Hyperpigmentation

Hyperpigmentation is the visible result of increased melanin production, increased transfer to keratinocytes, or melanin dropping into the dermis. Basal melanocytes synthesise melanin within melanosomes, with tyrosinase rate-limiting, and each melanocyte distributes melanosomes to a surrounding group of keratinocytes. Post-inflammatory hyperpigmentation follows acne, eczema, trauma, or procedures; melasma is a distinct hormonally and light-influenced pattern; solar lentigines follow cumulative ultraviolet exposure.

The clinically decisive variable is depth. Epidermal pigment is within reach of tyrosinase inhibitors, retinoids, and accelerated turnover and generally improves over months. Dermal pigment, where basement membrane damage has let melanin be taken up by dermal macrophages, can persist for years. Wood's lamp examination and dermoscopy help distinguish the two. Hydroquinone remains the reference tyrosinase inhibitor; in the United States over-the-counter hydroquinone products lost their marketing status under legislation enacted in 2020.

Depth should drive the approach, and so should phototype. Fitzpatrick types four through six carry the highest risk of post-inflammatory hyperpigmentation from procedures and from irritating topicals, a genuine tradeoff: an aggressive depigmenting regimen can inflame skin and worsen precisely what it targets.

Two evidential traps dominate this area. Before-and-after photographs of pigmentation are exceptionally sensitive to lighting angle, exposure, and camera white balance, so uncontrolled images can manufacture most of an apparent result. And brightening peptides are frequently supported only by inhibition of mushroom tyrosinase in a cell-free assay, an enzyme that differs substantially from human tyrosinase and predicts in-skin performance poorly.