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به نام خدا وند بخشنده و مهربان. Hyperpigmentation disorders. Dr Gita Faghihi Dermatology ASSOc. Professor Isf.Univ.Med.Sci. Skin color. Depends on: Amount of : Melanin , Chromophores such as :hemoglobin, carotenoids…. Causes of skin hyperpigmentation.

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hyperpigmentation disorders

Hyperpigmentation disorders

Dr Gita Faghihi




skin color
Skin color

Depends on:

Amount of :

Melanin ,

Chromophores such as :hemoglobin, carotenoids…

causes of skin hyperpigmentation
Causes of skin hyperpigmentation
  • Increase in amount of melanin or number of active melanocytes
  • deposition of exogenous pigments,…
  • Reticulate acropigmentation of Kitamura & Dohi
  • Naegeli–Franceschetti–Jadassohnsyndrome
  • Dyskeratosiscongenita , .…


  • Lentigo/Lentiginosis
  • Melasma
  • Erythema dyschromicumperstans
  • Lichen planuspigmentosus
  • Café au laitspot
  • Poikiloderma (Poikiloderma of Civatte),,(Poikilodermavasculareatrophicans)
  • Riehlmelanosis
  • PIP
  • Acanthosisnigricans
  • Periorbital hyperpigmentation
  • Photoleukomelanodermatitis of Kobori
  • Transient neonatal pustularmelanosis


  • Incontinentiapigmenti
  • Scratch dermatitis(flagellate bleomycin induced)
  • Shiitake mushroom dermatitis

linearity of the lesions is probably related to Blaschko’s lines, which suggests that the predisposition to develop ,,determined during embryogenesis


Others/unclassified(due to drugs, ,exogenous..)

  • pigments iron: Hemochromatosis • Iron metallic discoloration • Pigmented purpuricdermatosis (Schamberg disease, Majocchi's disease, Gougerot–Blum syndrome, Doucas and Kapetanakis pigmented purpura/Eczematid-like purpura of Doucas and Kapetanakis, Lichen aureus, Angiomaserpiginosum) • Hemosiderin hyperpigmentation
  • other metals: Argyria • Chrysiasis • Arsenic poisoning • Lead poisoning • Titanium metallic discoloration
  • Carotenosis , Tattoo,Tarmelanosis
postinflammatory hyperpigmentation pih
Postinflammatory hyperpigmentation (PIH)

acquired hypermelanosis…… after cutaneous inflammation or injury ….can arise in all skin types,


more frequently affects darker patients,

including : African Americans, Hispanics/Latinos, Asians

PostinflammatoryhyperpigmentationPIHin Fitzpatrick skin type 4 vs. 6Note the greater intensity of pigmentation in darker skin
a wide range of etiologies for pih
A wide range of etiologies for PIH:
  • Acne
  • Infect.(Dermatophytoses, viral exanthemsbacterials..,
  • allergic reactions ( insect bites or a contact dermatitis, medication-induced PIH from(.. hypersensitivity reactions,
  • papulosquamousdiseases (psoriasis or lichen planus, PR
  • cutaneous injury from irritants, burns, or cosmetic procedures
in pih melanocyte activity to be stimulated by
In PIH:melanocyte activity ….to be stimulated by:
  • LTC4,
  • prostaglandins E2 and D2, thromboxane-2, interleukin (IL)-1, IL-6,
  • tumor necrosis factor (TNF)-α,
  • epidermal growth factor, and
  • reactive oxygen species .
first line therapy pih typically consists of
First-line therapy (PIH) typically consists of :

Photoprotection(a sunscreen) + topical depigmenting

Topical tyrosinase inhibitors, such as:




arbutin, and

certain licorice extracts,

can effectively lighten areas of hypermelanosis.

recent clinical studies have shown that
Recent clinical studies have shown that:
  • topical 5% methimazole,
  • Topical2% dioic acid

can successfully treat hyperpigmentation secondary to a variety of etiologies../(PIH).


is an acquired symmetrical pigmentary disorder where confluent grey-brown patches typically appear on the face.

