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The Top 10 Things You Need to Know About Acquired Pigmentation Disorders

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The Top 10 Things You Need to Know About Acquired Pigmentation Disorders FEATURE ARTICLE 2.0 Contact Hours The Top 10 Things You Need to Know About Acquired Pigmentation Disorders Maggie L. Chow, Janiene Luke, Sharon E. Jacob ABSTRACT: Disorders of pigmentation can be acquired Jacob, 2015). Here, we describe the ‘‘top 10 things to know or inherited. The acquired disorders present an opportu- about’’ the disorders of hyperpigmentation and hypo- nity for surveillance and treatment to prevent morbidity pigmentation caused by functional abnormalities second- and improve quality of life. In this article, we delineate the ary to an acquired extrinsic or intrinsic cause. acquired causes, pathogenesis, and treatment options of disorders of skin hyperpigmentation or hypopigmentation. 1. Acquired Versus Inherited Pigmentary Disorders Key words: Acquired Pigmentation Disorders, Dyspigmen- Acquired disorders are medical conditions that develop tation, Hyperpigmentation, Pityriasis alba, Vitiligo over the course of an individual’s life. In contrast, an in- herited pigmentary disorder arises secondarily to genes elanin, a brown or black pigment, deter- passed on from parents to their offspring. Thus, an acquired mines the color of skin and hair. This pigmentary disorder is hypopigmentation or hyperpigmen- pigment is formed in melanocytes from tation that is not present at birth and is not secondary to tyrosine (Hurwitz, 2006). Melanocytes an inherited genetic defect from the parents. Examples of are cells derived from the neural crest such disorders include vitiligo, melasma, and postinflam- that migrate to the basal layer of the epidermis during matory pigment alterations secondary to tinea versicolor, Membryogenesis and become dendritic secretory cells when among others. In contrast, inherited pigmentary disorders mature. Abnormal skin hyperpigmentation or hypopig- are secondary to a genetic aberrancy and can include such mentation results from aberrant melanin production, syndromes as tuberous sclerosis, neurofibromatosis, and melanosome transport, or melanocyte development. the Carney complex. Defects in the melanin production pathway can be in- herited or acquired. The genodermatoses related to disorders 2. Pathophysiology of pigmentation are described in a separate article (Chow & Human skin color is primarily determined by the type, Maggie L. Chow, PhD, MD, Kaiser Permanente Los Angeles Medical quantity, and distribution of melanin pigment in the skin, Center, Los Angeles, CA. which is regulated by a complex array of genetic, environ- Janiene Luke, MD, Loma Linda University, Loma Linda, CA. mental, and endocrine factors (Costin & Hearing, 2007). Sharon E. Jacob, MD, Loma Linda University, Loma Linda, CA. Aside from determining skin color, melanin also protects Sharon E. Jacob served as an independent investigator on the safety the skin against ultraviolet (UV) radiation. Extrinsic and and efficacy of T.R.U.E. Test (Smart Practice, Phoenix, AZ) Panels intrinsic disturbances in the physiologic and biological pro- 1.1, 2.1, and 3.1 in children and adolescents, Pediatric Research Equity Act (PREA-1) trial, and now serves as an investigator on cesses that affect the production and transport of melanin, PREA-2. She has served as a consultant for Johnson & Johnson. such as UV light, certain medications, and the hormonal She has no conflicts of interest associated with the subject matter in changes that occur during pregnancy, can also affect skin color. this manuscript. Dr. Luke has no relevant disclosures or conflicts Melanocytes are the secretory cells that produce mela- of interest. Dr. Chow has no relevant disclosures or conflicts of nin. The quantity of melanocytes in human skin across interest. ethnicities is constant within each individual; however, skin Correspondence concerning this article should be addressed to Sharon E. Jacob, MD, Department of Dermatology, Loma Linda Uni- color is determined by the size, number, and distribution of versity, 11370 Anderson Street, Suite 2600, Loma Linda, CA 92354. melanosomes within keratinocytes (Haake & Holbrook, E-mail: [email protected] 1999). Melanocytes reside in the basal layer of the epidermis. DOI: 10.1097/JDN.0000000000000169 After the production of melanin, the melanocytes transfer 332 Journal of the Dermatology Nurses’ Association Copyright © 2015 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited. the pigment to surrounding keratinocytes through mela- 4. Epidemiology and Risk Factors nosomes, which are specialized membrane-bound organ- The epidemiology of acquired pigmentation disorders elles (Costin & Hearing, 2007). varies widely by disease association. These are described The synthesis and distribution of melanin