Melasma

Melasma, sometimes called chloasma, appears as a symmetrical blotchy, brownish pigmentation on the face. The pigmentation is due to overproduction of melanin by the pigment cells, melanocytes. It can lead to considerable embarassment and distress.

Melasma / chloasma

More images of melasma ...

What causes melasma?

The cause of melasma is complex. There is a genetic predisposition to melasma, with at least one-third of patients reporting other family members to be affected. In most people melasma is a chronic disorder.

There are several known triggers for melasma.

• Sun exposure – this is the most important avoidable risk factor.
• Pregnancy may provoke melasma – in affected women, the pigment often fades a few months after delivery.
• Hormone treatments seem to be a factor in about a quarter of affected women, including oral contraceptive pills containing oestrogen and/or progesterone, hormone replacement, intrauterine devices and implants. But in other women, hormonal factors do not appear important.
• Scented or deodorant soaps, toiletries and cosmetics may cause a phototoxic reaction triggering melasma that may then persist long-term.
• A phototoxic reaction to certain medications may also trigger melasma.
• Melasma has been associated with hypothyroidism (low levels of thyroid hormone).

More commonly, it arises in apparently healthy, normal, non-pregnant adults and persists for decades. Exposure to ultraviolet radiation (UVR) deepens the pigmentation because it activates the melanocytes.

Research is on-going to pinpoint the roles of stem cell, neural, vascular and local hormonal factors in promoting melanocyte activation.

Clinical features of melasma

Melasma is more common in women than in men; only 1-in-4 to 1-in-20 affected individuals are male (depending on the population studied). It generally starts between the age of 20 and 40, but can begin in childhood or not until middle-age. Melasma is more common in people that tan well or have naturally brown skin (Fitzpatrick skin types 3 and 4) compared with those who have fair skin (skin types 1 and 2) or black skin (skin types 5 or 6).

Melasma presents as macules (freckle-like spots) and larger flat brown patches. There are several distinct patterns.

• Centrofacial pattern: forehead, cheeks, nose and upper lips
• Malar pattern: cheeks and nose
• Lateral cheek pattern
• Mandibular pattern: jawline
• Reddened or inflamed forms of melasma (also called erythrosis pigmentosa faciei)
• Poikiloderma of Civatte: reddened, photoaging changes seen on the sides of the neck, mostly affecting patients older than 50 years
• Brachial type of melasma affecting shoulders and upper arms (also called acquired brachial cutaneous dyschromatosis).

Melasma is sometimes separated into epidermal (skin surface), dermal (deeper) and mixed types. A Wood lamp may be used to identify the depth of the pigment.

How is the diagnosis of melasma made?

The characteristic appearance of melasma means diagnosis is usually straightforward and made clinically. Other disorders that may be considered include:

• Postinflammatory pigmentation
• Solar lentigines and other forms of lentigo
• Drug-induced pigmentation, e.g. due to minocycline
• Lichen planus
• Naevus of Ota.

Occasionally, skin biopsy may be performed to confirm the diagnosis. Histology varies with the type of melasma. But some degree of each of the following features is usually found.

• Melanin deposited in basal and suprabasal keratinocytes
• Highly dendritic (branched) deeply pigmented melanocytes
• Melanin in the dermis within melanophages
• Solar elastosis and elastic fibre fragmentation

The extent and severity of melasma can be described using the Melasma Area and Severity Index (MASI).

Treatment of melasma

Melasma can be very slow to respond to treatment, so patience is necessary. Start gently, especially if you have sensitive skin. Harsh treatments may result in an irritant contact dermatitis, and this can result in postinflammatory pigmentation.

Generally a combination of the following measures is helpful.

General measures

• Discontinue hormonal contraception.
• Year-round sun protection. Use broad-spectrum very high protection factor sunscreen of reflectant type and apply it to the whole face every day. Reapply every 2 hours if outdoors during the summer months. Alternatively or as well, use a make-up that contains sunscreen. Wear a broad-brimmed hat.
• Use a mild cleanser, and if the skin is dry, a light moisturiser. This may not be suitable for those with acne.
• Cosmetic camouflage (make-up) is invaluable to disguise the pigment.

