Melasma
Chloe E. Ward
Janet Y. Li
Selina S. Hamill
Paul M. Friedman
BACKGROUND
Melasma is a common acquired pigmentary disorder characterized by light to dark brown hyperpigmented macules and patches with irregular circumscribed borders and confetti-like islands of normal appearing skin, resulting from increased melanin in the epidermis, dermis, or both. The term “melasma” is derived from a Greek word meaning “a black spot” and is synonymous with “chloasma,” meaning “a green spot.”1 This condition favors the face, but occasionally can involve the extensor forearms and trunk in what is termed extrafacial melasma. This condition is seen primarily in young to middle-aged women; however, men can also develop the same troublesome hyperpigmentation. It has been reported that at least 90% of patients are women, and it is often referred to as chloasma, or the “mask of pregnancy.”2 However, this rate may be closer to 75% when the rates of men in Southeast Asia and India are taken into account. The negative impact of melasma on quality of life is well known. It contends a phenotype of photodamaged skin and can be quite psychologically distressing for some patients.
Normal skin color is determined by a mixture of four biochromes in the skin, specifically, reduced hemoglobin (blue), oxyhemoglobin (red), carotenoids (yellow), and melanin (brown).1 Melanin is the main determinant of skin color. It is genetically determined by constitutive melanin pigmentation and can be increased in response to stimulants such as UV radiation or hormones, through inducible melanin pigmentation.1 Increased melanin in the epidermis, or hypermelanosis, reflects an increased number of melanocytes as in solar lentigines, or an increase in the production of melanin with no increase in the number of melanocytes, or melanotic hypermelanosis, as is marked by melasma.1 Irregularities in the appearance of skin pigmentation due to hypermelanosis, hypomelanosis, or a combination of both can be viewed or interpreted as a failure to present an attractive appearance. This is both a conscious and subconscious part of human nature.
Many chronic diseases, including pigmentary disorders, affect the way patients view and feel about themselves and the way they are perceived in society. This has significant psychosocial impacts for patients suffering from visible chronic skin diseases. Pigmentary disorders can cause great turmoil and grief for many patients. The psychosocial repercussions can be especially marked in populations with naturally darker skin phototypes, or where dyspigmentation of the skin may be viewed as hereditary or confused with Hansen disease. Of the many different pigmentary disorders that affect the appearance of the skin, melasma and vitiligo predominate. The anxiety and extraordinary distress attributed to melasma has been well documented. The impact can be profound, and patients may be willing to go to great lengths, even to reallocate money for necessities to the treatment in the appearance of melasma.
PRESENTATION
Patients typically present in child-bearing years or per-imenopausal years with complaints of dark spots on the face. They will sometimes give a history of having been prescribed oral contraceptives, a recent pregnancy, a sunny vacation, or a laser treatment followed by sun exposure precipitating its appearance.
DIAGNOSIS
Clinical Diagnosis
Melasma consists of irregular, well-demarcated, tan to brown macules patches distributed over the forehead, upper and mid cheek areas, and the upper lip. The subtypes are covered in detail later. Melasma is primarily a clinical diagnosis and a skin biopsy is typically unnecessary. Exceptions can be made when the clinical picture is unclear and another diagnosis with distinct histology, such as exogenous ochronosis, is in question. Otherwise, the risk of scarring and postinflammatory hyperpigmentation (PIH) in a cosmetically sensitive area should be strongly considered. Subdued lighting in the clinical examination room can enhance the contrast between hyperpigmented skin and normal skin, improving diagnostic acuity. This can be further enhanced by tangential lighting and a Wood’s light and other modern tools of skin visualization to ensure the lesions are flat and exclude any elevation or inflammation. Wood lamp emits UV longwave “black light” at 365 nm and can be used to help determine the depth of melanin pigmentation. Theoretically, light is increasingly absorbed in areas of increased epidermal melanin, enhancing the border contrast between melasma lesions and normal skin, as the affected skin appears darker relative to surrounding skin. In contrast, dermal melasma demonstrates less border contrast and blends with normal skin when irradiated, as the UV light travels deeper into the skin where the dermal macrophages are present. This can be a diagnostic challenge with darker skin phototypes and in cases of mixed melasma where there is both an epidermal and dermal component. Clinicopathologic studies using both lesional and adjacent skin suggest that Wood lamp examination has demonstrated that this technique does not always correlate the location of pigment on histology.3,4 Clinical photographs before and after treatment should always be done to assess progress.