%90 of individuals are women

It is A disease with considerable psychological impacts

The management of melasma is challenging and requires a long-term treatment plan.

factors implicated in the etiopathogenesis of melasma
factors implicated in the etiopathogenesis of melasma
  • One of the most important factors in the development of melasma is ultraviolet exposure from sunlight or other sources
  • photosensitizing and anticonvulsant medication
  • mild ovarian or thyroid dysfunction
  • certain cosmetics.
the centrofacial pattern
The centrofacial pattern

is the most common and involves:

  • the cheeks,
  • nose,
  • forehead,
  • upper lip, and
  • chin.

Wood's lamp examination is of benefit classifiyingmelasma(epidermal,dermal,mixed/..)

treatment of melasma remains a challenge
Treatment of melasma, remains a challenge
  • Kligman and Willis :



tretinoin (0.1%)


dexamethasone (0.1%).


In 2006, (FDA) released a statement proposing a ban on all OTC HQ agents based on rodent studies, which suggested that oral HQ may be a carcinogen


therapeutic effects
Therapeutic effects:

azelaic acid inhibit the energy production and/or DNA synthesis of hyperactive melanocytes,



This may also account for the beneficial effect on


azelaic acid 20% cream twice daily over a period of 12 weeks

melasma new treatment modalities
Melasma & new treatment modalities:
  • Tranexamic acid tabletswere prescribed at a dosage of 250 mg twice daily for a therapeutic period of 6 months.

75% good to excellent response

No side effects except hypomenorrhea and mild GI upset in <10%

other melasma drugs
Other Melasma drugs:
  • Arbutin ,(3-5 %) a herbal agent ,,

higher concentrations of arbutin can lead to a paradoxical hyperpigmentation.

Synthetic forms of arbutin, alpha-arbutin and deoxyarbutin,

exhibit greater ability to inhibit tyrosinase

Adding kojicacid, betulinic acid and niacinamide

To arbutin gives better inhibition of Tyrosinase and higher efficacy

cont melasma treatment
Cont… Melasma treatment

combination of

  • Tretinoin , and
  • kojic acid, and
  • azelaic acid

improve the melasma very effectively .

other melasma therapeutics
Other… melasma Therapeutics/ :
  • There is a lot of documented evidence about efficacy of adapalene gel 0.1%

in melasma

oral treatments
Oral treatments
  • Dioic acid
  • Resveratrol
procedures for melasma include
Procedures for melasmainclude:
  • chemical peel (such as glycolic acid,SA.. …etc..)
  • microdermabrasion
  • Laser (fractional ,ruby ,low fluence Q-switch nd:YAG …)
  • intense pulsed light (IPL)
erythema dyschromicum perstans

Most common in individuals with skin phototypesIII–IV(women are more commonly affected)

Ashy, gray–brown to blue–gray macules and patches in a symmetric distribution

Lesions favor the neck, trunk and proximal extremities


■ Genetic susceptibility

■Toxic effects of chemicals such as ammonium nitrate or barium sulphate

■ worm infestation

■ Viral infections

■ Adverse effect of drugs and medications

erythema dyschromicum perstans also known as ashy dermatosis
Erythema dyschromicumperstans(also known as "Ashy dermatosis," )
  • is a skin condition with age of onset almost always before 40 years old
  • characterized by skin lesions that are usually symmetrical and generalized

A consistently effective treatment is not currently available

But some case series responded to oral corticosteroids

treatment ashy dermatosis
Treatment/ ashy dermatosis ...
  • The use of narrow-band UVB phototherapy has shown success in a few patients
  • A low-potency topical steroid applied twice a day to the affected areas may be used, with or without a 4% hydroquinone cream for the hyperpigmentation
  • A patient from Turkey was described to have responded remarkably well to treatment with dapsone
lichen planus pigmentosus

Lichen planuspigmentosus (LPP) is an uncommon variant of lichen planus that favors individuals with skin phototypes III–V, including those from India Latin America and the Middle East.

