Melanin, the pigment responsible for skin and hair color, is produced by melanocytes beneath the skin. The amino acid L-Tyrosine acts as a precursor for melanin synthesis through enzymatic reactions (Raper Mason pathway). Melanin comes in two forms: darker Eumelanin (black and brown) and lighter Pheomelanin (yellow-red). Controlling L-Tyrosine and L-DOPA levels is important for regulating melanin production (1).
In the presence of oxygen, the tyrosinase enzyme converts tyrosine into DOPA and then into DOPA-quinone. The presence or absence of cysteine determines whether the pathway leads to eumelanin (darker pigment) or pheomelanin (lighter pigment). Different skin types have variations in how melanosomes (where melanin is stored) degrade during keratinocyte differentiation, resulting in diverse skin colors and complexions. Disruptions in the melanin production process, caused by internal and external factors, can lead to hyperpigmentation disorders (1, 2).
Hyperpigmentation refers to various skin disorders characterized by dark patches or discoloration. Examples include melasma, post-inflammatory hyperpigmentation, and solar lentigines (sun and age spots). Melasma specifically presents as brown patches on the skin, often becoming more noticeable after sun exposure.
Multiple factors contribute to the development of hyperpigmentation. These include genetics, hormonal imbalances, pregnancy, exposure to UV radiation, stress, hormone therapy, certain medications, and cosmetics. Among these, genetic predisposition and sun exposure play crucial roles.
Melasma involves increased melanin deposition, presenting as brown patches on the face. It commonly affects women of childbearing age, with an onset between 30-55 years (1, 2).