Newer imaging technologies have enhanced the clinical diagnosis of melasma and other pigmentary and vascular conditions, reducing the need for unnecessary skin biopsies in cosmetically sensitive areas such as the face. Spectrocolorimetry devices and RBX (Red/Brown/X) technology using cross-polarized light filters can be used to take skin images that depict the chromophores melanin and hemoglobin components.5 Identification and qualification of the red and brown components in melasma allows for an effective treatment plan in which the vascular and pigmented components can be targeted by vascular- and pigment-specific modalities, respectively. Spectrocolorimetry can be used to detect even subtle or subclinical telangiectatic erythema within lesions of melasma. Combined vascular- and pigment-specific targeted therapies may reduce the likelihood of recurrence.6 Other UV and cross-polarized light filters combined with photography in commercially available devices allow for increased visibility and quantification of not only brown and red areas, but also pores, wrinkles, the skin texture, and porphyrins. Many advances have been made in recent years, including three-dimensional imaging and stereotactical tables. Reflectance confocal microscopy is another emerging diagnostic test. Finally, videocapillaroscopy devices can also be used to quantify and qualify the skin microcirculation; however, it is not common practice in the assessment and management of melasma.
Further investigations are usually not necessary in the diagnosis of melasma, with the exception of pregnancy testing and thyroid function studies, when clinically relevant. A significant increase in thyroid abnormalities
in nonpregnant females with melasma relative to age- and sex-matched controls has been shown.7 A thorough review of medications, hormone therapy, triggers of phytophotodermatitis, and potential cosmetic allergens should be done in all patients.
in nonpregnant females with melasma relative to age- and sex-matched controls has been shown.7 A thorough review of medications, hormone therapy, triggers of phytophotodermatitis, and potential cosmetic allergens should be done in all patients.
The Melasma Area Severity Index (MASI) is a score originally developed by Kimbrough-Green et al for the assessment of melasma, based on a similar scoring system for psoriasis.8 The minimum score is 0, and the maximum is 48 for severe melasma. This tool is often used in clinical studies to compare the treatment outcomes and different variables in melasma with baseline. It is not commonly used in clinical practice, however, and new imaging technologies have streamlined quantification and qualification of both melanin and the vascular components of melasma. The severity of each of the four regions is assessed based on the percentage of the total area involved (A), darkness (D) compared with normal skin, and homogeneity (H) of hyperpigmentation. A score of 0 is given for darkness if there is no involvement, 1 for slight hyperpigmentation, up to 4 for severe hyperpigmentation, and a score of 0 to 4 is given for homogeneity of the hyperpigmentation where 0 appears unaffected and 4 corresponds to uniform skin involvement without any clear areas. The four regions included in the assessment are the forehead (F), right malar region (MR), left malar region (ML), and chin (C). Each region has a corresponding fixed numerical value representing the percentage body surface area of the face, by which the sum of the severity grade for darkness (D) and homogeneity (H), and the numerical values of the areas involved (A) are multiplied by (Table 1.2.1).
Clinically, the three most common distribution patterns involve the face (Table 1.2.2). Centrofacial is the most common, followed by malar and mandibular. Centrofacial melasma can involve the forehead, cheeks, nose, upper lip, and chin but spares the philtrum. Malar melasma affects the cheeks and nose, and mandibular melasma affects the jawline. Extrafacial melasma of the extensor forearms, mid-upper chest and back, and trunk is less commonly seen. Photo-protected sites are typically spared. The color ranges from light to dark brown, or brown-gray. The borders are well demarcated and irregular. Confetti-like macules or regularly pigmented skin within patches of melasma, termed the “Fitzpatrick macule,” is a more sensitive and specific finding in melasma than in its common mimickers, solar lentiginosis and poikiloderma of Civatte.9 Even with treatment, melasma is easily exacerbated or reactivated by pregnancy, the use of oral contraceptives, and ultraviolet and visible light exposure. Melasma is classically seen in women more than 75% of the time, with an increased incidence observed in pregnant women.
