Melasma

Melasma, also called chloasma or the mask of pregnancy, is a common disorder of hyperpigmentation that preferentially affects women. It is a circumscribed hypermelanosis with characteristic symmetric hyperpigmented patches occurring most frequently on the face, but can occur on the extensor arms. Melasma develops and progresses slowly and is often associated with hormonal changes, underlying genetic factors, and exposure to ultraviolet (UV) light as well as heat. In the United States melasma affects about 5 to 6 million individuals, and in one study the incidence of melasma in males was about 5% to 10%. It is more common among the Hispanic, Asian, African, and Middle Eastern populations, and tends to persist longer in those of darker phototypes. Melasma is an extremely prevalent and concerning problem in the Latino population. Sanchez and colleagues reported that melasma constitutes 8.2% of the diagnosis encountered in a Latino private practice population. Known exacerbating factors include pregnancy, oral contraceptives, and sun exposure. The pathogenesis, while not completely elucidated, is thought to involve UV exposure, or another exacerbating factor, in conjunction with hyperfunctional melanocytes that produce increased amounts of melanin. UV irradiation is thought to play the central role, and this is supported by the observation that melasma tends to improve during the winter months and by involvement of sun-exposed areas. Documented exacerbating factors are hormonal estrogen and possibly progesterone, medications such as phenytoin-related anticonvulsants and phototoxic medications, as well as increased expression of c-kit and stem cell factor within lesion skin. Perez and colleagues reported that fertile women who developed melasma without ever having been pregnant or on oral contraceptive medications may show a mild ovarian dysfunction consistent with polycystic ovarian syndrome. The melanocytes of melasma-affected skin have been shown to be highly dendritic, exhibit rapid DNA synthesis on UV sun exposure, and multiply rapidly. On histologic examination melanin deposition is seen in all layers of the epidermis, as well as an increased number of dermal melanophages.

In clinical terms facial melasma is divided into 3 patterns: 1) Centrofacial; 2) Malar; 3) Mandible. The centrofacial area is the most commonly affected area, seen in about two-thirds of patients. The malar area is the second most common, occurring in about 20% of patients, followed by the mandible area in about 16% of patients. Melasma is also subclassified into 4 subtypes based on illumination by Wood’s lamp: epidermal, dermal, epidermal and dermal (mixed), or intermediate. Lesions composed of epidermal pigment deposition are said to accentuate on Wood’s lamp illumination and those that are composed mainly of dermal pigmentation become less conspicuous or blend in on Wood’s lamp illumination. Melasma can be very disturbing for patients, and frustration can set in on recalcitrance to treatment. Factors that contribute to the severity of melasma are the surface area affected, intensity of pigmentation relative to the surrounding skim, and homogeneity of the lesions, with more surface area, 3 or more shade differences, and more homogeneous lesions all considered to be more severe.

Postinflammatory Hypermelanosis (PIH)

PIH, or postinflammatory hypermelanosis, is another frequently encountered, cosmetically concerning disorder of hyperpigmentation. As the name implies, PIH is an acquired hyperpigmentation that involves areas of prior cutaneous inflammation, allergic contact, irritant reactions, or trauma such as burns and friction. It can also occur after medication reactions or at sites of vesiculobullous diseases. Of course, cosmetic procedures such as chemical peeling, cryosurgery, laser therapy, intense pulse light therapy, and fillers can all produce PIH and therefore patients should be informed about the risk of such a development. PIH can affect all skin phototypes and is prevalent among the skin-of-color population. PIH can occur anywhere on the skin surface including the mucous membranes, and becomes apparent in the areas of inflammation once the initial erythema resolves. Patients of any age can be affected, and the incidence is equal in men and women. Although it occurs in all skin types, PIH may be more apparent in phototypes III to VI. Moreover, in these skin types the hypermelanosis may last longer and sometimes never fades completely. Halder and colleagues reported in 1983 that pigmentary disorders, other than vitiligo, were the third most common dermatoses among African American patients but were the seventh most common dermatoses among Caucasian patients. In 2007 Alexis and colleagues confirmed this observation by reporting that dyschromias was the second most common diagnosis among African American patients, whereas dyschromias did not make the top 10 most common diagnoses among Caucasian patients.

