Post-inflammatory Pigment Alteration
Post-inflammatory pigment alteration is a common sequela of acne vulgaris in darker skin types (Fitzpatrick skin phototypes IV–VI). Acne-associated dyschromia contributes considerably to the psychological and emotional distress experienced by acne patient
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Post-inflammatory Pigment Alteration Rajiv I. Nijhawan and Andrew F. Alexis
40.1
Introduction
Post-inflammatory pigment alteration is a common sequela of acne vulgaris in darker skin types (Fitzpatrick skin phototypes IV–VI). Acne-associated dyschromia contributes considerably to the psychological and emotional distress experienced by acne patients and can often be of greater concern to the patient than the acne itself [1–3]. Post-inflammatory hyperpigmentation is seen much more frequently than post-inflammatory hypopigmentation; however, it is important to keep in mind that in addition to acne itself, various acne treatments can cause hyper- or hypopigmentation as a result of irritation.
40.2
Background
Post-inflammatory pigment alteration especially hyperpigmentation is a common presenting concern, especially in acne patients [4, 5]. In a hospital-based dermatology practice in New York City, dyschromia was the second most common presenting diagnosis second to acne in black patients [5]. Of note, in another study, 65.3 % of African-Americans, 52.7 % of Hispanics, and 47.4 % percent of Asians all had hyperpigmented macules secondary to acne [6]. While the multifactorial pathogenesis of acne appears to be the same in all skin types and ethnic populations [1], the innate qualities of each patient such as skin color and sensitivity to inflammation markedly individualizes this disease. The differences in skin color are attributed to the varying degrees of epidermal density and distribution of the melanin, activity of R.I. Nijhawan, M.D. • A.F. Alexis, M.D., M.P.H. (*) Department of Dermatology, St. Luke’s-Roosevelt Hospital Center, 1090 Amsterdam Avenue, Suite 11B, New York, NY 10025, USA e-mail: [email protected]
J.A. Zeichner (ed.), Acneiform Eruptions in Dermatology: A Differential Diagnosis, DOI 10.1007/978-1-4614-8344-1_40, © Springer Science+Business Media New York 2014
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the enzyme tyrosinase, variations in number, size, and groupings of the melanosomes, as well as the efficiency of melanosome transfer to keratinocyte [7–10]. A key characteristic in skin of color is the tendency for melanocytes to exhibit labile responses to inflammation and injury [11, 12], which contributes to the high prevalence of post-inflammatory hyperpigmentation in darker skin types. Inflammatory mediators, including prostaglandins and leukotrienes, can stimulate increased melanin synthesis, which can lead to increased pigment in the epidermis alone or also in the dermis [13]. When there is dermal involvement, there is disruption of the basal layer that leads to macrophages engulfing the melanin and the formation of melanophages. In addition, a study by Halder et al. examined biopsies in thirty black patients with acne vulgaris and found the presence of inflammation histologically even in clinically noninflammatory lesions such as comedones. In addition, papules and pustules displayed considerable inflammation histologically that extended significantly beyond the margins of each lesion [
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