance of well-defined brown macules in areas of prior inflammation, with a latency period ranging from several days to several months (Fig. 2D–F).19 PIH may be particularly prolonged in SOC, sometimes persisting for 2–5 years.20 Dermoscopic findings in PIH are not well described in the literature. An accentuated pseudoreticular pattern with light- or dark-brown globules and dots sparing follicular openings may be observed. Pigmentation appears dark brown when the pigment is located in the epidermis or superficial dermis and grayish when deposited more deeply.21

Drug-induced hyperpigmentation

Drug-induced hyperpigmentation is classically associated with tetracyclines, nonsteroidal anti-inflammatory drugs, antimalarials, antipsychotics, amiodarone, diltiazem, or certain antiretroviral drugs.22 Its pathophysiology is complex: some drugs induce melanin accumulation (e.g., hydroxychloroquine), others stimulate melanin synthesis (e.g., lipofuscin), or lead to iron deposition (e.g., minocycline).23 Certain drugs such as voriconazole may induce phototoxic reactions.24 Some drugs have been particularly associated with facial pigmentation, including sunitinib (yellowish hyperpigmentation), phenytoin, polymyxin B, diltiazem, or imipramine.22 Clinically, drug-induced hyperpigmentation appears as hyperpigmented macules with focal or diffuse facial involvement, sometimes accompanied by pigmentation in other body areas.22,23 Only 1 dermoscopic description has been reported in the literature, showing accentuation of the facial pseudoreticular pattern with light- or dark-brown dots and globules.25

The late phase of fixed drug eruption (FDE) may present with isolated pigmentation. Dermoscopy in FDE shows pigment dots and globules with different shades ranging from brown to gray.12

Acanthosis nigricans

Acanthosis nigricans (AN) presents with grayish-brown hyperpigmented plaques with a velvety texture in flexural areas, particularly the neck, axillae, and groin, and less frequently on the face (Fig. 3). It is more common in adult SOC populations and is frequently associated with obesity and insulin resistance. Some authors reserve the term AN for cases not associated with drugs, neoplasms, or syndromic conditions, referring to obesity-related cases as pseudoacanthosis nigricans.26 Dermoscopically, AN shows a pattern known as “sulci and gyri/cristae,” characterized by accentuated skin grooves and ridges, sometimes hyperkeratotic and more pigmented, on a grayish-brown “dirty” background27 resembling “crocodile skin.”21 Occasionally, dark-brown dots or globules and, more rarely, telangiectasias may also be observed.25

Fig. 3.

(A, B) Acanthosis nigricans in a Central American man. (A) Brownish macules with a velvety appearance predominantly on both cheeks and the supraciliary areas. (B) Dermoscopy shows a “sulci and gyri/cristae” pattern (black arrows) along with follicular plugs (black arrowheads). (C, D) Acanthosis nigricans in an Indian man. (C) Brownish velvety macules on the cheek. Note the acanthosis nigricans on the neck. (D) Dermoscopy shows a “sulci and gyri/cristae” pattern (black arrows).

Frictional melanosis

Frictional melanosis (FM) is also more common in SOC (particularly in individuals from India). It appears in areas subjected to chronic or repeated friction. Clinically, it presents as well-defined dark-brown macules and plaques in areas exposed to trauma (Fig. 4). It is important to ask about possible causes of the lesions (e.g., forehead lesions caused by friction during prayer).28 Mutalik et al. described 6 clinical patterns in facial FM: zygomatic–supraorbital, metomelanosis (forehead), panfacial, parafacial, perioral, and mixed. These patterns show a characteristic symmetrical distribution with uniform brown-black pigmentation without textural changes.29 In contrast to FM, macular amyloidosis usually does not affect the face, tends to be more pruritic, and shows superficial amyloid deposition on histopathology. Dermoscopically, the most frequent finding in FM is exaggeration of the facial pseudoreticular pattern.12,29 Dark-brown or grayish dots and globules and prominent follicular openings have also been described.25,28

Fig. 4.

(A–C) Frictional melanosis secondary to allergic rhinitis in a 32-year-old African woman. (A) Hyperpigmented macules in the nasal region. (B) Repetitive gesture performed by the patient (frequent nasal rubbing). (C) Dermoscopy showing exaggeration of the facial pseudoreticular pattern (black arrows) and diffuse brown-gray dots/globules (black arrowheads).

