The mean age of patients with melasma in India is 37.2 ± 9.3 years. The prevalence of Melasma is higher in females and the female to male ratio is approximately 4:1. Studies suggest that the overall population with family history was 31%, highest in the northern region (38.5%) and lowest in the eastern region (18.2%). Also, the two prominent patterns of distribution in Indian patients are centrofacial (42%) and malar (39%) Melasma.
Melasma appears on sun-exposed areas and 20% may clear totally in a year but 80% have persistent, recalcitrant Melasma. Clearance – partial or total and maintenance are cornerstones in treatment. Melasma expressions include epidermal pigment, dermal pigment, mixed epidermal and dermal, erythemto-telangiectatic-vascular component, etc.
Interactions between altered cutaneous vasculature and melanocytes may influence the development of hyperpigmentation in the overlying epidermis. Vascular endothelial growth factor (VEGF) also has a direct influence on melanogenesis through its receptor on melanocytes, vascular endothelial cells, cytokines and soluble factors such as plasminogen are released on UV exposure, which might be a possible cause of hyperpigmentation in melasma – tranexamic acid.
UV melanogenesis by its direct effect on DNA and melanocyte membranes, release diacylglycerol and arachidonic acid, which have a putative role in melanogenesis. UV light increases cell surface expression of receptors for keratinocyte-derived paracrine melanogenic factors such as fibroblast growth factor, nerve growth factor, endothelin-1, and the proopiomelanocortin derived peptides such as melanocyte-stimulating hormone, adrenocorticotropic hormone, and beta-endorphin. Sun exposure, pregnancy, hormonal-oral contraceptives (estrogen production, ovarian dysfunction, thyroid dysfunction), and anti-seizure drugs are some of the triggers and perpetrators.
The goals of therapy in such cases are:
- To retard the proliferation of hyperactive melanocytes
- To inhibit the formation of melanin (melanosomes with mature melanin)
- To promote the degradation of melanosomes
- To protect the skin from UV
- To control inflammation
Topical therapies, sunscreens mandatory, lightening agents, antioxidant cosmeceuticals, and anti-inflammatory agents can be used to get visible influence on pigment components. Interventions are never first-line therapy in treating Melasma. They always are adjuvant to topical therapies and will be introduced for unresponsive or recalcitrant cases. For severe cases, treatment options are combination therapy, chemical peels, laser therapy, dermabrasion, and Camouflage.
Treating melasma has practical limitations such as:
- Achieving pigment reduction in dark skin is a challenge, especially dermal component
- The vascular component in melasma is the new highlight
- Unsatisfied patients as a clinical reduction in pigment take long time
- Superadded limitations from steroid and hydroquinone dependence and abuse
- Interventions are helpful but marred by PIH with aggressive modalities
- Recurrences are a rule
- LOSS OF ADHERENCE