TABLE 1.2.1 Calculation of the Melasma Area Severity Index (MASI) Score | ||||||||||
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TABLE 1.2.2 Common Clinical Distribution Patterns of Melasma | ||||||||||
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Histopathology
On histology, melasma is marked by increased melanin deposition in the skin relative to uninvolved adjacent skin. The histological subtypes can be differentiated by the presence of increased epidermal melanin, dermal melanin, or a combination of both. In darker skin
phototypes, this can be particularly challenging to diagnose even on histology and is termed indeterminate. Increased melanin in the epidermal and dermal layers may be accompanied by severe solar elastosis, damage to the basement membrane, increased vascularity, and an increased number of dermal mast cells.10
phototypes, this can be particularly challenging to diagnose even on histology and is termed indeterminate. Increased melanin in the epidermal and dermal layers may be accompanied by severe solar elastosis, damage to the basement membrane, increased vascularity, and an increased number of dermal mast cells.10
In epidermal melasma, the epidermal melanotic hypermelanosis is derived from increased melanocyte activity. Melanin is deposited in the basal and suprabasal layers, with highly dendritic melanocytes containing more melanin. In addition to the increase in epidermal melanin, an increased number of epidermal melanocytes and melanosomes has been described.3 The melanosomes are more widely dispersed among keratinocytes, and lesional melanocytes contain more organelles in their cytoplasm than normal skin. Dermal melasma is marked by superficial and deep perivascular melanophages throughout the dermis of affected skin.10 Mixed melasma involves a combination of both, as the name implies. Although patients may appear to have epidermal melasma clinically, significant dermal melanin and melanophages are often seen on histology.11 Clinically, this can be challenging to identify and may be mistaken for epidermal melasma. Indeterminate melasma can occur in darker skin phenotypes where it becomes difficult to distinguish increased melanin in melasma from their baseline melanin, thus diminishing the clinical contrast between affected and unaffected skin.
Subtypes
Melasma is best classified according to its histologic subtypes, which are based on the primary location of pigment in the skin. Histologically, the subtypes are epidermal, dermal, mixed, and indeterminate. The various subtypes may have important implications on prognosis and treatment. These can sometimes be distinguished clinically by their presentation, aided by the use of Wood lamp and other visualization tools. Clinically, melasma can be grouped into centrofacial, malar, mandibular, and extrafacial melasma, according to clinical distribution.
Differential Diagnosis
The differential diagnosis of melasma is broad. It should be differentiated from other causes of diffuse and circumscribed hyperpigmentation, specifically PIH, lichen planus, phytophotodermatitis, drug reactions, or drug-induced pigmentation related to minocycline, amiodarone, phenytoin, some chemotherapeutic agents, and exogenous ochronosis from hydroquinone-containing bleaching agents sometimes used to treat melasma, that can cause paradoxical darkening. Moreover, endogenous ochronosis due to a systemic deficiency of homogentisic acid oxidase can give scars a bluish pigmentation,100 in addition to other classic features of alkaptonuria. The clinical history, size, shape, and distribution pattern help distinguish PIH from melasma. Likewise, a history of systemic or topical medications, photoaggravation, or recurrent discrete oval or round-shaped plaques can differentiate drug-induced pigmentation, phototoxic and fixed drug eruptions from melasma. The clinical picture can become less clear if other cutaneous signs of photoaging are present, such as solar lentigines, PUVA lentigines, ephelides, thin seborrheic keratosis, and dyspigmentation associated with poikiloderma of Civatte, which can either be present with melasma or hard to distinguish from melasma at times.
