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Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Normal variations
  5. Abnormal hyperpigmentation
  6. The targeted treatment options of epidermal/dermal pigmentation
  7. References

Background  Pigment formation is highly complex. It is involved in inflammation, sun protection and many other processes. For practical purposes, such as exposure time for sun tanning, six skin types are distinguished according to Fitzpatrick, listed in decreasing lightness. The hyperpigmentation commonly occurs in Fitzpatrick skin types III to VI and can have a considerable impact on quality of life.

Material & Methods  In this article we will give an overview of normal variations of pigmentation and the most often common pigment abnormalities. It also reviews diagnostics and the current targeted treatment options of epidermal and dermal pigmentation.

Results  There are multiple hyperpigmented skin lesions, classification of pigmentation is based on histology or Woods light examination. Bleaching agents with phenolic compounds with non-phenolic agens as follow-up therapy appears to be the most beneficial treatment options for the hyperpigmentation.

Conclusions  The effective treatment of pigment disorders is characterized by influence of melanin formation, but the therapy should be based on a the correct diagnosis and always targeted to the other histopathological processes in the skin. The Woods light examination shows clinical aspect of the lesions and may be helpful in the determination of the diagnosis.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Normal variations
  5. Abnormal hyperpigmentation
  6. The targeted treatment options of epidermal/dermal pigmentation
  7. References

The tone of human skin can vary from a dark brown to nearly a colourless pigmentation, which may appear reddish because of the blood in the skin. Skin colour is determined primarily by the amount and type of melanin, the pigment in the skin. Variation in skin colour is largely because of genetics.

Virtually, every society tends to assign some valuation to skin colour differences, especially when these have corresponded to existing political and economic differentiations. Social isolation of individuals with discoloration in some countries such as India does happen because of the easy association with diseases like leprosy.

Differences in skin tone are the most readily perceptible phenotypes of human populations, and hence have historically lent itself to colour terminology for race. For practical purposes, such as exposure time for sun tanning, six skin types are distinguished according to Fitzpatrick, listed in decreasing lightness.

Pigment formation is highly complex. It is involved in inflammation, sun protection and many other processes. Melanocytes in cooperation with enzyme tyrosinase are responsible for the production and conversion of dopa to melanin; melanosomes containing pigment are ingested by the keratinocytes, and the melanin is shed with the stratum corneum cells. Melanin production and skin colour are affected not only by keratinocytes but also by Langerhans cells, mast cells and probably by lymphocytes. The effective treatment of pigment disorders is characterized by influence of melanin formation, but must be always targeted to the other histopathological processes in the skin.

The therapy of hyperpigmentation is based on accelerate epidermal turnover with removal of pigment in superficial layer (glycolic acid, salicylic acid and lactic acid), increase in melanosome transfer and downregulation of tyrosinase (Tretinoin), retard melanocyte proliferation, melanocyte secretory function and inhibition of inflammation (corticosteroids) and inhibition of enzyme tyrosinase with decrease melanogenesis (hydroquinone).

Classification of pigmentation based on histology (or Woods light examination 320–400 nm).

Epidermal melanosis

The hyperpigmented skin shows only excessive quantities of melanin, but a normal number of melanocytes. Clinical examples include café-au-lait spots and urticaria pigmentosa. The borders of these spots are sharply demarcated during Woods light examination and have dark brown colour. A drawing of normal skin is provided for comparison. This hyperpigmentation is most responsive to local treatment.

Dermal melanosis

This type of hyperpigmentation is caused by melanin within the dermis, between bundles of collagen, or within melanophages (clear cells). The epidermal melanin is normal. Clinical examples include fixed drug eruption, incontinentia pigmenti, lichen planus and many forms of post-inflammatory hyperpigmentation. The Woods light does not show any sharp demarcations of the lesions; the colour of the lesions is brown-grey. A drawing of normal skin is provided for comparison. This melanin incontinence and phagocytosis of melanosomes by macrophages is less responsive to local therapy such as bleaching creams containing for example hydroquinone.