Topical therapy

Tyrosinase inhibitors are the mainstay of treatment. The aim is to prevent new pigment formation by inhibiting formation of melanin by the melanocytes.

• Hydroquinone 2-4% as cream or lotion, applied accurately to pigmented areas at night for 2 to 4 months. This may cause contact dermatitis (stinging and redness in 25%). It should not be used in higher concentration or for prolonged courses as it has been associated with ochronosis (a bluish grey discolouration).
• Azelaic acid cream, lotion or gel can be used longterm, and is safe even in pregnancy. This may also sting.
• Kojic acid is often included in formulations as they interact with copper, required by L-DOPA (a cofactor of tyrosinase). Kojic acid can cause irritant contact dermatitis and less commonly, allergic contact dermatitis.
• Ascorbic acid (vitamin C) acts through copper to inhibit pigment production. It is well tolerated but highly unstable, so is usually combined with other agents.
• New agents under investigation include mequinol, arbutin and deoxyarbutin (from berries), licorice extract, rucinol, resveratrol, 4-hydroxy-anisole, 2,5-dimethyl-4-hydroxy-3(2H)-furanone and/or N-acetyl glucosamine

Other active compounds in use include:

• Topical corticosteroids , such as hydrocortisone, work quickly to fade the colour and reduce the likelihood of a contact dermatitis caused by other agents.
• Soybean extract, which is thought to reduce the transfer of pigment from melanocytes to skin cells (keratinocytes) and inhibit receptors.
• Tranexamic acid is a lysine analogue that inhibits plasmin (this drug is usually used to stop bleeding) and reduces production of prostaglandins (the precursors of tyrosine). Tranexamic acid has been used experimentally for melasma as a cream or injected into the skin (mesotherapy), showing some benefit. It may cause allergy or irritation.

Superficial or epidermal pigment can be peeled off. Peeling can also allow tyrosinase inhibitors to penetrate more effectively. Agents to achieve this include:

• Topical alpha hydroxyacids including glycolic acid and lactic acid, as creams or as repeated superficial chemical peels, not only remove the surface skin but their low pH inhibits the activity of tyrosinase.
• Topical retinoids, such as tretinoin are prescription medicines. They can be hard to tolerate and sometimes cause contact dermatitis. Do not use during pregnancy.
• Salicylic acid , a common peeling ingredient in skin creams and can also be used for chemical peels but it is not very effective in melasma.

Currently, the most successful formulation has been a combination of hydroquinone, tretinoin, and moderate potency topical steroid, which has been found to result in improvement or clearance in up to 60-80% of those treated. Many other combinations of topical agents are in common use, as they are more effective than any one alone. However, these products are often expensive.

Oral treatment of melasma

Oral medications for melasma are under investigation, including tranexamic acid (a prescription medicine in New Zealand). None can be recommended at this time.

Devices used to treat melasma

Machines can be used to remove epidermal pigmentation but with caution – over-treatment may cause postinflammatory pigmentation. Fractional lasers are preferred and have been approved by the FDA for treating melasma. Patients should be pretreated with a tyrosinase inhibitor (see above).

The ideal treatment for a quick result is just to destroy the pigment, while leaving the cells alone. Intense pulsed light (IPL) appears to be the most effective light therapy investigated so far. The topicals described above should also be used before and after treatment. Pigmentation may recur. Several treatments may be necessary and postinflammatory hyperpigmentation may complicate recovery.

Conventional carbon dioxide or erbium:YAG resurfacing lasers and pigment lasers (Q-switched ruby and Alexandrite devices) are no longer recommended because of the high risk of making melasma worse. Dermabrasion and microdermabrasion are not recommended, as they may also cause postinflammatory hyperpigmentation.

Outcome

Results take time and the above measures are rarely completely successful. About 30% of patients can achieve complete clearance with a prescription agent that contains a combination of hydroquinone, tretinoin and a topical corticosteroid.

Unfortunately, even in those that get a good result from treatment, pigmentation may reappear on exposure to summer sun and/or because of hormonal factors. New topical and oral agents are being studied and offer hope for effective treatments in the future.