Blue naevus and dermal melanocytosis

Meet the patient

A 25-year-old woman wants a stable 4 mm blue-black papule on the back of her hand removed for cosmetic reasons. It has been there, unchanged, since childhood. She asks why it is blue, and whether a laser will do. [1]

Two questions sit inside her request, and the whole topic lives between them: why is it blue? (an optical trick of deep melanin) and when is a blue lesion dangerous? (the moment it changes). Hold both, and the management writes itself — observe the stable classic lesion, excise anything that changes, and never laser a lesion you have not first confirmed benign. [1]

The colour is optical, not pigment — the one fact that runs the topic

There is no blue pigment in a blue naevus. The melanin is brown-black, but because it sits deep in the reticular dermis, the overlying collagen and epidermis scatter light so that the shorter blue wavelengths bounce back to the eye. This is the Tyndall effect — the same physics that makes a superficial vein look blue through the skin. [1]

Two facts follow and govern the whole topic. First, a blue naevus is a proliferation of dermal melanocytes — a discrete tumour — which separates it from the dermal melanocytoses (Mongolian spot, naevus of Ota, naevus of Ito), where scattered dendritic melanocytes simply persist in the dermis as a flat patch. [3] Second, because colour depends on depth and pigment density rather than biology, a long list of unrelated lesions — melanoma, a traumatic tattoo, a venous lake, a dermatofibroma, a pigmented BCC — can also look blue. The defining clinical skill is therefore not recognising the textbook lesion but separating the stable benign blue papule from a changing melanoma. [2]

Etymology for viva gold: a naevus is from the Latin naevus, "birthmark" or "mole"; the eponym Jadassohn–Tièche names the pathologists who first characterised the common blue naevus in 1906. Neither word tells you the biology — the Tyndall effect does. [3]

Classification — one family of ectopic dermal melanocytes

Blue naevi and the dermal melanocytoses are one biological family — ectopic dermal melanocytes — split by whether the cells proliferate into a tumour (the naevi) or simply sit in the dermis as a patch (the melanocytoses), and then by their characteristic territory. [3]

[3]

The common and cellular blue naevi are the two types an examiner expects you to separate cleanly: the common type is the everyday stable papule of the extremities with no malignant potential, while the cellular type is the larger, deeper, often congenital lesion of the buttock and scalp that carries a small but real risk of malignant blue naevus and is therefore excised. [1]

Epidemiology and the syndromic flag

The common blue naevus is one of the commonest acquired melanocytic lesions — present in roughly 1 to 3 percent of the general population, most appearing in childhood, adolescence or early adulthood, with a slight female predilection. [1]

The cellular blue naevus is rare and notable in that around half are present at birth or arise in early childhood — a congenital blue nodule of the scalp or buttock is a classical presentation. Its epidemiology matters because it is the variant with a recognised, if small, risk of malignant transformation. [3]

The dermal melanocytoses are ethnically patterned. The Mongolian spot is present in over 80 to 90 percent of Asian and Black neonates but in fewer than 10 percent of White neonates — so common in its characteristic populations that it is a normal variant. The naevus of Ota is most frequent in East Asian and Black women, is nearly always unilateral, and is permanent — unlike the Mongolian spot it does not fade. [7]

[1]

The principal risk factors for concern are not risk factors for getting a blue naevus but for a blue naevus behaving badly: a cellular subtype, large size (over 1 cm), congenital onset, a changing lesion, and — at the syndrome level — Carney complex, in which multiple blue naevi cluster with lentigines, cardiac myxomas and endocrine overactivity. [6]

Pathophysiology — arrested migration, scattered light, a shared driver

Embryological origin

Melanocytes originate in the neural crest and migrate to the basal epidermis in the first trimester. In blue naevi and dermal melanocytoses a clone is arrested in, or fails to complete, this migration and persists and proliferates within the dermis. The same developmental logic explains the characteristic sites: the lumbosacral Mongolian spot sits over the last region to be colonised, and naevus of Ota and naevus of Ito follow the trigeminal and cervical nerve distributions along which the cells travelled. [3]

