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.
Dr Gita Faghihi
Amount of :
Chromophores such as :hemoglobin, carotenoids…
linearity of the lesions is probably related to Blaschko’s lines, which suggests that the predisposition to develop ,,determined during embryogenesis
acquired hypermelanosis…… after cutaneous inflammation or injury ….can arise in all skin types,
more frequently affects darker patients,
including : African Americans, Hispanics/Latinos, Asians
Photoprotection(a sunscreen) + topical depigmenting
Topical tyrosinase inhibitors, such as:
certain licorice extracts,
can effectively lighten areas of hypermelanosis.
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.
is the most common and involves:
Wood's lamp examination is of benefit classifiyingmelasma(epidermal,dermal,mixed/..)
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
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
75% good to excellent response
No side effects except hypomenorrhea and mild GI upset in <10%
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
improve the melasma very effectively .
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
But some case series responded to oral corticosteroids
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
a spectrum of disorders characterized by the deposition of amyloid within the skin and other tissues .
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.
•Sedating antihistamines have been found to be moderately effective.
improvement of lichen amyloidosis with pulsed dye laser therapy595-nm-.Both pruritus and the papular eruption of lichen amyloidosis improved
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,
Most treatments attempted have been unsuccessful,
20 % azelaicacid gave significant improvement
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) 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
major consequence being:
is a cutaneous condition and refers to :
Poikilodermaof Civatte refers to erythema associated with a mottled pigmentation seen on the cheeks & sides of the neck
A little help in some patients but, a proven treatment approach for LWNH does not exist.
and usually represent the presenting signs. They are divided into four overlapping stages:
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.
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
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.
Treatment of mastocytosis
is a cutaneous condition characterized by :
light brown macules on mucosal surfaces
(ie, multiple lentigines syndrome) is a complex dysmorphogenetic disorder that is transmitted as an autosomal-dominant trait
Q -Switch lasers
is more common in Japanese, in women (9 times) with onset either in the perinatal period or around puberty
genetic factors are thought to be important but familial cases are rare.
Currently available lasers are
not particularly helpful for pigmented purpuricdermatoses
Bioflavonoid (Complex with Rutin)
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.
Although several classes of drugs are known to induce ‘hyperpigmentation’, the most common are:
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
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.
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