LPP usually has its onset during the third or fourth decade of life; it presents as oval or round, brown, gray–brown or dark brown macules and patches in either sun-exposed areas (especially the forehead, temples and neck) or intertriginouszones.

There may be no associated symptoms versus mild pruritus or burning, and, in contrast to some cases of EDP, early lesions do not have an erythematous border

Gray–brown to dark brown macules and patches in either a photodistribution or an inverse (intertriginous) pattern

a spectrum of disorders characterized by the deposition of amyloid within the skin and other tissues .

  • Primary (localized) cutaneous amyloidosis is subdivided into three major forms– macular, lichenoid and nodular

the first two are associated with hyperpigmentation.

The most common locations are the upper back (macular amyloidosis) and the extensor surface of the lower extremities (lichen amyloidosis).

Areas of involvement are often pruritic, and because rubbing plays a key role in the production of lesions, there is a characteristic rippled pattern with parallel bands or ridges of hyperpigmentation.

Histologically, melanophages as well as amyloid deposits that stain positively with antikeratin antibodies are seen within the upper dermis.


Diagnosis:Primary cutan .Amyloido/congored staining under polarized light forms a very sensitive and definitive methodfor confirmation.

treatment modalities in macular amyloidosis and lichen amyloidosis
treatment modalities in macular amyloidosis and lichen amyloidosis
  • relief of pruritus.

•Sedating antihistamines have been found to be moderately effective.

  • Topical dimethyl sulfoxide (DMSO), a chemical solvent
  • intralesionalsteroids are beneficial if combined with other modalities.
  • Treatment with ultraviolet B (UV-B) light can provide symptomatic relief.

improvement of lichen amyloidosis with pulsed dye laser therapy595-nm-.Both pruritus and the papular eruption of lichen amyloidosis improved

reticulate acropigmentation of kitamura1
Reticulate acropigmentation of Kitamura

usually autosomal-dominant fashion

punctate, irregular, atrophic, brown macules

involving the dorsa of the hands and feet, the dorsa of the knees

the extensor surface of the neck,

both axillary regions, the abdominal skin


the inguinal region,

treatment reticulate acropigmentation of kitamura
Treatment: Reticulate acropigmentation of Kitamura

Most treatments attempted have been unsuccessful,

  • but an attempt to treat the disease with

20 % azelaicacid gave significant improvement

  • Er-YAG laser treatment
reticulate acropigmentation of dohi rad
Reticulate acropigmentation of Dohi (RAD)

is characterized by the presence of hyperpigmented and hypopigmented pinpoint or pea-sized macules over the dorsa of the hands and feet and occasionally on the arms and legs

Naegeli-Franceschetti-Jadassohn(NFJ) syndromeis a reticulate pigmentarydisorder and a type of Ectoderm/ dysplasia/ syn..

Naegeli-Franceschetti-Jadassohn (NFJ) syndrome is a rare autosomal dominant form of ectodermal dysplasia that affects the skin, sweat glands, teeth and PPK .


Hypohidrosis dental anomalies PPKNo treatment is effective in Naegeli-Franceschetti-Jadassohn(NFJ) syndrome. As with other ectodermal dysplasias, exposure to heat should be limited and sufficient hydration is recommended.Tooth care to prevent early caries is indicated. Doxycycline has been found to interfere with tumor (TNF-alpha)–mediated signaling and apoptosis may have a role in future treatment

dyskeratosis congenita
  • Affected individuals often have fingernails and toenails that grow poorly or are abnormally shaped.
  • They also often have changes in skin coloring (pigmentation), especially on the neck and chest, in a pattern often described as "lacy."
  • White patches inside the mouth (oral leukoplakia
dyskeratosis congenita1

major consequence being:

  • bone marrow failure and/at increased risk of developing leukemia
  • People with dyskeratosiscongenita are also In addition have a higher risk of other cancers, especially head, neck, anus, or genitals
poikiloderma of civatte
Poikiloderma of Civatte

is a cutaneous condition and refers to :

