iMD - Dermatology - Fifth Edition - 67. Disorders of Hyperpigmentation PDF
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Gillian K. Weston and Mary Wu Chang
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This document is a chapter from a dermatology textbook, discussing disorders of hyperpigmentation. It covers key clinical features and introduces concepts including postinflammatory hyperpigmentation.
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67. Disorders of Hyperpigmentation BOOK CHAPTER Disorders of Hyperpigmentation Gillian K. Weston (chapter://search/Weston%20Gillian K./%7B%22type%22:%22author%22%7D) and Mary Wu Chang (chapter://search/Chang%20Mary Wu/%7B%22type%22:%22author%22%7D) Dermatology (chapter://browse...
67. Disorders of Hyperpigmentation BOOK CHAPTER Disorders of Hyperpigmentation Gillian K. Weston (chapter://search/Weston%20Gillian K./%7B%22type%22:%22author%22%7D) and Mary Wu Chang (chapter://search/Chang%20Mary Wu/%7B%22type%22:%22author%22%7D) Dermatology (chapter://browse/book/3-s2.0-C20191031798), 67, 1125-1154 Skin color depends upon the amount and distribution of melanin and other pigments such as hemoglobin, which can influence light absorption, reflection, and scattering. Disorders of hyperpigmentation usually result from an increase in melanin production and, on occasion, from an increase in the density of active melanocytes. Discoloration of the skin may also be caused by deposition of exogenous substances such as drugs, drug complexes (e.g. with melanin or iron), or heavy metals within the dermis. To aid in the clinical approach, disorders of hyperpigmentation can be divided into diffuse, circumscribed, linear, and reticulated subsets ( Fig. 67.1 (f0010) ). A discussion of each of these categories is followed by an overview of dyschromatoses, disorders characterized by both hypo- and hyperpigmentation. Keratinocytic disorders that present with hyperpigmentation are listed in Table 67.1 (t0010) , and benign melanocytic neoplasms are covered in Chapter 112 (chapter://content/3-s2.0-B9780702082252001128?scrollTo=%23c0112). Fig. 67.1 Approach to disorders of hyperpigmentation. Hyperpigmentation can also result from keratinocytic (epidermal) disorders (see Table 67.1 (t0010) ). Table 67.1 Hyperpigmentation related to keratinocytic (epidermal) disorders. HYPERPIGMENTATION RELATED TO KERATINOCYTIC (EPIDERMAL) DISORDERS Disorder Key clinical features Acanthosis nigricans Velvety and corrugated hyperpigmentation of flexural sites (e.g. neck, axillae) > extensor surfaces; often associated with insulin resistance (see Fig. 53.14 (chapter://content/3-s2.0- B9780702082252000536?scrollTo=%23f0075) ) Confluent and Hyperpigmented papules and thin plaques with a corrugated and papillomatous surface; reticulated form a reticulated pattern primarily on the central trunk, neck, and axillae; onset typically papillomatosis around puberty (see Figs. 67.20 (f0105) and 109.22 (chapter://content/3-s2.0- B9780702082252001098?scrollTo=%23f0115) ) Terra firma-forme Retention hyperkeratosis presenting as hyperpigmented plaques that favor concave dermatosis surfaces of the face, neck, chest, and ankles; removed by wiping with 70% isopropyl alcohol pads Nevoid Hyperpigmentation and thickening of the areola(s), more commonly bilateral; typically hyperkeratosis of the begins after puberty in women or men receiving hormonal therapy (see Fig. 109.21 nipple and areola (chapter://content/3-s2.0-B9780702082252001098?scrollTo=%23f0110) ) Epidermal nevus Linear hyperpigmented streaks following the lines of Blaschko (rarely hypopigmented); a variably papillomatous or verrucous texture; congenital or apparent by early childhood (see Chs. 62 (chapter://content/3-s2.0-B9780702082252000627?scrollTo=%23c0062) and Fig. 109.18 (chapter://content/3-s2.0-B9780702082252001098?scrollTo=%23f0095) ) Therapeutic options are discussed in cited chapters. DIFFUSE AND CIRCUMSCRIBED HYPERPIGMENTATION Introduction Diffuse and circumscribed hyperpigmentation are discussed together because both postinflammatory hyperpigmentation (PIH) and reactions to systemic drugs, two major causes of hyperpigmentation, can assume either of these patterns. Melasma is another common cause of circumscribed hyperpigmentation, whereas diffuse hyperpigmentation can also be a manifestation of metabolic diseases, sclerodermoid disorders, nutritional deficiencies, and occasionally HIV infection. POSTINFLAMMATORY HYPERPIGMENTATION SYNONYM: Postinflammatory hypermelanosis KEY FEATURES Extremely common, especially in individuals with more darkly pigmented skin Develops after inflammation or injury to the skin, but preceding inflammation may be transient or subclinical The increased melanin can be primarily within the dermis (e.g. following lichen planus) or in the epidermis (e.g. following acne or atopic dermatitis) Epidermal hyperpigmentation fades more readily than dermal hyperpigmentation Introduction PIH represents an acquired excess of melanin pigment following cutaneous inflammation or injury. It can occur anywhere on the skin surface, including the mucous membranes and the nail unit. PIH is extremely common and can have significant cosmetic and psychosocial consequences. Epidemiology PIH can occur at any age and there is no sex preference. Individuals with darkly pigmented skin tend to have a greater frequency, severity, and duration of PIH than those with lighter complexions. Pathogenesis In the epidermal form of PIH, there is increased melanin production and/or transfer to keratinocytes. Inflammatory mediators (e.g. prostaglandins E 2 and D 2 , IL-33) that enhance pigment production may play a role in this process. In dermal hyperpigmentation, melanin enters (“falls into”) the dermis via a damaged basement membrane, where it is phagocytosed by and subsequently resides within dermal macrophages (referred to as melanophages). Macrophages may also migrate into the epidermis, phagocytose melanosomes, and then return to the dermis. Melanin within dermal melanophages tends to persist for long periods of time (e.g. years). Clinical Features Asymptomatic hyperpigmented macules and patches range in color either from tan to dark brown (epidermal melanin) or from gray–blue to gray–brown (dermal melanin). Primary lesions of the underlying inflammatory disorder may be admixed with the hyperpigmentation or present elsewhere. When primary lesions are absent, the size, shape, and distribution pattern of the hyperpigmented lesions may provide clues to the underlying etiology ( Table 67.2 (t0015) ). PIH can be exacerbated by continued inflammation, trauma, exposure to ultraviolet (UV) irradiation, or treatment-related irritation. Table 67.2 Disorders associated with postinflammatory hyperpigmentation. Adapted from Bolognia JL. Disorders of hypopigmentation and hyperpigmentation. In: Harper J, Oranje A, Prose N (eds). Textbook of Pediatric Dermatology, 2nd edn. Oxford: Blackwell Science, 2006:997–1040. DISORDERS ASSOCIATED WITH POSTINFLAMMATORY HYPERPIGMENTATION Inflammatory disease Clinical clues Common Acne vulgaris Head/neck region, upper trunk;