TY - CHAP M1 - Book, Section TI - Disorders of Pigmentation A1 - Crowson, A. Neil A1 - Magro, Cynthia M. A1 - Janin, Anne A1 - Barnhill, Raymond L. A2 - Barnhill, Raymond L. A2 - Crowson, A. Neil A2 - Magro, Cynthia M. A2 - Piepkorn, Michael W. A2 - Kutzner, Heinz A2 - Desman, Garrett T. PY - 2020 T2 - Barnhill's Dermatopathology, 4e AB - The sources of pigment that cause hyperpigmentation of the skin range from endogenous products such as melanin and hemosiderin to exogenous agents such as tattoo dyes, ingested metals, and drugs. In some instances, these agents combine to produce hyperpigmentation. For example, in argyria- and chlorpromazine-related hyperpigmentation, silver particles along with melanin and drug metabolites plus melanin, respectively, contribute to dyschromasia. Ultraviolet (UV) rays often enhance pigmentation, so sun-exposed skin shows more intense discoloration. When the epidermis is heavily melanized, pigment incontinence may result in upper dermal melanization as well. Disorders of hypopigmentation and depigmentation are caused mainly by damage to and dysfunction of epidermal melanocytes (Figs. 15-1 and 15-2). In some congenital diseases (eg, piebaldism), melanocytes are absent, and in other conditions (eg, idiopathic guttate hypomelanosis) the melanocytes are dysfunctional with rudimentary dendritic processes. The circulation of blood through the superficial capillary plexus may influence the skin color, as evidenced by nevus anemicus. Both hyper- and hypopigmentations may be congenital or hereditary, postinflammatory, or induced by chemicals and foreign materials. SN - PB - McGraw Hill Education CY - New York, NY Y2 - 2024/10/06 UR - dermatology.mhmedical.com/content.aspx?aid=1178392603 ER -