Seborrheic melanosis

Seborrheic melanosis (SM), also known as sebomelanosis, is an entity almost exclusively observed in individuals with skin of color (SOC) (Fig. 5). For most authors, it is considered a post-inflammatory sequela of seborrheic dermatitis. However, cases of SM have also been described in patients without a prior history of seborrheic dermatitis and who are asymptomatic. SM is characterized by hyperpigmented macules and thin plaques with very superficial scaling, predominantly affecting the nasal grooves and nasolabial folds. It also typically involves the inferior nasal fold or the perioral region. It may or may not be pruritic and can involve other body areas such as the scalp or trunk.30,31 Dermoscopically, a prominent pseudoreticular pattern, brown granular structures, poorly defined vessels, prominent follicular openings, and yellowish-white perifollicular sebaceous scales are observed.12,30

Fig. 5.

(A, B) Thirty-year-old African woman with hyperpigmented lesions in the nasolabial folds and alar grooves. (A) Dark-brown macules in the alar grooves and nasolabial folds. (B) Dermoscopy: whitish scales (black arrows), predominantly in the alar groove, with background hyperpigmentation. (C, D) Latin American woman with pigmentation in the nasal groove and perioral region due to seborrheic dermatitis. Dermoscopy of the nasal groove showed prominent follicular openings, mild scaling, telangiectasias, and diffuse pigment.

Nevus of Ota

Nevus of Ota, also known as nevus fuscocaeruleus ophthalmomaxillaris, is an oculodermal melanocytosis characterized by coalescent macules distributed along the V1/V2 branches of the trigeminal nerve (Fig. 6A–C). It is more common in women of Asian or African ancestry. In 90% of cases it is unilateral and involves the sclera in 60% of patients.32 There is a slight increased risk of glaucoma, and rare cases of transformation into uveal or cutaneous melanoma have been described.32,33 Therefore, patients with nevus of Ota should undergo ophthalmologic follow-up.34 Dermoscopic features include structureless blue-gray areas and scattered brown-gray dots.12,35

Fig. 6.

(A–C) Nevus of Ota. (A) Blue-gray pigmented macule on the right hemiface, predominantly in the V1 and V2 territories. (B) Dermoscopy shows blue-gray coloration with light-brown and some lighter areas within the nevus. Photographs courtesy of Dr. Verónica Echeverry. (D–F) Lichen planus pigmentosus in a Latin American woman. (D–E) Grayish-brown macules affecting the entire face, predominantly on the cheeks (black arrows). (F) Dermoscopy shows perifollicular brown-gray dots and globules (black arrowheads) without obliteration of follicular openings.

Lichen planus pigmentosus

Lichen planus pigmentosus (LPP) is characterized by oval brown to gray-brown macules and plaques, predominantly affecting the preauricular and temporal regions, neck, cheeks, and/or intertriginous areas (Fig. 6D–F). Some authors classify LPP within acquired dermal macular hyperpigmentation (ADMH), which includes several dermal facial hyperpigmentation disorders such as pigmented contact dermatitis (Riehl's melanosis) and erythema dyschromicum perstans.12 LPP may sometimes be associated with other variants of lichen planus, such as lichen planopilaris or frontal fibrosing alopecia.36 Dermoscopically, there is accentuation of the facial pseudoreticular pattern with predominant blue-gray and brown dots and globules arranged in arcuate, perifollicular, and mottled patterns (or without a clear pattern),37 without obliteration of follicular openings.25 Other findings include diffuse erythema, telangiectasias, rhomboidal structures, follicular asymmetry, and reduction of vellus hair.38 Mulinari-Brenner et al. recently described additional dermoscopic features including decreased follicular openings, follicular hyperkeratosis, keratotic plugs, perifollicular erythema, simple loop interfollicular vessels, branching vessels, and white dots. Areas of reduced hair density or alopecia may also be observed.39

Pigmented contact dermatitis (Riehl's melanosis)

Riehl's melanosis (RM) predominantly affects SOC, particularly older women. It is characterized by reticulated to diffuse grayish-brown hyperpigmented macules or plaques on the face, neck, and upper chest (Fig. 7A–C). It may occasionally present with pruritus and superficial scaling. It is considered a type IV hypersensitivity reaction triggered by contact allergens such as fragrances, textiles, and cosmetics, although genetic factors, autoimmune alterations, and sun exposure may also contribute.40 Dermoscopically, a marked pseudoreticular pattern may be observed, with predominance of gray dots and globules, telangiectatic vessels, and an erythematous background.17,21,12 These findings are therefore very similar to those seen in LPP. Clinical history is useful to differentiate RM from LPP (history of allergen exposure in RM). Dermoscopic findings more specific to RM include fine scaling, follicular keratotic plugs, perifollicular hypopigmented halos,41 and obliteration of follicular openings.25

Fig. 7.