The Tyndall effect, restated for the mechanism

Melanin is brown-black, but in the deep dermis the overlying collagen and epidermis act as a scattering medium: shorter blue wavelengths are preferentially scattered back to the eye while longer red and brown wavelengths are absorbed or pass deeper. Depth and density set the shade — a superficial dermal deposit looks steel-blue, a deeper and denser deposit looks slate-blue to blue-black. [1]

Molecular driver

Most blue naevi carry activating mutations in the G-protein signalling pathway — most commonly GNAQ (the Q209 hotspot), and less often GNA11, PLCB4 or CYSLTR2. These drive the MAPK pathway constitutively, which is why a blue naevus sits on the same molecular spectrum as uveal melanoma (which shares the GNAQ/GNA11 driver). This shared biology explains why blue naevi only very rarely progress to melanoma but do so through the same pathway, and why atypical cellular blue naevus and melanoma can be histologically very difficult to separate. [1][2]

The biphasic histology of cellular blue naevus

The cellular blue naevus earns its name from a characteristic two-component architecture: a deep common-blue-naevus component (densely pigmented dendritic and spindled melanocytes with melanophages, hugging collagen bundles) plus a larger, more superficial nodular component of tightly packed fascicles and nests of plump spindle or ovoid cells, often extending into the subcutis in a wedge or dumbbell shape along skin appendages. The cells are low in atypia and rarely mitotic — and it is the loss of these benign features (atypia, mitoses, necrosis, deep infiltration) that defines malignant blue naevus. [3]

Clinical presentation — the pathognomonic story

Common blue naevus

The textbook lesion is a solitary, asymptomatic, well-circumscribed, dome-shaped blue-black to steel-blue papule, 2 to 10 mm across, firm, with overlying skin markings preserved. It most often sits on the dorsum of the hands and feet, then the scalp, face, wrists and forearms. Once it appears it is stable for years to life — the single most reassuring feature: a blue papule unchanged for a decade is a common blue naevus until proven otherwise. [1]

Cellular blue naevus

The cellular type is larger (1 to 3 cm) and deeper, presenting as a bluish-black nodule or plaque that may be multinodular. Its classical territory is the buttock and sacrococcygeal area and the scalp, and around half are congenital — a blue-black plaque present since birth over the sacrum or a blue nodule on the scalp of a child is the canonical stem. Any change in it is a red flag. [3]

Dermal melanocytoses

The Mongolian spot is a blue-grey patch over the lumbosacral area and buttocks present at birth, commonest in Asian and Black infants, that fades over the first two to four years as the melanocytes disperse. Naevus of Ota is a unilateral blue-grey or brown macular pigmentation of the first and second trigeminal dermatomes — temple, cheek, periorbital skin — almost always with scleral (and sometimes uveal) pigmentation; it is permanent. Naevus of Ito is the same process in the shoulder-girdle and lateral-neck distribution, without ocular involvement. [7]

Atypical and less common presentations

Examiners probe the edges of the distribution. A combined blue naevus presents as a blue papule within or beside a brown conventional naevus — a clinical melanoma mimic. An amelanotic blue naevus lacks the blue colour entirely and mimics a neurofibroma or appendage tumour. Subungual and periungual blue naevi produce a blue band or nodule under the nail and must be distinguished from subungual melanoma. [5] Mucosal blue naevi occur in the oral mucosa, conjunctiva and sinonasal tract. [2]

Differential — the blue lesion that is not a blue naevus

The differential of a blue or blue-black cutaneous lesion is long, because depth of pigment — from any source — produces the same optical effect. The task is not to list every mimic but to separate the benign stable lesion from melanoma, and to recognise the specific mimics that have their own management. [2][3]

[2]

For naevus of Ota specifically, the facial differential includes melasma, Hori naevus (acquired bilateral naevus of Ota-like macules), and post-inflammatory hyperpigmentation. In infants, a persistent or ectopic Mongolian spot must be distinguished from a bruise — a distinction with safeguarding implications, since a Mongolian spot is present at birth, sits in the classic lumbosacral area, does not evolve through the colour stages of a bruise, and is far commoner in pigmented infants. [7]

Bedside assessment — is it behaving like a benign blue naevus, or is it changing?