The pathogenesis of PIH depends on where the pigment resides. In the epidermal form there is an increase in melanin production and dendritic transfer to keratinocytes. In mice and possibly humans, mediators of inflammation such as prostaglandins E2 and D2 may enhance pigment production. In dermal hypermelanosis, melanin enters or “drops” into the dermis via a damaged epidermal basement membrane secondarily to the inflammatory process. This pigment incontinence is phagocytosed by the dermal melanophages where it resides. Some investigators report that patients with skin of color are more apt to develop postinflammatory pigmentation because of the large amount of melanin contained with the melanosomes within the epidermis. Others believe that the amount of PIH is related more to the individual’s type of melanocyte categorized as normal, weak, or strong. The difference is that weak melanocytes, after an inflammatory insult, lead to a decreased production of melanin, giving rise to clinical hypopigmentation, whereas strong melanocytes produce increased amounts of melanin after an inflammatory response, resulting in hyperpigmentation. Normal melanocytes remain unaltered, producing appropriate quantities of melanin. Although melanin is increased in this disorder, the number of melanocytes remains the same. On dermatopathologic examination, the epidermal form of PIH shows increased pigment in epidermal keratinocytes whereas the dermal form is characterized by melanin deposition within dermal macrophages. Although a biopsy is not routinely needed to make the diagnosis, if the diagnosis is questioned a biopsy is sometimes helpful. Included in the differential diagnosis of PIH are disorders such as melasma, exogenous ochronosis, amyloidosis, lichen planus, acanthosis nigricans, erythema dyschromicum perstans, morphea, and tinea versicolor. It is important to check for signs and symptoms and to rule out underlying Addison disease and systemic lupus erythematosus.

PIH presents clinically as asymptomatic macules or patches that range in color from tan to dark brown when there is epidermal melanin, and from blue-gray to gray-brown when there is dermal melanin. Wood’s lamp examination may be helpful when trying to distinguish between epidermal and dermal melanin deposition, with the epidermal melanin becoming accentuated under Wood’s lamp. Epidermal pigment will show fluorescence under Wood’s lamp illumination whereas dermal pigment should not. Mixed and intermediate level pigmentation will show a gradation between the former two. The deeper the pigment, the less fluorescence will occur on Wood’s lamp examination. Often the borders of these lesions are not distinct, due to the distribution in areas of prior inflammation. Often the areas of the hyperpigmentation are clues to the underlying inflammatory etiology. In acne vulgaris the resultant hyperpigmented lesions occur on the head, neck, and upper trunk area, are usually less than 1 cm, and tend to be perifollicular. In lesions resulting from lichen simplex chronicus, areas favored include the ankle and antecubital/popliteal fossae. For lesions due to an atopic dermatitis, in infants the face and forearms are affected whereas older children usually have involvement of the flexural areas. In suspected fixed drug eruptions, circular or nummular lesions are observed usually at a perioral, acral, or genital site. Epidermal hypermelanosis is more responsive to treatment than the dermal counterpart. Postinflammatory epidermal hyperpigmentation should resolve with time once the underlying inflammatory disorder is treated, which may take anywhere from 6 to 12 months. Conversely, dermal hypermelanosis is sometimes permanent.

Both melasma and PIH can be distressing for the patient, and the physician should not minimize the psychosocial impact that these disorders may have on the patient’s social and professional life. These conditions can have major detrimental effects on a patient’s quality of life. Patients may experience feelings of depression and social isolation. Often a feeling of frustration regarding multiple failed treatments as well as frustration with one’s self can arise from experience of both pigmentary disorders.

Explanation and discussion of the pathogenesis, clinical course, and treatment options before embarking on treatment can help to manage expectations and set realistic goals for the patient. Because there is no “quick fix,” patients must be counseled on the time that is required for treatments to take effect so that they themselves do not become discouraged. Because both disorders are characterized by increased epidermal and dermal melanin, production and deposition treatments for both are discussed together. The theme of a stepwise approach combining multiple modalities is emphasized, and prevention especially against ultraviolet radiation exposure is paramount. When approaching both clinical entities a stepwise approach to treatment is recommended while always assessing the patient’s clinical progress, satisfaction, and any adverse events that may occur. It is recommended to start with medical therapy, including topical bleaching agents, retinoids, and low-potency corticosteroids, with treatment durations described in the next section. If adequate resolution is not achieved, treatment can progress to chemical peels and laser therapies, although these should only be done by those who have extensive experience in treating disorders of hyperpigmentation, especially in skin of color. Due to the adverse effects of chemical peeling and laser therapy, including further hyperpigmentation and scarring, one should exercise caution when initiating such therapies.