Postinflammatory Hyperpigmentation
This acquired excess of pigment can be attributed to various preceding disease processes that affect the skin such as infections, allergic reactions, mechanical injuries, reactions to medications, phototoxic eruptions, trauma-like burning, and inflammator
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Sandra Ronger Savle
38.1 Clinical Presentation This acquired excess of pigment can be attributed to various preceding disease processes that affect the skin such as infections, allergic reactions, mechanical injuries, reactions to medications, phototoxic eruptions, trauma-like burning, and inflammatory diseases. This frequently follows lichen planus or lichen sclerosus in which the pigmentation may be persistent. It can develop on scars (obstetrical, gynecological). It is more common in individuals with darker skin (Fitzpatrick skin types III to VI). The classification known as the Fitzpatrick skin type (or phototype) depends on the amount of melanin pigment in the skin. This is determined by constitutional color (white, brown, or black skin) and the result of exposure to ultraviolet radiation (tanning). Type I is pale or white skin that burns easily and tans slowly and poorly: it needs more protection against sun exposure. Type VI is darker skin that burns less and tans more easily. It is also more prone to develop postinflammatory pigmentation after injury (brown marks). The lesions are macular pigmentation macules, unilateral or bilateral, and with tendency to confluence, on site of inflammatory lesions or on scars. The color of the lesions ranges from light
S. Ronger Savle (*) Department of Dermatology and Gynecology, Lyon 1 University and Centre Hospitalier Lyon Sud, Pierre Bénite, Lyon, France
brown to black, with a lighter brown appearance if the pigment is within the epidermis (i.e., epidermal melanosis) and a darker gray to bluish appearance if lesions contain dermal melanin (i.e., dermal melanosis). Furthermore, lesions of postinflammatory hyperpigmentation can darken with exposure to UV light and various chemicals and medications, such as tetracycline, bleomycin, doxorubicin, 5-fluorouracil, busulfan, arsenicals, silver, gold, antimalarial drugs, hormones, and clofazimine.
38.2 Histopathology The epidermal inflammatory response results in the release and subsequent oxidation of arachidonic acid to prostaglandins, leukotrienes, and other products. These products of inflammation alter the activity of both immune cells and melanocytes. Specifically, these inflammatory products stimulate epidermal melanocytes, causing them to increase the synthesis of melanin and subsequently to increase the transfer of pigment to surrounding keratinocytes. Such increased stimulation and transfer of melanin granules result in epidermal hypermelanosis. On the contrary, dermal melanosis occurs when inflammation disrupts the basal cell layer, causing melanin pigment to be released and subsequently be trapped by macrophages in the
© Springer International Publishing AG, part of Springer Nature 2019 J. Bornstein (ed.), Vulvar Disease, https://doi.org/10.1007/978-3-319-61621-6_38
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papillary dermis, also known as pigmentary incontinence.
38.3 Treatment Postinflammatory hyperpigmentation tends to fade with time and therapy. Remnants of epidermal hyperpigmentation may persist for indefinite periods, typically
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