Mixed type

This hyperpigmentation is characterized with increased melanin in epidermis and melanophages in dermis. The most common example is post-inflammatory hyperpigmentation after traumatization (peeling, laser treatment) or inflammatory dermatoses (acne). The Woods light inspection shows clinical aspect of both pigmentation types. The local bleaching is effective only in epidermal component of hyperpigmentation.

In the following section, we will give an overview of normal pigmentation, the most often common pigment abnormalities and the targeted treatment options of epidermal/dermal hyperpigmentation.

Normal variations

  1. Top of page
  2. Abstract
  3. Introduction
  4. Normal variations
  5. Abnormal hyperpigmentation
  6. The targeted treatment options of epidermal/dermal pigmentation
  7. References

Futcher’s or Voigt’s lines

These lines are normal colour patterns seen in pigmented individuals, especially in Asian people. This demarcation between darker and normal pigmented skin can be found on the upper arm anteromedially, the posterior portion of the lower limb, the pre-sternal area, the post-eromedial area of the spine and the bilateral aspect of the chest. There are no symptoms. The contact dermatitis and other inflammatory dermatoses can create similar lines of demarcation.

Hyperpigmentation at the extensor side of the joints

Stretching of the skin at the joints can possibly be a mechanical trigger for the melanocytes.1 Next causation of striking skin hyperpigmentation over the joints can be an episode of inflammatory arthritis. The phenomenon may be related to increased vascularity over areas of subcutaneous cellulitis.

Palmar and plantar hyperpigmentation

Macular hyperpigmentation usually involves palms and soles of healthy black people and is characterized by linear hyperpigmented macules. The lesions of Addison’s disease, lues, ephelides, nevi and melanoma form the base of differential diagnosis of palmar and plantar hyperpigmentation.

Familiar periorbital hyperpigmentation

Periorbital hyperpigmentation is a generally benign, extremely common condition which is characterized by dark circles around the eyes, often familial, and frequently found in individuals with dark pigmentation or Mediterranean ancestry. Usually, hyperpigmentation starts in the lower eyelid during childhood and progresses with age.2 A topic patients may also exhibit per orbital pigmentation (allergic shiners) thus none of the topical bleaching therapies will be effective.

Mongolian spot

Mongolian spots represent areas of dermal melanocytosis as result of arrest in migration of melanocytes from the neural crest to the epidermis. Approximately 80–100% of the Asian and black newborn have them.1 The grey-black macular lesions may be solitary or multiple. The sacrum, buttocks and back are the most common locations. These symptoms tent to fade in time.

Abnormal hyperpigmentation

  1. Top of page
  2. Abstract
  3. Introduction
  4. Normal variations
  5. Abnormal hyperpigmentation
  6. The targeted treatment options of epidermal/dermal pigmentation
  7. References

Post-inflammatory hyperpigmentation

Post-inflammatory hyperpigmentation is one of the most common and rather persistent in dark-skinned people. The different skin conditions like inflammatory dermatoses, trauma and medical interventions (such as laser therapy) are in dark people often the aetiology of remaining hyperpigmentation. Sunlight, some medication and chemicals often worsen the spots. The dyschromia follows the pattern and distribution of the original dermatoses, but its intensity is not necessarily related to the degree of previous inflammation. Epidermal pigmentation is mostly brown and fades out in several months. Dermal pigmentation has a grey-brown colour and is generally permanent for years.3 Treatment of post-inflammatory hyperpigmentation is difficult. The primary goal of therapy is treating the aetiology. Most significant clinical improvement for the lesions is directly correlated with different topical therapies such as depigmenting agents. Particularly important is the combination of these therapies with the frequented use of sunscreens.

Melasma/Chloasma

Most melasma develops on the faces of some women who are pregnant or taking birth control pills. Other aetiological factors include genetic influence, exposure to UV-radiation, phototoxic drugs, cosmetics and anti-convulsants. The usually symmetrical hyperpigmented spots are most prominent on the forehead, malar eminence and cheeks anterior to the ears. Sometimes it affects the upper lip and the chin. The goal of therapy is to decrease the production of melanin without killing melanocytes. Current treatment options include bleaching agents, chemical peels and the frequented use of sunscreens.

