Pigment International

: 2021  |  Volume : 8  |  Issue : 3  |  Page : 195--201

Approach to a case of melasma

Saloni Katoch1, Rashmi Sarkar2,  
1 Dr. KN Barua Institute of Dermatological Sciences, Guwahati, Assam, India
2 Department of Dermatology, Lady Hardinge Medical College and Hospital, New Delhi, India

Correspondence Address:
Dr. Rashmi Sarkar
Lady Hardinge Medical College and Hospital, New Delhi

How to cite this article:
Katoch S, Sarkar R. Approach to a case of melasma.Pigment Int 2021;8:195-201

How to cite this URL:
Katoch S, Sarkar R. Approach to a case of melasma. Pigment Int [serial online] 2021 [cited 2022 May 25 ];8:195-201
Available from: https://www.pigmentinternational.com/text.asp?2021/8/3/195/330898

Full Text

A 32-year-old female patient presents with the history of asymptomatic skin lesions on the face since 2 years. History reveals that the lesions started over the cheeks during her pregnancy and gradually became more prominent. She gives a history of the lesions becoming darker on prolonged sun exposure. Family history reveals similar lesions on her sister’s face. Treatment history includes usage of some topical creams, exact details of which are unavailable. There is no history of any drug intake and the patient does not suffer from any other illness.

On examination, there are bilateral symmetrical brown patches present over the forehead, malar region, upper lip, and bridge of the nose.

On Wood’s lamp examination accentuation of the pigmented patches is observed. Dermoscopic evaluation reveals a regular pigmentary network with homogeneous brown pigmentation in the background sparing the follicular and sweat gland openings.

Q. What is your diagnosis?

Melasma. It is a chronic acquired symmetrical hypermelanosis usually affecting the face and rarely extrafacial sites such as the neck, chest, and forearms. There is a female preponderance with the darker skin types being more affected. The age of onset is usually the third decade of life except the mandibular type which is more common in the perimenopausal age group. Etiologic factors include sunlight exposure, genetic predisposition, hormonal influences (pregnancy, oral contraceptive pills, hormone replacement therapy, thyroid disorders), and certain oral medications such as phenytoin that can cause a melasma-like pigmentation. Clinically, three different types have been identified. Centrofacial melasma affects the forehead, nose, upper lip, cheeks, and chin. The malar type involves the cheeks and nose and the mandibular presents with pigmentation in the mandibular region.[1] In the above case, the onset of the pigmentation during pregnancy highlights the underlying hormonal etiology of the hyperpigmentation. Also known as chloasma (mask of pregnancy), the prevalence of melasma during pregnancy increases and has been found to be up to 50.8% in an Indian study.[2] Family history is also positive in the above case and can be observed in 55% to 64% of patients with melasma.[1],[3] Cutaneous examination of the patient reveals patchy brown hyperpigmentation in the centrofacial distribution. Both Wood’s lamp examination and dermoscopy are in favor of an epidermal type of melasma.