depends on in Tables 1 and 2. Dyspigmentation can affect the young several steps. First, melanoblasts (melanocyte precursor or the older adults and both men and women around the cells) must develop and migrate from the neural crest to world. These epidemiologic clues can aid in diagnosis. For their final peripheral sites. Second, the melanoblasts must example, tinea versicolor should be near the top of the differentiate into melanocytes after migration. Finally, the differential diagnosis for scaly hypopigmented macules on melanocytes must then proliferate and begin producing the chest of a teenaged patient living in a humid environ- melanosomes, which must undergo a maturation process. ment. In endemic regions, infectious causes must also be Three enzymes are required to synthesize melanin within these ruled out; for example, pinta is a treponemal disease that organelles, including tyrosinase, dopachrome tautomerase, is similar to syphilis and causes hypopigmentation. and tyrosinase-related protein 1 (Haake & Holbrook, 1999). Melanosomes can produce several types of melanins: 5. Prevention eumelanin (black-brown), pheomelanin (yellow-red), a com- A critical intervention in the prevention of hyperpigmen- bination of eumelanin and pheomelanin termed mixed tation is sun protection, as exposure can exacerbate the melanins, and neuromelanin. These pigments differ in their dark areas through deposition of melanin into the skin. chemical, structural, and physical properties and play dis- Sun exposure can lead to both acute and chronic pigmentary parate molecular roles in different anatomic regions (Hearing, darkening. In the immediate (acute) setting, UV light (spe- 2000). Once the melanosomes are transferred to neigh- cifically UVA and, to a lesser extent, UVB) oxidizes tyrosine boring keratinocytes, the epidermal melanin unit becomes in the skin and ultimately forms melanin, causing skin a functional entity that can respond through paracrine darkening (Joshi, Carraro, & Pathak, 1987). In the chronic and autocrine mechanisms to environmental stimuli. Thus, setting, hyperpigmentation secondary to UVA/UVB ex- human skin pigmentation is a dynamic process determined posure arises from activation and proliferation of the ex- by numerous internal and external factors (Hearing, 2000). posed melanocytes (Gilchrest, Blog, & Szabo, 1979). 3. Causes of Human Skin Hypopigmentation or Furthermore, the cessation of aggravating or inciting Hyperpigmentation exogenous factors should be pursued, and infections should be treated appropriately. Underlying dermatoses, such as Internal and external processes that affect the steps in the acne, must be treated, and allergens and irritants need to complex melanin production and transport pathway can be avoided in contact dermatitis to prevent further develop- potentially lead to abnormalities in skin pigmentation. In- ment of dyspigmented lesions. ternal processes include autoimmune etiologies (e.g., vitiligo) and endocrine dysfunction (e.g., insulin resistance). In 6. The Social Impact of Dyspigmentation contrast, external processes can include medications (e.g., minocycline), sun exposure (e.g., solar lentigo), and post- Patients with dyspigmentation, for example, vitiligo and inflammatory hyperpigmentation responses to injury and pigmented contact dermatitis, both of which can affect the infections (e.g., tinea versicolor). face, may have their quality of life significantly affected For instance, numerous medications can cause skin dis- secondary to the impact that their disease has on appear- coloration. Heavy metals, such as silver, bismuth, arsenic, ance. Patients may experience depression, anger, embar- and gold, can cause hyperpigmentation through binding rassment, and shame. They may worry that their disease and inactivating sulfhydryl compounds that function to in- will continue to progress (Sampogna et al., 2008) or be hibit tyrosinase activity. This process results in melanogenesis contagious. Facial lesions in particular can be associated (Molokhia & Portnoy, 1973). Chemotherapy agents are with low self-esteem, social withdrawal, and lower school hypothesized to cause hyperpigmentation through toxic and work productivity. Furthermore, patients who elect to effects on melanocytes, stimulation of melanocytes, and in- pursue medical treatments and procedures can experience flammation (Costin & Hearing, 2007). Levodopa, which high financial burdens for results that may not reach their is used for the treatment of Parkinson’s disease, is hypoth- expectations (Handel, Miot, & Miot, 2014). esized to enhance melanin biosynthesis through possible Thus, it is important to discuss the etiology of the dys- extracellular oxidation (Hendrix & Greer, 1992). Other pigmentation with patients and explore their level of distress medications that have been associated with skin
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