Pregnancy, with or without other forms of pregnancy-associated hyperpigmentation, suggests melasma with the right distribution. Nevus of Ota presents as a blue-gray-brown unilateral or bilateral facial patch, typically in Asian and African Americans, sometimes with scleral involvement. Acquired bilateral nevus of Ota-like macules, also known as acquired dermal melanocytosis or Hori nevus, is commonly seen in middle-aged Asian women and can easily be confused with melasma. Typically, a more grayish-brown hue to the macules arising on the malar cheeks, forehead, eyelids, temples, and nose helps elicit this diagnosis. Actinic lichen planus can also have a melasma-like appearance, as it presents on sun-exposed sites, particularly on the face, neck, and dorsal arms, in young adults and children typically of Middle Eastern or East Indian descent. The presence of inflammation, scale, a violaceous hue, or red-brown annular plaques can help distinguish it from melasma. Similarly, lichen planus pigmentosus can also be easily confused with melasma; however, involvement of the temples, preauricular area, neck, intertriginous sites, and coexistent lichen planus if present should prompt this diagnosis. Erythema dyschromicum perstans presents with slate-gray to blue-brown lesions, occasionally with a rim of erythema early on, and may involve sun-protected sites. Additional causes of diffuse hyperpigmentation include a pigmented contact dermatitis (Riehl melanosis), which can be more reticulated in appearance, erythromelanosis follicularis faciei et colli, which presents as red-brown patches on the lateral cheeks and neck with superimposed pale follicular papules, Poikiloderma of Civatte marked by the presence of atrophy and telangiectasias in addition to dyschromia, actinic lichen nitidus,
metabolic diseases, sclerodermoid disorders, nutritional deficiencies, cutaneous mercury deposits, and rarely, human immunodeficiency virus (HIV).
metabolic diseases, sclerodermoid disorders, nutritional deficiencies, cutaneous mercury deposits, and rarely, human immunodeficiency virus (HIV).
In men, the differential diagnosis of melasma is very similar. It should include PIH, pigmented contact dermatitis, lichen planus pigmentosus, nevus of Ota or nevus of Hori, frictional melanosis, facial acanthosis nigricans, ephiledes, lentiginoses, and Becker melanosis.12
Diagnostic Pitfalls
One of the most common reasons melasma gets worse or does not improve with treatment is misdiagnosis. Diagnostic uncertainty can lead to suboptimal treatment and poor management of patient expectations. Several historical factors can help distinguish melasma from other disorders, including any preceding inflammation or primary inflammatory lesions, irritation, pruritus, burning, application of any topical agents, systemic medications, the color and onset of the lesions, the pattern of distribution, and the histologic features, when a biopsy is done. A prompt and accurate diagnosis allows for appropriate preventative and therapeutic measures to be initiated, for the best cosmetic outcome in this challenging condition to be achieved. Despite an accurate clinical diagnosis and appropriate therapeutic measures, one must remember melasma is a chronic disease, which is not entirely understood. Refractory or recurrent melasma is not uncommon and patient expectations should be managed accordingly.
Melasma in Men
Although less common, melasma can be acquired in men, and there are some subtle differences in features that can be seen between men and women. It is most common on the face, and the clinical patterns are the same as in women, even for extrafacial melasma.12 Epidermal melasma is the most common subtype on examination with Wood’s light, as seen in women; however, in men a malar clinical distribution is more prominent, whereas centrofacial is usually more common in women.12,22 The histopathologic findings appear to be the same in both genders. Similarly, treatment can be challenging in both men and women, and overall, treatments do not really differ between the two, with some minor exceptions in terms of patient preferences around time and complexity of treatments, camouflage options, product formulations, and product packaging.
As melasma is often regarded as a disease of pregnant women by many, some men experience a certain social stigma around this. The quality of life in men with melasma has been shown to be significantly less than in those without it, as observed in a study of Latino men working in the United States.23 The prevalence appears to be increased in Fitzpatrick skin types III to VI and has been reported to range from 14.5% in Latino migrant workers in the United States, 20% in South East Asia, and up to 20.5% to 25.83% in India.22,23,24,25 The average age of onset is around 30 years.12 Little is known about the etiology in men; however, some of the common factors implicated in the pathogenesis in women would not apply. Sun exposure and family history in a first- or second-degree relative appear to be important factors, both significantly higher in men than in women.22 It has been suggested that luteinizing hormone may be elevated and testosterone lowered in men, and that men who have received diethylstilbestrol therapy for prostate cancer are at increased risk of developing melasma.26
PATHOGENESIS
Melasma is multifactorial in etiology. It appears to mostly affect adult women of child-bearing age with Fitzpatrick phototype III to VI skin. It has a genetic and racial predilection for individuals of Asian, Hispanic/Latino, and African American descent. Although the etiology is not completely known, several factors have been implicated. Common etiologic factors include a genetic predisposition, ultraviolet (UV) radiation and visible light, specifically blue light exposure, barrier abnormalities, hormone sensitivities relating to pregnancy, and exogenous hormones from oral contraceptives, or hormone replacement therapy. UV light both precipitates and exacerbates melasma. Endogenous and exogenous estrogen, combined with progesterone and sunlight, can lead to significant darkening of pigmentation in melasma. Less common risk factors include thyroid disorders, photosensitizing medications, and type 4 hypersensitivity reactions to common allergens found in cosmeceuticals and topical preparations.10,13,14 A pilot study examining the role of cosmetic contact allergy found that a significant portion of melasma patients had positive results when patch tested to the Indian Cosmetic and Fragrance Series, the Indian Sunscreen Series, p-phenylenediamine, and some of the patients’ own cosmetic products. Nearly half (43.3%) had positive patch test results to the Indian Cosmetics and Fragrance Series, with cetrimide (52%), gallate mix (31%), and thiomersal (24%) being the most common contact allergens tested.14 The role of contact dermatitis
should not be overlooked in melasma, and products containing these allergens should be avoided. Although melasma has many associated triggers, it can also be termed idiopathic when no clear predisposing factors can be identified. Melasma tends to be more persistent in more darkly pigmented skin types and tends to fade over the winter months in northern latitudes where there is less daytime UV exposure.
