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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.

Skin's acidic pH supports barrier repair and antimicrobial defense; pH stays raised for hours after even a single wash.

Surfactants remove not just grease and dirt but also corneocytes, lipids, and proteins; repeated over-exposure causes irritant dermatitis.

Management of hand-hygiene-driven irritant contact dermatitis is choosing less-irritating products plus frequent moisturizer, not washing less.

Triterpene constituents of shea butter's unsaponifiable fraction have anti-inflammatory activity.

Shea butter is a component of evidence-backed eczema barrier formulations.

Traditional wound-healing use of shea butter is documented.

The water-transport resistance of a deposited occlusive or emulsion film can increase stratum-corneum hydration and alter permeability and TEWL; the relevant mechanism is the film left on skin.

No study located shows shea BUTTER fades hyperpigmentation: the published melanogenesis-inhibition result is for a lab extract of the defatted kernel, not the butter; the Library declines the "shea fades dark spots" claim.