The focused assessment of any blue-black lesion is built around a single question: is this lesion behaving like a benign blue naevus, or is it changing? History establishes the age of onset, duration, and — critically — any change in size, shape, colour, elevation, or any new symptom (itch, pain, bleeding, ulceration). A stable lesion unchanged for years in a typical site is the classic benign pattern; a new, enlarging or symptomatic blue lesion reopens the question of melanoma every time. [1]

Examination confirms the morphology, site, colour homogeneity, and the presence or absence of the ABCDE features of melanoma. Dermoscopy is the decisive bedside tool: a classic common blue naevus shows structureless, homogeneous, steel-blue to blue-black pigmentation with no pigment network, no globules, no regression and no atypical vessels — the absence of melanoma features is as important as the presence of the blue field. [4]

Three named bedside manoeuvres resolve the common mimics at the chairside and cost nothing. Diascopy (pressing a glass slide over the lesion) empties a venous lake — a compressible vascular papule on the lower lip or ear blanches to nothing, whereas a blue naevus does not change. The dimple sign marks a dermatofibroma. Cold sensitivity with paroxysmal pain points to a glomus tumour, classically a tender bluish subungual nodule. [3]

A whole-skin examination is mandatory for two reasons: to look for multiple blue naevi (which flag Carney complex), and, in any blue lesion of concern, to search for a primary melanoma elsewhere. For naevus of Ota, the examination extends to the eyes — document the scleral pigmentation and arrange tonometry for glaucoma and a dilated fundus examination for uveal melanoma. [6][7]

Investigations — dermoscopy first, biopsy when the pattern breaks

A typical common blue naevus is a clinical diagnosis confirmed by dermoscopy; no biopsy, blood test or imaging is required for a stable, classic, asymptomatic lesion in a typical location. Investigation in that setting is over-investigation. [1]

The dermoscopic signature of a common blue naevus is a structureless, homogeneous, steel-blue to blue-black area occupying the whole lesion, with no network, no globules, no streaks, no regression areas and no atypical vessels. The cellular blue naevus may add a central structureless blue area with peripheral regular globules or streaks. The key point is the negative feature: the absence of melanoma structures is what permits observation. [4]

Biopsy or excision is mandated the moment the lesion departs from the reassuring template — any change, an atypical dermoscopic pattern (asymmetry, atypical network, blue-white veil, regression, irregular vessels), a new blue lesion in an adult, a lesion over 1 cm or a cellular blue naevus, any diagnostic uncertainty, or a lesion in a site that cannot be reliably monitored (scalp, mucosa, subungual). Where biopsy is indicated, the preferred technique is a complete excisional biopsy with a narrow margin of normal skin, because the distinction between atypical cellular blue naevus and melanoma can require the entire architecture and the deep margin. [1][2]

The common blue naevus on histology shows densely pigmented, elongated dendritic and spindled melanocytes lying between and within collagen bundles of the reticular dermis, with numerous melanophages and variable fibrosis, no junctional activity, no atypia and no mitoses. The cellular blue naevus shows the biphasic pattern of plump spindle or ovoid cells extending in a wedge into the subcutis. Malignant blue naevus is defined by cytological atypia, mitoses (especially atypical), necrosis and infiltrative growth. [3]

Management — the diagnostic safety step first

Blue naevus is not a time-critical emergency, but every blue lesion must pass a diagnostic safety step: exclude melanoma before reassuring. A new, rapidly enlarging blue-black nodule in any age group, or any blue lesion that bleeds or ulcerates, is treated as possible melanoma and undergoes prompt complete excisional biopsy. [1][2]

Multiple new blue lesions in an adult should prompt a search for the syndrome or the occult melanoma, not blanket reassurance — multiple blue naevi raise Carney complex, and a blue-naevus-like lesion may rarely be a melanoma mimicking a blue naevus. [6]

Management — definitive and stepwise

Definitive management follows the lesion's behaviour and subtype, not its colour. [1]

Step 1 — the stable classic common blue naevus: observe and reassure. Document the lesion with a photograph and dermoscopy, explain the benign natural history, teach self-examination, and advise the patient to return if it changes. No treatment is needed unless removal is requested for cosmetic reasons. This is the correct answer to the common stem of a stable blue papule on the hand of a young adult. [1]