Q. Based on the history and examination, what differential diagnosis would you like to consider in the above patient?

The diagnosis of melasma is primarily clinical and needs to be differentiated from other causes of facial melanosis which are as follows:Macular hyperpigmentary disorders of unknown etiology such as erythema dyschromicum perstans (EDP) and Lichen planus pigmentosus (LPP). These present with gray brown to bluish gray macules and need to be differentiated from mixed and dermal melasma. Apart from the face, neck and upper trunk can also be involved. EDP may be associated with a history of ammonium nitrate or barium sulfate ingestion. An association with viral infections such as HIV, hepatitis C, and whipworm infestation has also been reported. On examination, the bluish gray macules may start on the trunk and then progress to involve other sites. An erythematous border may be appreciated in the lighter skin types in the initial phase.[4],[5]LPP is insidious in onset with symmetrical slate gray to brownish black hyperpigmentation on photoexposed sites. It is usually diffuse and may be associated with pruritus or burning sensation. A waxing and waning pattern may be reported by the patient. Up to 30% of the patients may give present or past history of lichen planus. Associated mucosal lesions may also be reported.[5],[6]Riehl’s melanosis, a pigmented contact dermatitis, presents with a history of contact with a cosmetic. Symptoms such as itching and redness may precede the onset of brown to gray brown hyperpigmentation at the site of contact. The hyperpigmentation may be diffuse, patchy, or reticular. Satellite brown macules in perifollicular distribution are often reported.[7],[8]Exogenous ochronosis (EO) is a complication of prolonged usage of topical hydroquinone and other phenolic compounds leading to deposition of homogentisic acid in the papillary dermis. Early stage of EO can be confused with melasma where further usage of hydroquinone-based therapy will lead to worsening of the condition. Clinically the patient can present with diffuse gray brown to blue black hyperpigmentation with reticulate sooty blue macules, erythema, and caviar like papules, atrophy, guttate hypopigmentation, and papulonodular lesions.[8],[9]Hori’s Naevus or acquired, bilateral naevus of Ota-like macules (ABNOM) is mostly reported in Asian women and presents after the third decade of life. It is an acquired dermal melanocytosis with melanocytes in the papillary and middle dermis. Patients present with speckled blue gray to gray brown macules which can be distributed over the forehead, temples, malar region, nose, and eyelids [Figure 1]. Unlike nevus of Ota, mucosa is not involved here. Patients do not respond to topical therapy but improvement is observed with Q-switched laser treatment.[8],[10]{Figure 1}Facial acanthosis nigricans can present with bilateral symmetrical velvety hyperpigmented plaques distributed over the forehead, temples, malar region, periocular, and perioral areas. It is usually associated with obesity, diabetes, insulin resistance, and other entities of the metabolic syndrome. Patients may also have acanthosis in other areas such as the neck and axilla.[8],[11]Pigmentary demarcation lines are physiologic in nature and present as areas of sudden transition from hyper- to hypopigmented or normal skin. There is a female preponderance with an increased incidence during pregnancy. Types F, G, and H need to be differentiated from melasma. F and G lines are “V” and “W” shaped, respectively, found between the temple and malar regions, whereas type H extends from the angle of the mouth to the lateral part of chin.[12]Postinflammatory hyperpigmentation results due to an acute or chronic injury to the skin. The site, clinical pattern, and distribution follow the preceding inflammatory condition. The hypermelanosis is acquired and could be due to an inflammatory disease (lichen planus, fixed drug eruptions, psoriasis, etc.), infection (tinea, viral exanthems), or external causes (burns, trauma, etc.).[8],[13]

Q. What investigations can be performed in a patient with melasma?

Melasma is largely diagnosed by its clinical presentation of irregular symmetric hyperpigmented macules and patches over the face [Figure 2]. Investigations aid in diagnosis, assessing the depth of pigmentation, response to treatment, prognosis, and complications of therapy.{Figure 2}

Wood’s lamp examination is an economical and simple outpatient procedure. It emits long wave ultraviolet (UV) light that can help in assessing the depth of pigmentation. An enhancement in pigmentation favors epidermal melasma; absence of enhancement is a feature of dermal melasma; and mixed melasma shows patchy enhancement. This classification of melasma based on Wood’s lamp, however, has now been found to be not very accurate with dermal melanin being under detected by the same.[1],[14]

Dermoscopy is a very valuable noninvasive tool in diagnosis and assessment of melasma. It has been found to be more objective, specific, and applicable when compared with a Wood’s lamp, in classifying melasma into the epidermal, dermal, and mixed types based on pigment color and pattern. It also aids in differentiation of melasma from other facial hyperpigmentary disorders thereby alleviating the need for a biopsy. Treatment efficacy and complications such as telangiectasia, atrophy, and depigmentation can be identified at an early stage. A global feature of melasma is the reticular pattern, which may be superimposed by globules, blotches, or granules. Sparing of the sweat gland and follicular openings leads to a pseudo network pattern with concave borders referred to as “Jelly sign.” Homogeneous brown pigmentation with a regular pigment network is a feature of epidermal melasma. Blue to bluish gray pigmentation is characteristic of dermal melasma with an irregular pigment network. Mixed melasma can show features of both.[14] Dermoscopic features of differential diagnosis of melasma are enumerated in [Table 1].[15]{Table 1}

Mexameter is a narrowband reflectance spectrophotometer that can be used for objective grading of hyperpigmentation in patients with melasma. This instrument emits lights in the green, red, and infrared spectrum. The intensity of light absorbed and reflected in the red (669 nm) and infrared (880 nm) spectrum gives us the melanin index.[16]

Reflectance confocal microscopy (RCM) is an in vivo imaging tool which gives real-time images of the skin and can be used for evaluation up to the level of the papillary dermis with resolutions almost as good as histopathology. It can be used for classifying melasma and for assessing treatment response in patients. Hyperpigmented basal keratinocytes can be observed as hyperrefractile cobblestone-like cells on RCM. Dendritic cells on RCM correspond to activated melanocytes on histology. Melanophages in the dermis can be viewed as plump bright cells. Solar elastosis and blood vessels are observed as ragged lacy structures and dark round to tubular structures, respectively.[1],[16],[17]

Skin biopsy is usually not required for diagnosis on a routine basis and may be performed to confirm or rule out other differential diagnosis. On histology epidermal melasma shows an increased pigmentation in all the epidermal layers especially the suprabasal and basal. Melanocytes have increased number of melanosomes and are larger and more dendritic. The melanocyte number does not increase. Melanophages in the dermis is a feature of dermal melasma and the source of dermal melanin has been found to be the epidermis only. Increased number of vessels and solar elastosis may also be reported in the dermis. Mixed melasma presents with features of both epidermal and dermal melasma.[1],[17]

