Melasma pathogenesis involves which interaction that drives epidermal hyperpigmentation beyond simple sun exposure?
- A Stem cell factor (SCF)/c-Kit and endothelin-1 (ET-1) from keratinocytes activating melanocytes ✓
- B IL-17A from T-cells directly stimulating melanocytes
- C Autoimmune destruction of surrounding melanocytes causing rebound hyperpigmentation
- D TGF-beta-mediated dermal fibrosis stimulating melanogenesis
Explanation
In melasma, UV exposure induces keratinocytes to secrete SCF (stem cell factor), endothelin-1, and prostaglandins, which activate c-Kit receptor on melanocytes leading to increased melanogenesis and dendricity. Additionally, hormonal factors (estrogen/progesterone activate ERα in melanocytes) and vascular changes (increased VEGF, dermal neovascularization) contribute. This explains why sun protection alone is insufficient and why oral tranexamic acid (which inhibits plasminogen activator-mediated prostaglandin release) is effective.
Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.