Step 2 — cosmetic or definitive removal when desired: complete surgical excision. Excision is both treatment and a source of tissue for histology, and is preferred whenever removal is contemplated. Q-switched lasers (ruby, alexandrite or Nd:YAG) can lighten the dermal pigment of naevus of Ota and dermal melanocytoses over multiple sessions, but are less reliable for nodular blue naevi and crucially provide no tissue diagnosis — a laser must never be applied to a lesion not first confirmed benign. [8]

Step 3 — the cellular blue naevus and any atypical or uncertain lesion: complete surgical excision. Excision with a margin of normal skin is recommended for the cellular blue naevus and for any lesion with atypical features, change or diagnostic uncertainty — both diagnostic (the whole lesion for histology) and therapeutic. Submit the specimen in full. [3]

Step 4 — malignant blue naevus: treat as melanoma. Malignant blue naevus is managed within the melanoma pathway: wide local excision with margins guided by Breslow thickness, sentinel lymph node biopsy where appropriate, staging imaging, and multidisciplinary-team management — exactly as for a cutaneous melanoma of equivalent thickness. [2]

Dermal melanocytoses. The Mongolian spot needs only reassurance — it fades. The naevus of Ota is permanent: Q-switched laser is the treatment of choice for the cutaneous pigmentation, typically over multiple sessions, and the patient requires lifelong annual ophthalmology review for glaucoma (tonometry) and uveal or ocular melanoma (dilated fundus examination). [7][8]

Self-test: a 9-year-old has a 3 mm blue-black papule on the back of the hand, unchanged for three years. What next, and what would change your plan?

The lesion is a classic common blue naevus — stable, small, in a typical site, with a homogeneous structureless blue dermoscopic pattern. The correct management is reassurance, photographic documentation and self-examination advice; no biopsy is needed. The plan changes — to complete excisional biopsy — the moment the lesion shows any change (growth, colour, shape, elevation), any symptom (itch, pain, bleeding), any atypical dermoscopic feature, or any diagnostic uncertainty. The cardinal rule: never reassure a blue lesion that is changing. [1]

Specific subtypes and syndromes

Cellular blue naevus

The cellular blue naevus deserves individual attention because it is the variant with malignant potential. It is larger (1 to 3 cm), deeper and often congenital, occupies the buttock, sacrum and scalp, and shows biphasic histology. Its management is complete surgical excision because the whole lesion must be examined to exclude atypia, and it carries a small risk of malignant blue naevus. Recurrence after incomplete excision is well described, and the recurrence may be histologically atypical. [1][3]

Naevus of Ota, naevus of Ito and Mongolian spot

Naevus of Ota is permanent and carries the ocular risk that defines its follow-up: roughly 10 percent of patients develop glaucoma (which can present at any age), and a smaller but significant minority develop uveal or ocular melanoma. Both mandate lifelong annual ophthalmology review — tonometry for glaucoma and dilated funduscopy for melanoma. The cutaneous pigmentation is treated with Q-switched laser for cosmetic reasons. [7][8] Naevus of Ito is the same lesion in the shoulder-girdle distribution and carries no ocular risk. The Mongolian spot fades by age two to four and needs only reassurance, with the safeguarding caveat that an atypical or ectopic lesion in an infant must be distinguished from a bruise. [7]

Carney complex (NAME and LAMB)

Multiple blue naevi are the cutaneous clue to Carney complex, an autosomal-dominant multiple-neoplasia syndrome (PRKAR1A). Its eponyms encode the features: NAME (Naevi, Atrial myxoma, Myxoid tumours, Ephelides) and LAMB (Lentigines, Atrial myxoma, Mucocutaneous myxomas, Blue naevi). The life-threatening component is the cardiac myxoma, so a patient with multiple blue naevi must be screened with an echocardiogram, and the endocrine overactivity — most characteristically Cushing syndrome from primary pigmented nodular adrenocortical disease — demands a targeted endocrine workup. Recognising the cutaneous sign can prevent sudden death from an atrial myxoma. [6]

[6]