Q. What are the different types of melasma?

The classification of melasma is as follows[16],[17]:Based on depth of pigmentation and histopathologyEpidermal: Increased melanin in all epidermal layersDermal: Presence of melanophages in the dermisMixed: Increased melanin in epidermis and dermisBased on Wood’s lamp examinationEpidermal: Pigment enhancement reportedDermal: No pigment enhancementMixed: Enhancement observed in some areasWood’s light nonapparent in skin types V and VI: cannot be appreciated under Wood’s lightBased on clinical presentationCentrofacialMalarMandibularExtrafacialBased on natural historyTransient: Lesions resolving within one year of cessation of risk factors such as oral contraceptive pillsPersistent: Lesions persisting even after a year of cessation of risk factors

Q. How is severity of melasma assessed clinically?

The severity of melasma can be assessed clinically by the modified Melasma Area Severity Index (mMASI). The score takes into account the area of involvement and darkness in four areas of the face namely the forehead, left malar region, right malar region, and chin. The formula for the same is as follows:

mMASI = 0.3 (A × D) forehead + 0.3 (A × D) left malar region + 0.3 (A × D) right malar region + 0.1 (A × D) chin

where A stands for area and is rated as follows:

0 = absent, 1= <10%, 2 = 10–29%, 3 = 30–49%, 4 = 50–69%, 5 = 70–89%, 6 = 90–100%

D stands for darkness and is rated as follows:

0 = absent, 1 = slight, 2 = mild, 3 = marked, 4 = severe

The score can range from 0 to 24. The component of homogeneity has been eliminated from the original scoring method during its validation.[16],[18] Another global score that has been used in research studies and trials is the Melasma Severity Score (MSS) which grades melasma into clear, mild, moderate, and severe.[18]

Q. What are the recent updates in the etiopathogenesis of melasma?

Recent insights into the etiopathogenesis of melasma reveal that this common disorder of hyperpigmentation results due to an interplay between hyperactive melanocytes, keratinocytes, dermal fibroblasts, vascular factors, neural factors, basement membrane damage, inflammatory factors, and a defective skin barrier. RCM has thrown light upon how all types of melasma are actually of the mixed variety with both epidermal changes and dermal features such as solar elastosis and increased vasculature.[19]

In melasma, the melanocytic activity is heightened but the melanocyte number remains the same. The genes associated with melanogenesis are also increased. Migration of active melanocytes and melanin in the dermis due to probable basement membrane damage may be responsible for persistent pigmentation in patients.[16]

Role of visible light and infrared light has now been established in the etiology of hyperpigmentation especially in the darker skin types. Visible light such as UV radiation (UVR) can increase melanogenesis by causing lipid peroxidation and release of reactive oxygen species. Infrared light can stimulate melanin production via endothelin receptor B and mitogen-activated protein kinase. UVR also causes dermal inflammation leading to activation of fibroblasts and increased melanogenesis.[19]

An increase in the size and number of dermal vessels has been found in melasma under the influence of angiogenic factors such as the vascular endothelial growth factor. Interaction of hyperactive melanocytes with an altered dermal microvasculature stimulates melanin production. UVR also leads to increased plasminogen production from dermal vessels. Binding of plasminogen to keratinocytes can increase melanin synthesis.

Mast cells and histamine have been reported to play a significant role in pathogenesis of melasma. Estrogens have been found to act via estrogen receptors on melanocytes and by upregulating enzymes involved in melanin synthesis. Increased expression of nerve growth factor receptors has also been found in lesional skin.[16],[19] These recent updates in the etiopathogenesis will help guide the evolution of melasma management with new targets for both topical and systemic agents.

Q. Management of melasma

Management of melasma can be very challenging due to multifactorial etiology, frequent recurrences, patient compliance, and sometimes the unyielding nature of the pigmentation. Intense sun protection continues to be the mainstay of therapy especially for maintenance and prevention. Broad spectrum sunscreens with a SPF 30 or above with filters blocking UV, visible and infrared light are now recommended due to better efficacy and results. Iron oxide is one such inorganic filter blocking visible light, it also adds a tint to the sunscreen which aids in cosmetic camouflage. Patients with melasma should also apply sunscreens when indoors due to the potential role of infrared light. The application should be repeated every 2 to 3 hours between 9 am to 4 pm with more than half a teaspoon (3 mL) being applied to the face and neck.[20],[21]

