Hyperpigmentation

Pigmentation of the skin normally varies according to racial origin (see Fitzpatrick phototypes) and the amount of sun exposure. Pigmentation disorders are often more troublesome in skin of colour.

The pigment cells or melanocytes are located at the base of the epidermis and produce the protein melanin. Melanin is carried by keratinocytes to the skin surface. The melanocytes of dark skinned people produce more melanin than those of people with light skin. More melanin is produced when the skin is injured, for example following exposure to ultraviolet radiation. The melaninisation process in dark skin is protective against sun damage, but melanisation in white skin (for example after sunburn) is much less protective.

Hormonal effects of oestrogen during pregnancy or due to medication can cause pigmentation of nipples, vulva and abdomen (linea nigra).

Some skin diseases and conditions result in generalised or localised hyperpigmentation (increased skin colour), hypopigmentation (reduced skin colour), or achromia (absent skin colour).

A Wood lamp may be used to assess pigmentation during the examination of the skin, as pigmentary changes are often easier to identify while exposing the affected skin to long wavelength ultraviolet rays (UV-A).

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Generalised hyperpigmentation may rarely arise from excessive circulating melanocyte stimulating hormone (MSH), when it often has a bronze hue. It occurs:

In 95% of patients with Addison disease when it is more prominent on pressure areas, in skin folds, on scars and within the mouth
In 90% of patients with haemochromatosis, when it is more prominent on the genitals, in skin folds and on sun-exposed sites
Rarely in metastatic melanoma: diffuse melanosis cutis
In people treated with afamelanotide

Localised pigmentation may be due to melanin, haemosiderin or externally-derived pigment.

If dark patches are observed, the main diagnoses to consider are:

Benign pigmented skin lesions, such as melanocytic naevi (moles), seborrhoeic keratoses and lentigos
Skin cancers, such as melanoma and pigmented basal cell carcinoma
Post-inflammatory pigmentation due to prior injury, current or prior inflammatory skin disease such as eczema, especially in dark skinned individuals or fixed drug eruption
Current or previous superficial skin infection, particularly pityriasis versicolor and erythrasma.
Chronic pigmentary disorders, particularly melasma (facial pigmentation)
Photocontact dermatitis to certain plants
Thickened skin eg acanthosis nigricans or ichthyosis
Pigmented purpura due to bleeding into the skin, eg capillaritis, senile purpura, as a sign of venous disease, or after varicose vein surgery or sclerotherapy

If pigmentation affects an exposed site, daily application of broad-spectrum SPF 50+ sunscreen is important to minimise darkening caused by UVR. Cosmetic camouflage can be used.

The following agents can be used to lighten epidermal melanosis, alone or, more effectively, in combination:

Hydroquinone
Topical retinoid
Topical corticosteroid
Glycolic acid and other fruit acids
Azelaic acid
L-Ascorbic acid (vitamin C)

Resurfacing using chemical peels, laser, intense pulsed light (IPL) or dermabrasion may be effective but unfortunately risks further damage to the epidermis and formation of more pigment. Cautious cryotherapy to small areas of postinflammatory pigmentation can be effective but risks causing permanent hypopigmentation.

Cosmetic camouflage using make-up is sometimes the best advice

Generalised reduction in pigmentation at birth (congenital) may be racial in origin or due to albinism. Pituitary failure resulting in lack of MSH rarely results in acquired generalised hypomelanosis. Pallor is much more frequently due to blood loss or anaemia.

Localised hypopigmentation may be due to partial or complete loss of melanin (achromia or leukoderma). If single or multiple pale or white patches are observed, the main diagnoses to consider are:

Congenital piebaldism and Waardenburg syndrome (with deafness)
Pityriasis alba
Pityriasis versicolor
Idiopathic guttate hypomelanosis
Progressive macular hypomelanosis
Postinflammatory hypopigmentation or scarring
Vitiligo
Lichen sclerosus
Leprosy

The hypopigmentation due to inflammatory skin disorders and infections usually resolves by itself over weeks to months once the underlying disorder has been cleared. There is no effective treatment for achromia due to scarring. The response of vitiligo to therapy is highly variable.

The Ellipse Selective Waveband Technology (SWT®) treatment works by directing well-controlled pulses of light into the upper skin layer. The light is absorbed by two of the body's own natural chromophores - melanin in the pigment. The pigments convert the light energy into heat. This heat is used to destroy the parts of the cells in which the melanin is stored. This technique is called "Selective Photothermolysis”. Ellipse treatments offer clinically proven, removal of pigmented lesions in the epidermis.

The visible light produced by the Ellipse systems is carefully controlled to produce the correct pulse length and wavelengths energy to destroy the target without damaging surrounding tissue.

The combination of the Ellipse Square Pulse Technology which minimises the risk of side effects by ensuring consistent intensity of energy throughout the pulse and the Dual Mode Filtering that eliminates unnecessary and potential harmful wavelengths, allowing only those that are beneficial to the treatment. This ensures that the treatment is done without damaging the surrounding tissue, without the need for active skin cooling. The results are further enhanced by the short pulse available in the Nordlys system.

Most often seen I fair skinned individuals, ephelides are caused by an overproduction of melanosomes, changing the colour of the skin.

The colors range from light brown to red or black and are mainly found on, hands, face, shoulders, arms and forehead, and the scalp (if bald), the skin most exposed to the sun.

Age spots / liver spots / solar lentigo

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Hyperpigmentation