Complications and pitfalls

The common blue naevus has effectively no complications: it is benign, stable, and does not transform. The cellular blue naevus carries the small risk of malignant transformation. Naevus of Ota causes glaucoma and uveal or ocular melanoma, and significant cosmetic distress from the facial pigmentation. Carney complex, signalled by multiple blue naevi, brings the sudden-death risk of atrial myxoma. [6][7]

[1]

The five classic pitfalls: (1) the melanoma pitfall — reassuring a changing blue lesion; (2) the amelanotic pitfall — missing a blue naevus that lacks the blue colour; (3) the laser-without-histology pitfall — lasering a lesion that turns out to be melanoma; (4) the Ota pitfall — failing to arrange ophthalmology review; (5) the multiple-blue-naevi pitfall — missing Carney complex and not screening for an atrial myxoma. [1][6]

Prognosis and disposition

The common blue naevus has an excellent prognosis — benign, unchanged for life, no malignant potential. The cellular blue naevus is benign in the great majority but carries a small, recognised risk of malignant blue naevus, which is why it is excised and followed. Malignant blue naevus has the prognosis of a melanoma of equivalent thickness, governed by Breslow thickness, ulceration and nodal status. Naevus of Ota requires lifelong ophthalmology surveillance; the Mongolian spot fades with an excellent prognosis. [1][7]

Disposition follows the lesion. A typical common blue naevus is managed in primary care or general dermatology with reassurance. A cellular blue naevus, any changing or atypical lesion, naevus of Ota, or multiple blue naevi should be referred to a dermatology or specialist pigmented-lesion service. The safety-net for every patient is the same advice: return if the lesion changes. [1]

Special populations

Children and neonates. The Mongolian spot is a normal variant in Asian and Black infants and fades by age two to four; parents need reassurance and the lesion should be documented. A congenital cellular blue naevus of the scalp or buttock merits excision. A congenital giant cellular blue naevus in a bathing-suit distribution (scalp, posterior neck, spine) demands an MRI of the brain and spine to exclude neurocutaneous melanosis. [3]

Pregnancy. Blue naevi and dermal melanocytoses (including naevus of Ota) may darken under hormonal influence. The approach is reassurance and dermoscopy; excision is deferred to the postpartum unless the lesion is changing, in which case it is biopsied on its own merits. [1]

Darker phototypes carry blue naevi and dermal melanocytoses more commonly and more visibly; the cosmetic impact of facial naevus of Ota is greater, and laser results are variable with a higher risk of post-inflammatory dyspigmentation. [8]

Anticoagulated patients. Excision of an atypical blue lesion should not be deferred for anticoagulation — minor cutaneous surgery is routinely performed without interrupting warfarin provided the INR is in range, and direct oral anticoagulants are managed per local protocol. A changing blue lesion is excised on its merits; the anticoagulation is managed around it. [1]

Evidence and regional differences

The conceptual framework for the blue naevus family was laid down in the 1994 differential-diagnostic review of González-Cámpora, which remains a useful single reference for the histological separation of common, cellular and related entities. [3] The 2016 concise review by Sugianto, Ralston and Metcalf is the best modern single overview of common, cellular and malignant blue naevus, and the 2017 comprehensive review by Borgenvik of blue-naevus-like and blue-naevus-associated melanoma underpins the malignant-transformation and biopsy rules. [1][2]

The biology is the same everywhere; what varies is the threshold for biopsy and the intensity of screening. [1]

Exam pearls

Exam application bank (NEET-PG and INICET)

One-line answer

A blue naevus is a benign melanocytic lesion of heavily pigmented dermal melanocytes in the reticular dermis, whose blue colour is an optical effect (Tyndall scattering) of deep pigment rather than blue pigment. The common blue naevus is a small, stable blue-black papule of the extremities; the cellular blue naevus is larger, deeper, on the buttock or scalp, with a small malignant potential; dermal melanocytoses (Mongolian spot, naevus of Ota, naevus of Ito) are persistent ectopic dermal melanocytes distributed by site. Stable classic lesions are observed; any changing or atypical blue lesion is excised to exclude melanoma; naevus of Ota needs lifelong ophthalmology; multiple blue naevi flag Carney complex. [1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose and route if drug therapy is standard. [1] Stem 2 — Unstable or complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote or reperfusion — and what you do in the first 15 minutes. [1] Stem 3 — Atypical group. Elderly, pregnancy, child or immunocompromised: how presentation and thresholds change. [1] Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1] Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU, ICU or theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition and classification
2. Pathophysiology chain
3. Bedside signs and criteria
4. Score with exact components
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline or trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Blue naevus and dermal melanocytosis. [1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the stable blue papule that wants a laser (answer)