should not be overlooked in melasma, and products containing these allergens should be avoided. Although melasma has many associated triggers, it can also be termed idiopathic when no clear predisposing factors can be identified. Melasma tends to be more persistent in more darkly pigmented skin types and tends to fade over the winter months in northern latitudes where there is less daytime UV exposure.
In pregnancy, up to 90% of women develop some form of hyperpigmentation, which can manifest as hyperpigmented areolae, linea nigra, and/or melasma.2 These skin lesions arise from the quality and quantity of the physiologic hormone changes in pregnancy, specifically elevated serum levels of melanocyte stimulating hormone (MSH), estrogen, and possibly progesterone.2,15 In pregnancy, pituitary enlargement is accompanied by an increase in the blood level of MSH, in addition to an increased output of gonadotropins, and corticotrophin.15 Moreover, cortisol levels are increased from increased adrenocortical activity, which is thought to weaken and rupture dermal elastic fibers as seen in striae distensae, and high levels of circulating estrogen lead to the vascular changes seen in pregancy.15 Up to 70% of pregnant women may develop melasma, which either first appears or becomes noticed by the patient during pregnancy.16 It is estimated that between 5% and 34% of nonpregnant women taking oral contraceptives may also develop melasma.2 The onset often follows or may be exacerbated by UV exposure. This “mask of pregnancy” often fades or even disappears after parturition in more lightly pigmented skin types but can persist following pregnancy and discontinuation of oral contraceptives in more darkly pigmented individuals.2
The pathogenesis of melasma is complex and, although not entirely known, is thought to be related to hyperfunctional melanocytes, which can be stimulated by various factors, with concomitant angiogenesis. Ongoing research has led to an increased understanding of the complex pathogenesis of this disorder. Melanocytes, keratinocytes, and even dermal cells including mast cells and fibroblasts have all been described as playing a role in the pathogenesis. Advancements in molecular techniques have allowed for the identification of certain genes, cytokines, chemokines, angiogenic factors, and defects in the structural integrity of affected skin.
Hyperfunctional Melanocytes
It is believed that following exposure to an inciting agent, such as UV radiation, hyperfunctional melanocytes in the skin produce increased amounts of melanin.4,10 On histology, increased melanin is always seen, often with overlying solar elastosis. This suggests a role of UV radiation and dermal damage in the pathogenesis.3 The role of UV radiation is further supported by relative fading of the lesions during the winter months in northern latitudes and sparing of sun-protected sites such as the philtrum. The expression of KIT within lesional epidermis, and stem cell factor within lesional dermis, is increased.
