You found us. Start with what brought you.

L-ascorbic acid is the most-studied vitamin C form (direct tyrosinase inhibition); requires pH 2.5-3.5 to penetrate, which can itself trigger PIH on reactive Fitzpatrick IV-VI skin.

Oral tranexamic acid 250mg twice daily for 3 months produced a 49% mMASI reduction vs 18% placebo.

Tranexamic acid is an antifibrinolytic lysine analogue that binds the lysine-binding sites of plasminogen and so reduces plasmin generation. In guinea pigs, topical tranexamic acid applied after UV exposure reduced UV-induced pigmentation and arachidonic-acid-induced pigmentation; the authors propose that UV raises epidermal plasmin activity, plasmin promotes arachidonic acid release and prostaglandin production, and these arachidonic-acid metabolites stimulate melanocyte tyrosinase (arachidonic-acid metabolites do stimulate tyrosinase in cultured human melanocytes). This chain rests on animal and cell-culture data and is not established in humans.

In cultured melanocytes and keratinocyte-melanocyte models, tranexamic acid reduces melanin content, tyrosinase activity and tyrosinase protein by acting on signalling upstream of the enzyme, rather than being characterised as a direct tyrosinase-enzyme inhibitor. It does so both through a keratinocyte paracrine route (tranexamic acid raised keratinocyte TGF-beta1, which suppressed melanogenesis in melanocytes) and directly on melanocytes (ERK-MITF degradation; cAMP-PKA-CREB-MITF; VEGF-receptor signalling). The evidence is in vitro; in a 30-patient refractory-melasma series, oral tranexamic acid was followed by lower epidermal pigmentation and Melan-A staining.

2-5% niacinamide produced statistically significant melanin-density reduction over 4-8 weeks (35-68% melanosome-transfer inhibition in coculture).

The core PIH mechanism (melanocytes overproduce pigment in response to inflammation on elevated-melanin-density skin).

Chronic friction induces hyperpigmentation (frictional melanosis).

PIH is often chronic; improves only partially and slowly.

Iron-oxide sunscreen protects against visible-light-induced pigmentation in Fitzpatrick III-VI, including melasma, where SPF alone did not.

Visible light is ~45% of solar spectrum and can induce persistent darkening, especially in skin of color.

Tranexamic acid produced significantly greater melasma improvement (MASI) than ascorbic acid mesotherapy in skin-of-color patients.

Azelaic acid inhibits tyrosinase and accelerates keratinocyte turnover.

Niacinamide at 10-12% blocks melanosome transfer.

Visible light induces pigmentation in darker skin; iron-oxide tints block it, plain nanoparticle mineral filters do not.

Iron-oxide/tinted photoprotection corroboration for skin of color.

Physical sunscreens with iron oxide and silicones give a photoprotective + camouflage effect in melasma.

Visible light's role in melasma is established; its role in PIH specifically remains to be demonstrated.

L-ascorbic acid penetrates skin only below pH 3.5, optimal absorption ~20%; several derivatives did not raise skin vitamin C levels in the same study.

PIH affects darker skin with greater frequency/severity; azelaic acid, niacinamide, ascorbic acid are recognized topical depigmenting agents in skin of color.

Citrus-induced phytophotodermatitis can present as hyperpigmentation without preceding inflammation, especially in dark-skinned people.

On skin of color, irritation itself can trigger PIH; clinical approach is to start low and titrate up.

Topical retinoids reduce hyperpigmentation in patients with skin of color and should be started early.

All-Black-patient RCT: 0.1% tretinoin improved melasma (MASI) 32% vs 10% vehicle over 40 weeks; side effects limited to mild retinoid dermatitis in 67%.

Frictional melanosis is an acquired pigmentary disorder — brown pigmentation from repeated rubbing — recognized among frictional dermatoses, prevalent in more pigmented skin.

In richly pigmented skin, frictional/postinflammatory pigmentation is common; PIH risk requires cautious, individualized treatment.

The Fitzpatrick scale (developed 1975 by Thomas Fitzpatrick) classifies UV response, not appearance; Types I-VI run from always-burns/never-tans to never-burns/tans-deeply; higher melanin density means higher PIH risk, not more protection; product concentrations formulated/tested on Fitzpatrick I-III can inflame IV-VI skin.