Disorders of Pigmentation

Abstract

Propiomelanocortin (POMC) is also the precursor for Adrenocorticotropic Hormone (ACTH), which is raised in Addison’s disease. This accounts for the cutaneous hyperpigmentation seen in this condition. Once synthesized, melanin is then packaged into melanosomes and transported to neighboring keratinocytes. The depigmentation is more prominent during the summer months, when the surrounding skin takes on more pigment giving a stark comparison. The presence of a white forelock, a depigmented patch, sensorineural deafness, and iris heterochromia are consistent with Waardenburg’s syndrome. Spontaneous repigmentation may occur but is uncommon. Treatment options include topical therapy (e.g., topical corticosteroids and calcineurin inhibitors), phototherapy, immunosuppression (especially in unstable vitiligo), and grafts. The use of cosmetic camouflage is often useful, and it can provide psychologic support. Hyperpigmentation can be localized (e.g., melasma, nevus of Ota) or generalized (e.g. Addison disease) in distribution, and circumscribed, linear, or reticulate in configuration. © 2022 Taylor & Francis Group, LLC.