Unit 2.30 – Post Inflammatory Hyperpigmentation (PIH) Copy

Post-inflammatory hyperpigmentation

History can include infestation, allergic reactions, mechanical injuries (picking acne lesions) or reactions to medications, phototoxic eruptions, burns, bruising and inflammatory skin diseases from eczema/dermatitis family. This type of pigmentation can darken with exposure to UV light and with the use of various chemicals and medications, such as tetracycline, bleomycin, doxorubicin, 5-fluorouracil, busulfan, arsenicals, silver, gold, antimalarial drugs, hormones and clofazimine.

Dermal pigmentation caused by trauma

A combination of the inflammatory response and ultraviolet causes the inflammation to disrupt the basal cell layer, a combination of melanin pigment being released and subsequently trapped by macrophages in the papillary layer. Once the wound healing has completed and the junction repaired the melanin pigment granules caught within the dermal layer have no way of escape and thus a more difficult type of pigment granule to eliminate. Post inflammatory hyperpigmentation is a darkening of skin that’s the result of acne scarring or skin injury due to inflammatory response in skin. The cells associated with melanin production are closely linked with the skin immune system cells; meaning you can’t stimulate one without stimulating the other.

Post inflammatory hyperpigmentation can be seen after endogenous or exogenous inflammatory conditions. Essentially any disease with cutaneous inflammation can potentially result in post inflammatory hyperpigmentation in individuals capable of producing melanin. Several skin disorders such as acne, atopic dermatitis, allergic contact dermatitis, incontinentia pigmenti, lichen planus, lupus erythematosus, and morphea have post inflammatory hyperpigmentation as a predominant feature. Exogenous stimuli, both physical and chemical, can cause injury to the skin followed by PIH these include mechanical trauma, ionizing and nonionizing radiation, heat, contact dermatitis, and phototoxic reaction.

Optimal treatment for PIH includes prevention of further pigment deposition and clearing of the deposited pigment. Chemical peels work best when used in combination with topical bleaching regimens. Laser therapy should be used with extreme caution and care. Given the propensity of darker-skin types to develop post inflammatory hyperpigmentation, superficial peels work best, while minimizing complications. Tyrosinase inhibitors, such as vitamin C, arbutin, kojic acid and mulberry, have been favored for their ability to inhibit melanin by targeting the tyrosinase enzyme, which covers the amino acid phenylalanine into the melanin precursors. Effective topical vitamins include niacinamide and several forms of vitamin C, including L-ascorbic acid, magnesium ascorbyl phosphate (MAP) and tetrahexyldecyl ascorbate, an oil soluble version. In addition to having a direct skin-lightening effect, vitamin C can help protect against sun damage by neutralizing free radicals that contribute to hyperpigmentation. Studies have shown that vitamin C and E in combination can improve the efficacy of sunscreen. A great all around skin vitamin, vitamin A helps pigmentation problems by treating slight discoloration and evening skin tone. Vitamin A can be taken orally as well as applied topically in the form of a retinol cream or other retinol. If a client suffers from PIH they need to be using a tyrosine inhibitor two weeks before treatment to avoid further PIH.