  • Reticulated red-brown patches with telangiectasias

Poikilodermaof Civatte refers to erythema associated with a mottled pigmentation seen on the cheeks & sides of the neck

reddish-brown pigmentation and telangiectasis surmounted with pale, tiny follicular papules involving periauricular area
linear and whorled nevoid hypermelanosis lwnh
Linear and whorled nevoid hypermelanosis(LWNH)
  • Reticulate and zosteriform(“Zebra-like”) hyperpigmentation, in whorls and streaks
  • is a disorder of pigmentation that develops within a few weeks of birth and progresses for one to two years before stabilizing.
treatment lwnh
Treatment ((LWNH)) :
  • chemical peel
  • Q-S laser

A little help in some patients but, a proven treatment approach for LWNH does not exist.

IncontinentiapIgmenti(x-linked dominant)typical neonatal vesicular rash with eosinophilia; typical blaschkoidhyperpigmentation
cutaneous findings are the most common manifestation of ip
Cutaneous findings are the most common manifestation of IP

and usually represent the presenting signs. They are divided into four overlapping stages:

  • (1) vesiculobullous, which favors the extremities during the first few months of life (but occasionally recurs during childhood in association with a febrile illness);
  • (2) verrucous, which favors the distal extremities in patients one to six months of age (and sometimes adolescents);
  • (3) hyperpigmented, which favors the trunk and intertriginous sites from three months of age through adolescence; and
  • (4) hypopigmented/atrophic, which affects the calves in adolescents and adults

The hyperpigmentation of the third stage(IP)is seen in just about all patients, beginning at 3-6 months of life. In contrast to the vesicular and verrucous lesions, the pigmentary changes are generally truncal in distribution and not proceeded by inflammatory changes.

ip assoc
  • Hyperpigmented lines arefading in adolescence
  • linear, atrophic hairless lesions.
  • dental anomalies,
  • alopecia, wooly hair, and
  • abnormal nails
  • Seizure or MR
  • Retinal /ophthalmic disorders(blindness..)
laugier hunziker syndrome
Laugier-Hunziker syndrome

is a rare acquired macular hyperpigmentation of oral mucosa and lips frequently associated with longitudinal pigmentation of the nails

The pathogenesis is unknown,


no systemic involvement no family history of the disease or no intestinal polyposis, or

no malignant predisposition has been described

laugier hunziker syndrome1
Laugier-Hunziker syndrome

flat brown marks on the lips and inside the mouth, and frequently brown stripes on the nails.


Rubbing the skin lesions causes a hive-like bump. Younger children may develop fluid-filled blisterThe face may also flushed.In severe cases, the following symptoms :•Diarrhea•Fainting•Headache• tachycardia


usually affects the neck, arms, legs and trunk of children and young adults. The rash consists of reddish-brown spots


The exact cause of this uncommon disease is unknown but recent research suggests genetic change in a protein (called c-kit) on the surface of mast cells may result in the abnormal proliferation of these cells.

  • Variety of factors can cause or worsen the symptoms of urticariapigmentosa:
  • Physical stimuli such as heat, friction, and excessive exercise
  • Bacterial toxins
  • Venom
  • Eye drops containing dextran
  • Alcohol
  • Morphine
  • Emotional stress
Cetirizineloratadinefexofenadinemore superior to first generations Mast cell stabilizerscalcium channel blockers

Treatment of mastocytosis



sun-exposed areas

mucosal lentigines also known as labial penile and vulvar melanosis and melanotic macules
Mucosal lentigines(also known as "Labial, penile, and vulvar melanosis," and "Melanotic macules")

is a cutaneous condition characterized by :

light brown macules on mucosal surfaces

Lentiginosisrefers to the presence of lentigines in large numbers or in a distinctive configuration
leopard syndrome
LEOPARD syndrome

LEOPARD syndrome

  • Lentigines,
  • electrocardiographic conduction defects,
  • ocular hypertelorism,
  • pulmonary stenosis,
  • abnormal genitalia,
  • retardation of growth, and
  • deafness syndrome)

(ie, multiple lentigines syndrome) is a complex dysmorphogenetic disorder that is transmitted as an autosomal-dominant trait

caf au lait macules calm
Café au lait macules(CALM)
  • pigmented birthmarks
  • The name café au lait is French for "coffee with milk" and refers to their light-brown color

Nevus of Ota

  • Epidemiology

is more common in Japanese, in women (9 times) with onset either in the perinatal period or around puberty

  • Etiology

genetic factors are thought to be important but familial cases are rare.


