Chloasma or melasma is a condition of the skin characterized by the presence of brown to greyish pigmentation usually on the face. Although more common in women and dark-skinned people living in sunny climates, there is no delineation between genders or ethnic origin. Chloasma is more pronounced in the summer and becomes less conspicuous during the winter months. It is not an allergic condition and neither is it infectious nor cancerous.
Chloasma is recognized by the characteristic brownish patches on the face and neck, and sometimes the arms and sternal regions  . The pigmentation appears in susceptible individuals upon exposure to the sun's ultraviolet light. The lesions consist of symmetric, hyperpigmented macules with irregular but clearly delimited borders. These are found most frequently on the forehead, chin, nose, cheeks, and upper lips or other sun-exposed areas of the body. The chloasma are mainly light to dark brown in color of epidermal origin, blue or black in patients with dermal chloasma.
Facial lesions are of two types: centrofacial and peripheral. Centrofacial lesions as the name implies are distributed on the face, i.e., in the frontal, nasal, glabellar, zygomatic, upper lip and chin areas. The peripheral type is found in the preauricular, fronto-temporal, and mandibular areas. Malar involves only the nose and cheeks and mandibular, the ramus of the mandible. While there is no definite explanation for these patterns, the presence and activity of sebaceous glands in these regions may be relevant. Lesions have been observed on the forearms of women undergoing treatment with exogenous progesterone and among Native Americans.
There are no specific laboratory tests for chloasma. Diagnosis is based mainly on the clinical assessment of patient, family history, exposure to the sun, visual examination of the lesions, and confirmatory tests on thyroid function, pregnancy, hormonal treatment and other predisposing factors.
Wood's lamp examination by a dermatologist can verify the nature of the lesions that is, whether they are of epidermal or dermal origins, to guide treatment strategies . Wood's lamp examination (at 340 to 400 nm) can distinguish epidermal from dermal pigmentation as it is important to recognize that dermal chloasma requires a more tedious and prolonged treatment regimen. It has been shown that Wood's light examination has made possible more effective treatment with topical medication  .
Treatment for chloasma is time consuming since pigment development and resolution are both slow processes. Resistance to treatment and recurrences tend to complicate or delay recovery because of repeated exposure to sunlight. All wavelengths of sunlight, including the visible spectrum can induce melanogenesis. The method of choice is a combination of topical hydroquinine cream, avoidance of sunlight and estrogen therapy. Oral contraceptives are to be avoided by all means even among women without a family history of the disorder.
The standard treatment for chloasma is based on the application of topical depigmenting agents such as, hydroxyquinone (HQ) alone or in conjunction with other agents . However, long-term use of HQ is not recommended due to possible deleterious side effects. Topical retinoids (trans- retinoic-acid) can be used as monotherapy and being derivatives of vitamin A may increase keratinocyte regeneration while decreasing melanocyte activity. Superficial skin peels containing glycolic or salicylic acid-based compounds are presumed to accelerate hyperpigmented keratinocytes turnover. These are applied slowly in graduated increments with minimal initial concentration of 20% active ingredients applied weekly. Care must be observed for adverse side effects. Superficial peels can be used with skin lightening agents. Lasers therapy is currently indeterminate.
So far, successful treatment of chloasma has been with the use of topical agents, as a monotherapy or in combination with chemical peels and physical therapy (with laser or intense pulse light sources). Nonetheless, patients should be informed of the nature of the disease and the need for long-term therapy as well as the importance of strict compliance with preventive measures. Treatment is based on whether the pigmentation is epidermal or dermal in origin, which is better assessed with a Wood's light examination or biopsy. First-line therapy for epidermal pigmentation includes 2 to 4% hydroquinone with 0.05 to 1% tretinoin and a class V to VII topical corticosteroid. Prolonged treatment with 2% hydroquinone B.I.D. is recommended as a maintenance dose. Hydroquinone is usually tested on one ear or the forearm for irritability or allergenicity one week week before application on the face. Azelaic acid 15 to 20% cream can be used as an alternative to hydroquinone and/or tretinoin. These three chemical compounds are bleaching agents.