Topical therapies are the main modality of treatment and include agents such as 4% hydroquinone, kojic acid, azelaic acid, glycolic acid, retinoids, niacinamide, arbutin, ascorbic acid, etc. The above agents can be used as first line agents in treatment of mild melasma. Intermittent hydroquinone can be used for up to 6 months for maintenance. Triple combination creams continue to be a first-line modality in initiation of therapy for moderate to severe melasma and should be prescribed only after counseling as the tendency for misuse and abuse is high. The original Kligman formulation contained 5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone. Over the years, various modifications have been carried out. The combination containing 4% hydroquinone, 0.05% tretinoin, and 0.01% flucinolone acetonide is FDA approved and has a level of evidence A in treatment of melasma leading to near complete resolution in about 8 weeks. Daily usage for more than 6 months has been associated with adverse effects such as telangiectasia, atrophy, hypertrichosis, acneiform eruptions, etc. [Figure 3]. Mometasone-based combinations lead to quick results but also quicker relapses on cessation. Long-term use is associated with adverse effects. The patient should be evaluated at 4 and 8 weeks for response. If the response is good, the patient can be switched to other depigmenting agents for maintenance.{Figure 3}

Chemical peels and lasers are reserved for those patients who do not respond to the conventional modalities of treatment. Chemical peels such as glycolic acid, salicylic acid, trichloroacetic acid, Jessner, retinoids, and combination peels have been found to be effective and are combined with the medical management. The response is good in epidermal and mixed melasma. Newer peels with better safety profile include lactic, mandelic, arginine, and pyruvic acid.

Laser and light devices are reserved for patients with refractory melasma. Longer wavelengths are used to target dermal melanin. Q-switched Nd:YAG laser with a large spot size and low fluence has been found to be effective. IPL (Intense Pulsed Light), copper bromide, and vascular lasers such as pulse dye laser (PDL) have also been tried. PDL works on the vascular component of melasma and is an emerging modality. Nonablative fractional resurfacing with transdermal elimination of melanophages has shown improvement in patients with melasma after a single session. Laser toning with Q-switched Nd:YAG laser has also shown good results. Recurrence is almost always the rule unless combined with medical management and other preventive measures.[16],[20]

Q. Role of systemic drugs in melasma

Tranexamic acid is a fibrinolytic drug which inhibits the conversion of plasminogen to plasmin and hence its binding to epidermal keratinocytes. A synthetic derivative of lysine, it decreases production of prostaglandins and fibroblast growth factor. It also inhibits angiogenesis and mast cells. A dose of 250 mg twice daily for 8 to 12 weeks has been found to give a rapid and sustained result. It is contraindicated in patients with history of thromboembolic disorders. Side effects in dermatologic doses are mild and include gastrointestinal upset, skin rashes, hypomenorrhea and alopecia.

Polypodium leucotomos is a fern extract being researched as an adjunct photoprotective agent. It acts by enhancing the endogenous antioxidant systems, modulating inflammatory responses, and promoting p53 suppressor gene expression. Recent studies have demonstrated the efficacy of 240 mg twice daily for 12 weeks with patients reporting a greater reduction in MASI when compared with placebo.

Other oral agents that are being tried include glutathione, melatonin, procyanidin, and pycnogenol. More studies are needed to establish their efficacy in melasma.[20],[21]

Q. Enumerate some of the newer drugs being used in treatment of melasma

With newer insights into the etiopathogenesis of melasma, various new agents are now being studied in its management. Some have been enumerated below depending on their potential target:Drugs targeting hyperactive melanocytes: linoleic acid, ascorbic acid, N-acetyl-4-S-cystaminylphenolMelanogenesis inhibitors: arbutin, deoxyarbutin, aloesin, rucinol, flavonoids, ellagic acid, epigallocatechin gallate, gentisic acid, hydroxycoumarins, cinnamic acid, antisense oligonucleotidesAnti-inflammatory agents targeting reactive oxygen species: licorice extract, orchid extracts, mulberry extracts, coffeeberry extractInhibition of melanosomal transfer to keratinocytes: liquiritin, soy milk, soybeanRestoring skin barrier: soy moisturizerDrugs targeting vascular component and mast cells: tranexamic acidAgents inhibiting effects of estrogen: antiestrogen drugs such as tamoxifen, anastrozole, etc., may have a probable role in the futureOthers: flutamide, curcumin, lignin peroxidase, platelet-rich plasma, methimazole, glutathione, cysteamine

Triple combination of the future may have a formulation including hydroquinone, a vascular endothelial growth factor inhibitor, and an antiestrogen.[19],[21] Response to therapy is good in epidermal melasma, poor in dermal melasma, and varies in mixed melasma. Due to its chronicity and frequent recurrences, melasma still remains a therapeutic challenge and warrants more research into the safety and efficacy of these newer agents for long-term application.


Photograph’s courtesy: Dr. KN Barua Institute of Dermatological Sciences, Guwahati, Assam, India.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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