Oral tranexamic acid has emerged as an adjunct in refractory melasma. Its proposed mechanism of action is:

• A Competitive inhibition of tyrosinase copper binding
• B Blockade of alpha-melanocyte-stimulating hormone receptors on melanocytes
• C Acceleration of epidermal turnover carrying melanin outward
• D Plasmin-mediated reduction of melanocyte activation by keratinocytes exposed to ultraviolet light ✓

Explanation

Ultraviolet exposure increases plasmin in keratinocytes, which triggers release of arachidonic acid and alpha-MSH pathways activating melanocytes. Tranexamic acid blocks plasminogen conversion to plasmin, thereby reducing this melanogenic signalling. Tyrosinase inhibition is the action of hydroquinone and kojic acid, enhanced turnover describes retinoids, and MSH receptor blockade is not an established melasma pathway.

Reference: Fitzpatrick's Dermatology, 9th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.