Defects in the basement membrane may facilitate the fall or migration of melanin, and active melanocytes into the dermis.17 This can be exacerbated by aggressive treatments, which may disrupt the basement membrane, trigger dermal inflammation and destruction of melanocytes, upregulate stem cell factors, and increase vascularity, which effectively promotes melanogenesis and causes PIH, worsening the appearance of melasma.18
Angiogenesis
Angiogenesis also plays a role in the pathogenesis of melasma. Lesions of melasma display an increased number and size of blood vessels, and vascular endothelial growth factor (VEGF) appears to be upregulated.19 VEGF receptors are found on human melanocytes.20 VEGF stimulates the release of arachidonic acid, in addition to the phosphorylation and activation of cytosolic phospholipase A2.21 There appears to be a complex link between the VEGF and arachidonic acid pathways with inflammatory cytokines induced by the effects of UV on cutaneous blood vessels in the melanogenesis seen in melasma.19
TREATMENT
Melasma is a chronic pigmentary disorder that can be challenging and refractory to treatment. Although no cures have been developed as of yet, several technological and pharmacologic advances have led to promising approaches in the accurate diagnosis, prevention, and the long-term management of this chronic pigmentary disorder. In a Cochrane review of 20 melasma studies, a standard therapy for melasma could not be recommended
because of the heterogeneity, poor quality, or inadequate follow-up in the studies reviewed.27 The best therapeutic outcomes are achieved when an accurate diagnosis is made, a strong adherence to preventative measures is achieved, and a combination treatment approach is used (Algorithm 1.2.1). It is typically felt that epidermal melasma due to superficial increases of melanin in the epidermis responds best to treatment. Management of melasma is both a science and an art.
because of the heterogeneity, poor quality, or inadequate follow-up in the studies reviewed.27 The best therapeutic outcomes are achieved when an accurate diagnosis is made, a strong adherence to preventative measures is achieved, and a combination treatment approach is used (Algorithm 1.2.1). It is typically felt that epidermal melasma due to superficial increases of melanin in the epidermis responds best to treatment. Management of melasma is both a science and an art.
Melasma is chronic, recalcitrant and recurrent in nature, thus it can be a real therapeutic challenge. Because this condition is inherently more prevalent in individuals with darker skin, the risk of PIH associated with some treatments can be high if caution is not exerted. In general, prevention and modification of exacerbating risk factors is fundamental to successful management. In some pregnancy-related cases, melasma may resolve spontaneously postpartum, and in women taking an oral contraceptive pill, alternative forms of contraception or switching to a low estrogen oral contraceptive can be considered. Similarly, treatment of thyroid disease and management of medications contributing to hyperpigmentation should be done where applicable. Avoidance of other triggers, such as sun, UV radiation, heat, hot yoga, and visible light, especially blue light should be advised. Broadly speaking, management of melasma can be broken up into behavioural measures, topical lightening agents, superficial chemical peels, and light or laser therapies. The response to monotherapy is generally limited and disappointing for both the patient and the clinician. Optimal cosmetic results are achieved in melasma when a combination of treatments tailored to the individual patient is used. Diligent photoprotection and sun avoidance are necessary to maintain treatment results.
Medical
Prevention
Despite the medical and procedural interventions, which can be performed by the clinician, the general everyday lifestyle measures of the patient cannot be overemphasized. Although sunscreens alone have not been extensively studied in the treatment of melasma, there is a general consensus that protection from UV light, in addition to infrared light (IR) and visible light including blue light, from both sun and artificial light sources is of utmost importance. Artificial light sources include digital screens, fluorescent and light-emitting diode (LED) lighting, and high-energy visible (HEV) light or blue light. A significant portion of free radicals formed during sun exposure are thought to be due to IR and blue light, not only UVR. A daily sunscreen with high factor, broad-spectrum protection against both UVA and UVB, and visible light (VL) is recommended for all patients. Especially in darker skinned patients, VL has been shown to produce reactive oxygen species, inflammatory cytokines, matrix-degrading enzymes such as matrix-metalloproteinase-1, and the resultant pigmentary changes similar to those of UV radiation.28 Moreover, regular use of a VL-absorbing pigment such as iron oxide in addition to a UV-only broad-spectrum sunscreen can enhance the efficacy of other lightening treatments and prevent the effects of VL that includes blue light in the pathogenesis of melasma.29 UV sunscreens combined with skin-lightening agents can improve MASI scores up to 75%, as was shown with topical hydroquinone 4%; UV-VL photoprotection appears to further improve melasma more than UV protection alone.29,30
Regular use of an opaque sunscreen containing a high concentration of zinc oxide and/or titanium dioxide, with a camouflage makeup containing iron oxide can be suggested. Sun avoidance, the use of UV protection factor (UPF) clothing, wide-brimmed hats, and UV protective sunglasses can also be helpful.
