Melasma

In women, genetic predisposition and increased exposure to hormones (through pregnancy, the use of oral contraceptives or other hormonal treatments, or endocrine dysfunction) are key factors in the aetiology of melasma.[11]Ortonne JP, Arellano I, Berneburg M, et al. A global survey of the role of ultraviolet radiation and hormonal influences in the development of melasma. J Eur Acad Dermatol Venereol. 2009;23:1254-62. http://www.ncbi.nlm.nih.gov/pubmed/19486232?tool=bestpractice.com Men may have melasma, but hormone exposure does not seem to play an important role in these patients. Cosmetic agents and phototoxic drug exposure can trigger melasma in men and women.[12]Grimes PE. Melasma. Etiologic and therapeutic considerations. Arch Dermatol. 1995;131:1453-7. http://www.ncbi.nlm.nih.gov/pubmed/7492140?tool=bestpractice.com Ultraviolet light exposure also plays an important role in this condition, and those with increased sun exposure are more likely to develop melasma.

Melasma is caused by an increase in dermal and epidermal melanin production and retention. Skin biopsies from patients with melasma show an increase in the number of melanocytes and melanin-laden macrophages (melanophages). In addition, later-stage melanocytes containing greater numbers of melanosomes may be present; these are the cellular organelles responsible for melanin synthesis.[3]Nicolaidou E, Antoniou C, Katsambas AD. Origin, clinical presentation, and diagnosis of facial hypermelanoses. Dermatol Clin. 2007 Jul;25(3):321-6, viii. http://www.ncbi.nlm.nih.gov/pubmed/17662897?tool=bestpractice.com In keratinocytes, there is an overexpression of vascular endothelial growth factor (VEGF). It is thought that VEGF may be related to melanocyte behaviour.[13]Kang HY, Ortonne JP. What should be considered in treatment of melasma. Ann Dermatol. 2010 Nov;22(4):373-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991712/?tool=pubmed http://www.ncbi.nlm.nih.gov/pubmed/21165205?tool=bestpractice.com Solar elastosis is increased by 83% in melasma patients, which also correlates with the fact that this disease is a process that involves cumulative sun exposure as an important risk factor for its occurrence.[14]Torres-Álvarez B, Mesa-Garza IG, Castanedo-Cázares JP, et al. Histochemical and immunohistochemical study in melasma: evidence of damage in the basal membrane. Am J Dermatopathol. 2011;33:291-295. http://www.ncbi.nlm.nih.gov/pubmed/21317614?tool=bestpractice.com Some of the pathological changes found in the skin of melasma patients compared with non-affected perilesional skin include photodamage, vascularisation, inflammation, and melanogenic activity.[15]Miot LD, Miot HA, Polettini J, et al. Morphologic changes and the expression of alpha-melanocyte stimulating hormone and melanocortin-1 receptor in melasma lesions: a comparative study. Am J Dermatopathol. 2010;32:676-682. http://www.ncbi.nlm.nih.gov/pubmed/20534990?tool=bestpractice.com

Histological subtypes[2]Victor FC, Gelber J, Rao B. Melasma: a review. J Cutan Med Surg. 2004 Mar-Apr;8(2):97-102. http://www.ncbi.nlm.nih.gov/pubmed/15685388?tool=bestpractice.com

• Epidermal type: most common type; melanin is increased in the epidermis, with only a few melanocytes in the upper dermis; enhances on Wood lamp examination

• Dermal type: many melanophages throughout the entire dermis; does not enhance on Wood lamp examination

• Mixed type: melanin is increased in the epidermis, and many melanophages throughout the dermis; spotty enhancement on Wood lamp examination

• Indeterminate type: seen in people with Fitzpatrick type V or VI skin (skin that very rarely burns or never burns); Wood lamp examination is not helpful.

Clinical subtypes[3]Nicolaidou E, Antoniou C, Katsambas AD. Origin, clinical presentation, and diagnosis of facial hypermelanoses. Dermatol Clin. 2007 Jul;25(3):321-6, viii. http://www.ncbi.nlm.nih.gov/pubmed/17662897?tool=bestpractice.com

• Centrofacial: involves forehead, cheeks, upper lip, nose, and chin

• Malar: involves upper cheek area

• Mandibular: involves the ramus of the mandible.

Fitzpatrick skin-type classification

• Type I: white, always burns easily, never tans

• Type II: white, always burns easily, tans minimally

• Type III: white, burns minimally, tans gradually

• Type IV: light brown, burns minimally, tans well

• Type V: brown, rarely burns, tans profusely

• Type VI: dark brown or black, never burns, tans profusely.

[Figure caption and citation for the preceding image starts]: Fitzpatrick skin type classificationCreated by BMJ Knowledge Centre [Citation ends].

Melasma Area and Severity Index (MASI) Score

This classification is primarily used in research and provides a quantitative index of the severity of melasma. Even though the MASI score is a subjective measure, one study showed reliability, stability, and consistency.[4]Pandya AG, Hynan LS, Bhore R, et al. Reliability assessment and validation of the Melasma Area and Severity Index (MASI) and a new modified MASI scoring method. J Am Acad Dermatol. 2011 Jan;64(1):78-83, 83.e1-2. http://www.ncbi.nlm.nih.gov/pubmed/20398960?tool=bestpractice.com

• Area of involvement (A): includes analysis of four areas including the forehead (f) 30%; right malar region (rm) 30%; left malar region (lm) 30%; and the chin (c) 10%. The area of melasma involvement is given a numeric value from 0 to 6.

  • 0 = no involvement

  • 1 = <10% involvement

  • 2 = 10% to 29% involvement

  • 3 = 30% to 49% involvement

  • 4 = 50% to 69% involvement

  • 5 = 70% to 89% involvement

  • 6 = 90% to 100% involvement

• Darkness (D): estimated and given a value from 0 to 4.

  • 0 = absent

  • 1 = slight

  • 2 = mild

  • 3 = marked

  • 4 = maximum

• Homogeneity (H): estimated and given a value from 0 to 4 using the same scale as darkness.

The MASI score is then calculated by the following formula: 0.3 A(f) [D(f) + H(f)] + 0.3 A(rm) [D(rm) + H(rm)] + 0.3 A(lm) [D(lm) + H(lm)] + 0.1 A(c) [D(c) + H(c)].