Prognosis is good with adequate treatment and avoidance of exposure to sunlight and other known predisposing factors. Meanwhile, new topical or oral medications are being studied for more effective treatment of chloasma. With successful treatment, reduction in prevalence of chloasma and intensity of lesions with age can be expected.
The goal of treatment is to attenuate or minimize pigmentation, a process which takes time because dermal pigment is difficult to remove. Since dermal pigment derives from the epidermis, inhibition of epidermal melanogenesis will eventually remove the source of dermal pigmentation. Treatment of epidermal pigmentation should be maintained for long periods. Recurrence is likely to occur with repeated exposure to sunlight as well as the persistence of hormonal influences. Therefore, it can not be overemphasized that recovery from melasma requires absolute compliance with treatment and preventive measures.
The precise cause of chloasma is not known. Multiple predisposing factors have been cited in the literature e.g., exposure to the sun, pregnancy, hormone replacement therapy (HRT), oral contraceptives and other steroids, ovarian tumors, certain kinds of food, intestinal parasitoses, liver disease, cosmetics and photosensitizing drugs, inflammation, dermatological procedures, and stress    . These indicate a complex interaction involving the environment, host factors and possibly, family history.
The single most important environmental factor is the sun. Ultraviolet radiation directly induces and accelerates melanogenic activity, resulting in the appearance of epidermal pigmentation which tends to be more intense in sites where there are previous lesions than in the adjacent unaffected skin  . Ultraviolet radiation causes peroxidation of lipids in cell membranes which, in turn, leads to the generation of free radicals. Free radicals stimulate melanocytes to produce more melanin. The choice of sunscreens is relevant. Sunscreens that are able to block only UV-B radiation (short wavelengths of 290-320 nm) are ineffective. Longer wavelengths (UV-A and visible radiation, 320-700 nm) like free radicals cause melanocytes to produce melanin.
Hormones are implicated in the occurrence of chloasma in women. The so called "mask of pregnancy" is a familiar term among obstetrics patients although the exact mechanism behind this phenomenon is not clear. Elevated progesterone, estrogen, and melanocyte-stimulating hormone (MSH) levels are known to coincide with the development of melasma in women during the third trimester of pregnancy. On the other hand, normal levels of estrogen or MSH are maintained in circulation in nulliparous patients with chloasma, but with functional estrogen receptors at the site of the lesions. Evidence shows that oral contraceptive containing estrogen and/or progesterone, HRT, intrauterine devices and implants are linked to chloasma in about 25% of affected women.
Anti-cancer therapy, scented toiletries and cosmetics may cause phototoxicity that possibly account for persistent episodes of chloasma. Hypothyroidism, stress and genetic predisposition likewise contribute to the incidence of chloasma. To recapitulate, sunlight (UVL), pregnancy, genetics, and hormones are the important risk factors in chloasma. Women are more prone than men and persons with light-brown complexion residing in the tropics where exposure to UVL is intense are more susceptible.
Melasma gravidarum or the mask of pregnancy occurs in 15-50% of pregnant women. It is also more common in women taking oral contraceptives. Nulliparous women and men with dark complexion constitute 10% of all cases of chloasma. In addition, episodes of chloasma persist longer in persons with dark skin (i.e., skin types IV to VI) than in lighter skin types. It is more prevalent among people living in the tropics (e.g., East Asian, Southeast Asian, and Hispanics) who are constantly exposed to intense ultraviolet light waves. Chloasma is also common among Indians . The clinical presentation and histology of chloasma in both men and women are identical . There is no delineation with regards to ethnic origin. The disorder rarely occurs before puberty but peaks in women of reproductive age.
Elevated levels of estrogen, progesterone, and melanocyte-stimulating hormone (MSH) have been observed in women with chloasma during the third trimester of pregnancy whereas, nulliparous patients have normal levels of estrogen or MSH in circulation. Furthermore, the intake of estrogen and progesterone oral contraceptives has been linked to melasma. Postmenopausal women on progesterone medication have been known to develop melasma but not those who are given estrogen only. Thus, progesterone is the principal determinant in this case. Exposure to the sun's spectrum (UV-B, UV-A, and visible light) can trigger melanogenesis.
