What is postinflammatory hyperpigmentation?
Postinflammatory hyperpigmentation is temporary dark discolouration of the skin after an underlying skin disease has healed.
More severe injury results in postinflammatory hypopigmentation, which is usually permanent.
What causes postinflammatory hyperpigmentation?
Conditions causing postinflammatory hyperpigmentation include:
- Skin infections due to bacteria, fungi, viruses, parasites
- Trauma, eg thermal burns, abrasions
- Reactions to medications, eg fixed drug eruption and other drug eruptions
- Phototoxic eruptions, eg some forms of plant dermatitis
- Inflammatory reaction, eg acne, dermatitis, lichen planus and psoriasis
What are the clinical features of postinflammatory hyperpigmentation?
Postinflammatory hyperpigmented patches are located at the site of the original disease after it has healed. The lesions range from light brown to black in colour. The patches may become darker if exposed to sunlight (UV rays).
Some medications may also darken postinflammatory pigmentation. These include antimalarial drugs, clofazimine, tetracycline, anticancer drugs such as bleomycin (flagellate erythema), doxorubicin, 5-fluorouracil and busulfan.
Postinflammatory hyperpigmentation can occur in anyone, but is more common in darker skinned individuals, in whom the colour tends to be more intense and persists for a longer period. Pigmentation tends to more pronounced in sun-induced skin conditions such as phytophotodermatitis and lichenoid dermatoses (skin conditions related to lichen planus including erythema dyschromicum perstans).
Lichen planus actinicus
Violin playing (friction)
Postinflammatory hyperpigmentation (inflamed cyst)
Flagellate reaction to bleomycin
What causes postinflammatory hyperpigmentation?
Postinflammatory hyperpigmentation can be due to increased melanin or melanosis within epidermal cells (the outer layer of the skin) or deposited in the dermis (the deeper layer of the skin).
Epidermal melanosis follows inflammatory responses of the epidermis to disease or trauma, which results in the release and oxidation of arachidonic acid to prostaglandins, leukotrienes, interleukin-1 and other products. Fibroblasts in the dermis produce keratinocyte and melanogenic growth factors. These products alter the activity of immune cells and melanocytes. An increased number of melanocytes produce more melanin (skin pigment), which is transferred to surrounding keratinocytes (skin cells).
Dermal melanosis is a deeper pigmentation that occurs when inflammation disrupts the basal cell layer (the bottom of the epidermis), causing melanin pigment to be released into the papillary dermis (the top part of the dermis). The dermal pigment may be trapped by large immune cells called tissue macrophages.
How is postinflammatory hyperpigmentation diagnosed?
Postinflammatory hyperpigmentation is diagnosed by taking a careful history and examining the skin. Dermal melanosis gives a characteristic hue to the skin colour (grey-purple-brown).
Sometimes the diagnosis is only made after skin biopsy. Histopathology reveals patchy epidermal melanosis and/or dermal melanosis.
What is the treatment for postinflammatory hyperpigmentation?
Usually, hyperpigmentation will gradually lessen over time and normal skin colour will return. However, this is a long process that may take up to 6–12 months or longer. Patients should be advised to use broad spectrum sunscreens daily to reduce further darkening when outdoors.
Cosmetic camouflage using pigmented makeup can also be used to disguise hyperpigmented skin to a hue that is similar to surrounding unaffected skin.
A variety of topical treatments are available to lighten/bleach hyperpigmented lesions in epidermal hypermelanosis. Varying degrees of success are achieved but combinations of the treatments below are usually required for significant improvement.
- Azelaic acid
- Vitamin C cream
- Tretinoin cream
- Corticosteroid creams
- Glycolic acid peels
- Others: kojic acid, arbutin, licorice extracts, mequinol, niacinamide, N-acetyl glucosamine, soy
These treatments are not effective in dermal hypermelanosis.
- Cardinali G, Kovacs D, Picardo M. Mechanisms underlying post-inflammatory hyperpigmentation: lessons from solar lentigo. Ann Dermatol Venereol. 2012 Dec;139 Suppl 4:S148-52. doi: 10.1016/S0151-9638(12)70127-8. Review. PubMed PMID: 23522630.
- Lamel SA, Rahvar M, Maibach HI. Postinflammatory hyperpigmentation secondary to external insult: an overview of the quantitative analysis of pigmentation. Cutan Ocul Toxicol. 2013 Mar;32(1):67-71. doi: 10.3109/15569527.2012.684419. Epub 2012 Jun 6. Review. PubMed PMID: 22667459.
- Book: Textbook of Dermatology. Ed Rook A, Wilkinson DS, Ebling FJB, Champion RH, Burton JL. Fourth edition. Blackwell Scientific Publications.
- Callender VD, St Surin-Lord S, Davis EC, Maclin M. Postinflammatory hyperpigmentation: etiologic and therapeutic considerations. Am J Clin Dermatol. 2011 Apr 1;12(2):87-99. doi: 10.2165/11536930-000000000-00000. Review. PubMed PMID: 21348540
On DermNet NZ:
- Postinflammatory Hyperpigmentation – Medscape Reference
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