Diagnosis

Discussion

Melasma is one of the most common chronic acquired pigmentary disorders. It is characterized by hyperpigmented macules present symmetrically mainly on the sun exposed areas of face. Sun-exposure and hormones are major triggering factors. Several clinical patterns of melasma including facial and extra-facial types have been described. Woods lamp examination helps in identifying epidermal, dermal or mixed types. There are several method of treatment including topical and oral medical treatment, chemical peels and lasers available for melasma.

The term chloasma (comes from Greek word chloazein meaning to be green) or the mask of pregnancy had been used in past, whereas the term melasma comes from the Greek melas, meaning brown. It occurs most commonly in Fitzpatrick skin phototype III and IV. Prevalence of melasma ranges from 1.5% in western countries [1] to as high as 40% Southeast Asian populations [2]. Melasma is much more common in women and occurs during reproductive years. It is present in 15–50% of pregnant patients.

The exact etiopathogenesis of melasma is not well understood; several factors have been reported. These risk factors are genetic predisposition, exposure to ultraviolet (UV) light, pregnancy, oral contraceptives and hormone replacement therapy [3]. Many studies have suggested higher incidence of melasma in family members indicating genetic predisposition a major risk factor. Sun exposure is a commonly reported aggravating factor because of UV-induced upregulation of melanocyte stimulating cytokines. Hormonal influence plays a role in development or exacerbation of melasma in some individuals. With pregnancy or oral contraceptive use onset or worsening of melasma has been noted in many patients but clinical evidence to date does not clearly associate serum hormone level to melasma. Other less common reported risk factors are cosmetic abuse, nutritional deficiency, thyroid disorders and phototoxic medications. Recent studies have suggested possibility of neural mechanism because of increased expression of nerve growth factor receptor (NGFR) in keratinocytes and more hypertrophic nerve fibers in superficial dermis of lesional skin compared to non-lesional skin. Increased expression of vascular endothelial growth factor (VEGF) by keratinocytes and more numerous large blood vessels in lesional skin indicate vascular component in pathogenesis of melasma. Histopathological studies have documented solar elastosis, basal layer vacuolar degeneration and basement membrane disruption, increased vascularity (evident by increased number, size and density of blood vessels), and increased mast cells in the lesional skin; the clinical and therapeutic implications of these findings are being explored. Considering increased vascularity of the lesional skin, tranexamic acid has been successfully tried in the treatment of melasma.