Ashy dermatosis

Ashy dermatosis or erythema dyschromicum perstans is a progressive pigmented disorder. The pathogenesis of this discoloration remains unclear. Most cases have been in blacks, especially those from Latin America and Asia. The disease has been called ashy dermatosis because of its peculiar slate like grey coloration occasionally demonstrated, in its beginning stages, by an erythematous raised border.4 The disorder is usually asymptomatic. Multiple brown-grey macules and patches develop over the trunk and extremities. The face and neck, palms, soles and mucous membranes are usually not affected. The differential diagnosis should include lichen planus pigmentosus, fixed drug reaction, Addison’s disease, argyria, photodermatoses or leprosy. None of the therapies is presently effective.5 Patients, especially those suffering from hyperpigmentation on visible places such as the face, hands and neck, can camouflage these areas using skin-coloured cosmetics.

Nevus of Ota and nevus of Ito

These nevi are seen in all races, but affect mostly Asian people. Nevus of Ota (nevus fuscocoeruleus ophthalmomaxillaris) is a blue to grey-brown pigmented patch located on the face, usually within the distribution of the ophthalmic and maxillary branches of the trigeminal nerve with involving of the sclera in some cases. The nevus of Ito is located unilaterally on the shoulder and neck. The macules are present at birth or soon thereafter. The start of puberty is likewise possible. The lesions look like Mongolian spots but are not self-limiting. Malignant transformation has been observed in rare instances. The therapy with pigment laser, has been in the literature reported as an effective treatment.6

Lentigo solaris

These lesions are characterized by increased numbers of epidermal melanocytes that are producing excessive quantities of melanin within the epidermis. Commonly, the epidermal morphology is also hyperplastic. Lentigines are the prototype of melanocytic epidermal hypermelanosis accompanied by epidermal hyperplasia. Histologically, they are characterized by an increased number of melanocytes producing an excessive amount of melanin in the epidermis and prolongation of the epidermal rete pegs. Bleaching creams containing hydroquinone are not usually effective. Kligman found that lentigines solares were resistant to topical treatment with a combination of tretinoin, hydroquinone and dexamethasone in a hydrophilic ointment. Solar lentigo is actually being treated with an increasing variety of ablative and non-ablative lasers.

The targeted treatment options of epidermal/dermal pigmentation

  1. Top of page
  2. Abstract
  3. Introduction
  4. Normal variations
  5. Abnormal hyperpigmentation
  6. The targeted treatment options of epidermal/dermal pigmentation
  7. References

Epidermal pigmentation responds to many treatments, but concomitant dermal pigment is often present in the lesions.

The dermal pigmentation is less/not responsive to local therapy such as bleaching creams. The laser therapy is in many cases of dermal melanin not effective too. The post-inflammatory hyperpigmentation after laser treatment is frequently occurring.

For the epidermal pigmentation still is hydroquinone one of the most effective depigmenting agents.

Bleaching agents with phenolic compounds are: hydroquinone (2–5%), monobenzon (20%), 4-methoxy-phenol (20%), isopropylcatechol and N-acetyl-4-S-cystaminylphenol.

With non-phenolic compounds are: N-acetylcystein, 4-N-butylresorcinol, tretinoin – (0.05–0.1%), azealic acid (20%), kojic acid, ascorbic acid and corticosteroids. Combinations: Kligman formula (tretinoin, hydroquinone and dexamethasone).

The often used hydroquinone containing bleaching formula is mostly effective, but has the following disadvantages: high recurrence rate, first effect after 3–4 months applications, high concentration required and not effective in all cases. The following side-effects after prolonged use may occur: contact dermatitis/irritation, dermatosis ‘en confetti’ and risk of exogenous ochronosis.

The indication for 4-N-butylresorcinol is the role of keeping up the bleaching result after ending therapy with hydroquinone. The application of this agents by a mild form of epidermal hyperpigmentation can be effective too. The 4-N-butylresorcinol is optimal indicated for long-term use because of absence of the side-effects as appear by the use of hydroquinone and other phenol containing creams.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Normal variations
  5. Abnormal hyperpigmentation
  6. The targeted treatment options of epidermal/dermal pigmentation
  7. References