The 25-year-old with a stable 4 mm blue-black papule on the back of her hand since childhood, who wants it lasered. What is it, what do you advise, and why not laser? Model: This is a classic common blue naevus — stable, small, homogeneous steel-blue on dermoscopy, in a typical site. The blue colour is a Tyndall effect of deep dermal melanin, not blue pigment. The first advice is reassurance; no treatment is needed. If she still wants it off, complete surgical excision is the appropriate technique because it removes the lesion and provides histology. Do not laser it — a laser destroys the lesion and forfeits the tissue diagnosis, and the one lesion you must never miss, melanoma, can mimic a blue naevus. A laser is reserved for confirmed-benign dermal melanocytoses such as naevus of Ota. [1]

Stem 2 — the changing blue scalp lesion (answer)

A 42-year-old man has a blue-black nodule on his scalp that has enlarged from 8 mm to 14 mm over four months, darkened, and bled once. Dermoscopy shows asymmetry, a blue-white veil and irregular vessels. What is the concern and the action? Model: This is melanoma (or a blue-naevus-like melanoma) until proven otherwise — the evolution (enlargement, darkening, bleeding) and the atypical dermoscopy (asymmetry, blue-white veil, irregular vessels) are incompatible with a stable common blue naevus. The action is a complete excisional biopsy with a narrow margin of normal skin, promptly — a shave or incisional biopsy is avoided because separating atypical cellular blue naevus from melanoma can require the entire architecture and the deep margin. Do not laser. If histology confirms malignant blue naevus, manage within the melanoma pathway (wide local excision guided by Breslow thickness, sentinel node biopsy as appropriate, staging imaging, MDT). [2]

Stem 3 — the sister with 'lots of these blue moles' (answer)

The 25-year-old now tells you her sister has many blue moles. What does that change? Model: Multiple blue naevi raise Carney complex (NAME/LAMB syndrome), an autosomal-dominant multiple-neoplasia disorder. The life-threatening component is the cardiac myxoma, so I would examine her whole skin for lentigines and myxomas, and arrange an echocardiogram and an endocrine workup (Cushing from primary pigmented nodular adrenocortical disease). I would offer genetic counselling if the syndrome is confirmed. [6]

The mantra: the colour is optical, the biology decides — observe the stable classic lesion, excise anything that changes, and never laser a blue lesion you have not first confirmed benign. [1][7]

References

1. [1]Sugianto JZ, Ralston JS, Metcalf JS Blue nevus and malignant blue nevus: A concise review Semin Diagn Pathol, 2016.PMID 27199078
2. [2]Borgenvik TL, Karlsvik TM, Ray S Blue nevus-like and blue nevus-associated melanoma: a comprehensive review of the literature ANZ J Surg, 2017.PMID 28318130
3. [3]González-Cámpora R, Galera-Davidson H, Vázquez-Ramírez FJ Blue nevus: classical types and new related entities. A differential diagnostic review Pathol Res Pract, 1994.PMID 7984522
4. [4]Salas-Callo CI, Riera-Monroig J, Podlipnik S Blue Nevus With Rosettes on Polarized Light Dermoscopy Dermatol Pract Concept, 2020.PMID 31921504
5. [5]Satolli F, Gandolfi M, Rovesti M Blue nevus of the nail: A case report and review Dermatol Ther, 2020.PMID 32500667
6. [6]Bertherat J Carney complex (CNC) Orphanet J Rare Dis, 2006.PMID 16756677
7. [7]Williams NM, Gurnani P, Labib A Melanoma in the setting of nevus of Ota: a review for dermatologists Int J Dermatol, 2021.PMID 32808287
8. [8]Shah VV, Bray FN, Aldahan AS Lasers and nevus of Ota: a comprehensive review Lasers Med Sci, 2016.PMID 26563954