The pathophysiological basis of chloasma is not clearly understood. A causal association with female hormonal status is apparent which explains why chloasma is more frequently found in females than in males. Pregnancy and oral contraceptives provide the stimuli for melanogenesis and one out of every melasma case presents initially during pregnancy. Estrogen receptors appear to be activated in chloasma lesions . The association of hormonal levels with male chloasma remains contestable.
Other factors that predispose to chloasma are the use of photosensitizing medications, scented cosmetics, and mild ovarian or thyroid dysfunction. Exposure to UV radiation (UV-B, UV-A and visible light) is paramount in the pathogenesis of chloasma. Ultraviolet radiation catalyzes the production of alpha-melanocyte-stimulating hormone and corticotropin, and the pharmacologically active interleukin 1 and endothelin 1 that altogether facilitate melanin production by intraepidermal melanocytes. Furthermore, genetic factors may be involved based on the family history of more than 40% of patients claiming to have relatives affected with the disease.
Chloasma is a self-limiting disorder. Spontaneous cure is possible although it takes a long time for the pigmentation to disappear. The best preventive measure is to avoid exposure to the sun. Photoprotection can be achieved in a number of ways, including wearing of hats and application of broad-spectrum sunscreens. Sunscreens with physical blockers (e.g., titanium dioxide and zinc oxide) provide broader protection than chemical blockers. These measures have been proven to be efficacious, however, clinical studies are lacking on their role in disease prevention. Regardless of treatments used, the important critical factor in any case is "staying away from the sun's way" so to speak. UV-B, UV-A and visible light can stimulate melanogenesis and trigger a new bout of chloasma in between treatments. Facial make-ups containing zinc oxide or titanium dioxide can both protect and provide cosmetic effect of minimizing the discoloration. Patients should be made to understand the importance of photoprotection and that resolution is a long tedious process but recovery is certain.
Chloasma is a chronic abnormality of the skin resulting in the development of patchy, brownish discoloration on the face. As such, this condition may be a cause of concern if not embarrassing for some individuals. Hypermelanosis called "the mask of pregnancy" affects 50 to 70% of women during the gestation period. Upon exposure to the sun, symmetric hyperpigmented macules appear on the cheeks, upper lip, chin and forehead, which are either confluent or punctuate. The exact relationship between pregnancy and melanogenesis is unknown. Chloasma may also develop in other parts of the body that are exposed to the sun.
Chloasma, also referred to as melasma and sometimes called "the mask of pregnancy", is a chronic disorder of the skin presenting as brown patches or macules with irregular borders on areas of the body that are customarily exposed to the sun. The usual sites that are affected are the face, neck, and sometimes the forearm. Apart from the embarrassing appearance for individuals who are particular with their looks, chloasma is typically a harmless condition, which is neither infectious nor cancerous.
Persons who are susceptible to chloasma are those with light-brown to dark brown complexion living in areas where they are constantly exposed to the sun, such as in the tropics. Melasma can develop in adult male or female regardless of age or ethnicity although it is said to be more common in women particularly those who are pregnant or on oral contraceptives.
Exposure to the sun's ultraviolet rays is the most critical factor. UV radiation can stimulate the melanocytes found in the skin to produce pigments. Other risk factors that can trigger melanogenesis are hormonal treatments, infectious diseases, thyroid and liver diseases, stress, cosmetics and photosensitizing drugs. Although chloasma is self-limiting and spontaneous cure may be expected, it takes a long time. Treatment with topical medication and avoidance of exposure to the sun can hasten recovery. Recurrence may occur without photoprotective measures such as wearing of hats and the use of appropriate sunscreens. Cosmetic remedies can be done but care must be taken to avoid the side effects or to cease the practice altogether if they do not help in preventing the occurrence of chloasma.