In a study of 200 pregnant women from Morocco, with application of a broad-spectrum sunscreen with SPF 50/UVA PF 28 several times per day independent of sun exposure, only 2.7% developed melasma.30 The same investigators had previously observed a rate of 53% in the same geographical area and time frame in pregnant women not using strict photoprotection, and rates have been reported to range anywhere from as low as 10% to 15%, up to as high as 70%, depending on skin phototype and racial predilection.16,30,31 Most women on average also experienced lightening of their skin by the end of the study, or improvement of melasma in the 8 out of 12 women noted to have preexisting melasma.30 The regular use of broad-spectrum sunscreen thus appears to be well tolerated and effective in preventing the development of melasma in pregnant women.
Polypodium leucotomos (PL) is an oral dietary supplement from a fern of the Polypodiaceae family in Central and South America, gaining interest in the management of melasma for its antioxidant and potential photoprotective properties. PL is rich in polyphenols, including ferulic, vanillic, chlorogenic, and caffeic
acids. These help the skin maintain protection against free radicals and reactive oxygen species (ROS) related to sun exposure.
acids. These help the skin maintain protection against free radicals and reactive oxygen species (ROS) related to sun exposure.
 ALGORITHM 1.2.1 Treatment algorithm for melasma. AHA, alpha-hydroxy acid; BHA, beta-hydroxy acid; BID, bis in die; mo, months; Nd:YAG, neodymium-doped yttrium aluminium garnet; nm, nanometer; PDL, pulsed dye laser; QS, quality-switched; TCA, trichloroacetic acid; TCC, triple combination cream; UPF, ultraviolet protective factor; UV, ultraviolet. |
Camouflage
Camouflage techniques can be particularly helpful in managing the emotionally and psychologically devastating sequelae of melasma in visible locations, especially in patients who have had an unsatisfactory response to treatment. Feelings of embarrassment, depression, and social inhabitation associated with the disease can be mitigated. Camouflage makeup has been shown to significantly improve the quality of life in patients with pigmentary disorders and other dermatologic conditions.32
Mineral makeups may contain titanium dioxide, zinc oxide, and iron oxide or ferric oxide. They can be helpful in camouflaging visible discoloration on the skin, in addition to offering adjuvant protection against the sun and visible blue light.103 Popular commercially available lines of camouflage makeup include Dermablend, Jane Iredale, Bare Minerals, Covermark, and CoverFX. Lines and products should be selected based on patient preferences and skin type, and should be color-matched to the patient’s unaffected skin. Typically, topical treatments, bland emollients and sunscreen are applied first, followed by a fine layer of color-matched camouflage cream and a setting powder. Camouflage makeup can be touched up or reapplied throughout the day as needed.
Skin-Lightening Agents
Topical skin-lightening agents are the mainstay of treatment in melasma, after photoprotection. Most lightening agents target tyrosinase, which converts L-tyrosine to L-3,4-dihydroxyphenylalanince (L-DOPA), the rate-limiting enzyme in melanin synthesis. Topical lightening agents can be used first-line and alone with photoprotection, before physical treatments to prepare the skin, as adjuvant therapy with procedures that deliver the drug transepidermally or transdermally, or ongoing as mainstay after a procedure.
Traditional melasma treatments include hydroquinone 2% to 5% cream, azelaic acid, triple combination creams (TCCs) containing hydroquinone, tretinoin and fluocinolone, and tretinoin cream alone, which will be discussed separately (Table 1.2.3). Topical tranexamic acid is a more recent treatment option, gaining popularity for its safety and efficacy profile. Cosmeceuticals
and botanicals with skin brightening and anti-oxidant properties are often added. TCC containing fluocinolone acetonide 0.01%, hydroquinone 4%, and tretinoin 0.05% is the only hydroquinone-containing drug currently approved by the FDA for the treatment of melasma.
and botanicals with skin brightening and anti-oxidant properties are often added. TCC containing fluocinolone acetonide 0.01%, hydroquinone 4%, and tretinoin 0.05% is the only hydroquinone-containing drug currently approved by the FDA for the treatment of melasma.
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