This type of hyperpigmentation occurs in all skin types but is most common in those with darker skin.
It occurs after a skin condition or skin injury that causes the skin to become inflamed with resultant damage to the melanocytes, which are the cells that produce melanin pigment. Sometimes the preceding condition is barely noticeable.
Damage to the melanocytes causes melanin to be deposited in the dermis or epidermis (upper layer of the skin). This is important as epidermal hyperpigmentation fades faster than dermal hyperpigmentation, and in fact the dermal type may be permanent.
This type of hyperpigmentation can occur at any age, and on any part of the body.
It may appear tan, various shades of brown or blue gray. A blue gray appearance points to dermal melanin and a more prolonged and difficult treatment. Sometimes a dermatologist may be able to see lesions of the preexisting condition making it easier to make a diagnosis.
Common causes of post inflammatory hyperpigmentation that I see in my practice every day are acne, eczema, insect bites and skin infections. We need to treat the underlying disorder if it is still present to prevent more PIH from developing. If left untreated PIH may take years to resolve.
Melasma or chloasma is a common disorder of hyperpigmentation that mainly involves the face. It usually affects both sides almost symmetrically and occurs in both males and females, though commoner in females. At least 90% of patients with melasma are women.
It can affect all races but is most common in darker skins where it is also the most difficult to treat.
Nevertheless melasma is a very distressing condition as it occurs somewhat out of the blue, sometimes seemingly without any precipitating factors.
Common precipitants are sunlight and hormonal influences (OCP and pregnancy). There is a genetic predisposition as in most diseases.
It may not seem fair that some of us will never get melasma even with reckless sun behavior and others will get it even with strict sun avoidance. The hyperpigmentation of melasma is due to increased melanin production by melanocytes i.e. increased activity of the melanocytes and not an increased number in the cells.
These melanocytes are called ‘reactive’ melanocytes. They produce an excess of melanin pigment, which is transferred to the skin cells called keratinocytes. Some of this pigment also ‘falls’ into the dermis where it gives a blue gray appearance to the skin. The key enzyme in the process of melanin pigment production is called tyrosinase.
Melasma is a clinical diagnosis based on a typical presentation. We do not do any tests to confirm the diagnosis. The hyperpigmentation of melasma can be described as flat coalescing brown, gray or bluish patches with irregular edges.
There are three typical patterns of distribution.
Centrofacial involves the forehead, nose, chin and cheeks. Malar pattern involves the cheeks and nose and mandibular pattern involves the area over the jawline.
Melasma may also occur on the neck and forearms i.e. extrafacial melasma.
Melasma is a common condition, but the treatment remains difficult particularly in darker skinned individuals where the condition may often either persist or recur.
Apart from classification according to distribution on the face, melasma is also classified according to where in the skin the pigment sits. As with PIH, epidermal melasma is more likely to respond to treatment than dermal melasma.
Melasma is managed with a combination of treatment modalities. Treatment needs to target various stages in the production and clearance of the excess melanin pigment.
Treatment of hyperpigmentation
Three pronged approach.
1. Avoid factors that stimulate melanocytes and cause them to produce more melanin ie avoidance of sun exposure, meticulous use of sunscreen and protective clothing. I must stress that protecting your skin from the sun is critical to the treatment and ongoing maintenance for patients with melasma. If you are on an oral contraceptive pill, consider an alternative form of contraception.
2 . Inhibit the production of melanin by melanocytes by targeting the enzyme tyrosinase.
The gold standand treatment to inhibit tyrosinase is hydroquinone. This treatment is only available by prescription. Other options are Arbutin, Kojic Acid and ellagic acid which are gentler and less likely to cause a worsening of the hyperpigmentation when discontinued.
3. Increasing the epidermal turnover will help to shed those keratinocytes which have been loaded with melanin pigment.
Topical creams and chemical peels help to remove the pigmented epidermal skin layers. Good options for accelerating epidermal turnover include glycolic acid and lactic acid
Proceed cautiously especially with darker skin types as there is no quick fix and epidermal injury from aggressive treatments could worsen hyperpigmentation
Remember that to maintain results as long as possible you will need to continue with your maintenance products.