(A–C) Latin American woman with Riehl's melanosis. (A, B) Dark brown-gray macules and patches diffusely affecting the face, especially the nose, cheeks, and perioral region. (C) Dermoscopy highlights follicular keratotic plugs (black arrows) and perifollicular pigmented halos (black arrowheads). (D, E) Latin American woman with ashy dermatosis. (D) Blue-gray macules on the left cheek. (E) Dermoscopy shows a brown reticular pattern without evident vascular structures.

Ocronosis exogena

Exogenous ochronosis (EO) is characterized by dark-brown or even blackish macules and plaques.42 Papules resembling “caviar” (colloid milium) or interspersed atrophic hyperpigmented patches may be observed. Dermoscopically, EO presents with exaggerated facial pseudoreticular pattern, hypopigmented areas, telangiectasias, and dark-brown curvilinear or amorphous structures with obliteration of follicular openings.17,21,12 Histological examination is particularly useful, showing the characteristic ochre-colored “banana bodies” in the upper dermis.12

Maturational hyperpigmentation

Maturational hyperpigmentation (MH) is a recently described entity, almost exclusive to SOC (especially individuals from India), characterized by dark-brown macules predominantly on the cheeks, temples, and forehead. Macroscopically, the lesions often show a “granular” surface and poorly defined borders. It is considered a marker of metabolic syndrome.43 Dermoscopically, it shows a nonspecific pattern with a light-brown background overlaid by multiple dark-brown globules and clods. The most distinctive feature is circular to oval dark-brown structures with perifollicular accentuation. Unlike acanthosis nigricans, it does not show sulci or ridges.43,44

Ashy dermatosis (erythema dyschromicum perstans)

Ashy dermatosis (erythema dyschromicum perstans) is a condition of unknown etiology, more common in SOC (Latino, Afro-descendant, and Asian populations). It is characterized by grayish or bluish hyperpigmented macules that appear on the trunk, extremities, neck, and less frequently on the face (Fig. 7D–E). Dermoscopy helps differentiate it from other conditions such as melasma, PIH, fixed drug eruption, and LPP. Dermoscopy typically shows a reticulated pattern with gray and brown networks, grayish or black pigment globules in more advanced lesions, and absence of vascular structures.21,45

Discussion

Given globalization and migratory flows, improving dermatologic training in diseases that more frequently affect individuals with skin of color (SOC) is necessary.46 FHD are very common in this population, and certain conditions such as seborrheic melanosis or maturational hyperpigmentation are almost exclusive to SOC. Although studies on dermoscopy in SOC have increased over the last decade, few specifically evaluate FHD,21,25,12 and we did not find systematic reviews or meta-analyses addressing this topic.

The diagnosis of FHD may be complex, and histological examination is not always particularly useful (except in certain conditions such as exogenous ochronosis or lichen planus pigmentosus). A thorough medical history (for example, to rule out the use of topical products that may favor Riehl's melanosis, a history of inflammatory dermatoses in post-inflammatory hyperpigmentation, among others), physical examination, and dermoscopy will often allow an accurate diagnosis of FHD in SOC or at least a very close diagnostic approximation. Dermoscopy can provide important diagnostic clues, although no pathognomonic findings have been identified.

Limitations

The present review has the limitation of being narrative rather than a systematic review or meta-analysis, implying that study selection may be subject to bias. In addition, many of the included studies did not specifically address FHD but extrapolated facial findings from observations made in other body areas. Most of the reviewed studies correspond to small case series or retrospective studies, which limits the generalizability of the findings and the ability to establish causal relationships. Furthermore, it should be noted that not all the reviewed publications were strictly focused on higher phototypes.

Conclusions

FHD are very common in individuals with skin of color and may significantly affect quality of life. A thorough medical history, physical examination, and dermoscopic evaluation can assist in establishing the diagnosis.

Conflict of interest

The authors declare that they have no conflict of interest.

Acknowledgments

We thank Elena Morgado Pizarro for her assistance in preparing Fig. 1 and Dr. Verónica Echeverry for providing the photographs of the patient with nevus of Ota.

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