  • represents aborted embryonic migration of melanocytes from neural crest to epidermis. Late pubertal onset is explained by pigmentation of the amelanotic nevoid cells present at birth by adolescent spurt of sex hormones.

Clinical features

  • is characterized by speckled or mottled coalescing blue-grey pigmentation of the area supplied by ophthalmic and maxillary divisions of trigeminal nerve. It is usually unilateral (90%).
topical therapy is of no value q switch lasers
topical therapy is of no valueQ-switch lasers
  • The sclera is involved in two-thirds of cases (causing an increased risk of glaucoma).
Crops of red-brown flat patches with cayenne pepper spots on their borders appear for no apparent reason. most common on the lower legs,

Schamberg disease

topical steroids can be helpful for itching but rarely clear the capillaritis
Topical steroids can be helpful for itching but rarely clear the capillaritis.

Currently available lasers are

not particularly helpful for pigmented purpuricdermatoses

treatment cont d
  • (pentoxifylline) circulation,
  • Vitamins (Vitamin C 500mg twice daily )

Bioflavonoid (Complex with Rutin)

avitaminosis esp vit b12 def caused hyperpig of skin resolves after vit supplement
Avitaminosis esp.Vit. B12 Def.Caused hyperpig. of skinresolves after Vit . Supplement
in patients with vitamin b12 deficiency the following skin lesions are reported
In patients with vitamin B12 deficiency, the following skin lesions are reported:
  • skin hyperpigmentation,
  • vitiligo,
  • hair changes,
  • recurrent angular stomatitis

Hyperpigmentation of the extremities

especially over the dorsum of the hands and feet, with accentuation over the interphalangealjoints and terminal phalanges


Drug-induced pigmentary abnormalities classified into 3 groups, hyperpigmentation/melanosishypopigmentation/leukodermaand dyspigmentationor occurrence of unusual skin color.

drug induced hyperpigmentation

Although several classes of drugs are known to induce ‘hyperpigmentation’, the most common are:

  • minocycline,
  • phenothiazines
  • antimalarials,
  • chemotherapeutic agents
  • Zidovudine
  • Amiodarone

mucosal pigmentations and Longitudinal or horizontal melanonychia may also be present


pigmentation usually resolves with discontinuation of the offending drug,

but the course may be prolonged

photoleukomelanodermatitis of kobori
Photoleukomelanodermatitis of Kobori
  • thiazides
  • tetracyclines

followed by exposure to sunlight

Edematous erythema with slight itching appeared on the sun-exposed areas ,the cutaneous lesions almost disappeared after drug stop

but pigmentations and depigmentationsdevelop in spots in sun-exposed areas.

Photopatch and oral challenge tests were positive.


Facial melanoses (FM) are a common presentation in dermatologic patients, causing cosmetic disfigurement with considerable psychological impact.

Some of the well defined causes of FM include melasma, Riehl'smelanosis, Lichen planuspigmentosus, and poikiloderma of Civatte. But there is considerable overlap in features amongst the clinical entities.

Etiology in most of the causes is unknown, but some factors such as UV radiation in melasma, exposure to chemicals in EDP, exposure to allergens in Riehl'smelanosis are implicated.

Diagnosis is generally based on clinical features.

The treatment of FM includes removal of aggravating factors, vigorous photoprotection, and some form of active pigment reduction either with topical agents or physical modes of treatment.

Topical agents include hydroquinone (HQ), which is the most commonly used agent, often in combination with retinoic acid, corticosteroids, azelaic acid, kojic acid, and glycolic acid.

Chemical peels are important modalities of physical therapy, other forms include lasers and dermabrasion.

The end


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