Hypopigmented disorders - Clinical Tree

Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports

Hypopigmented disorders present as areas of skin that are lighter than normal due to reduced melanin. In contrast, depigmented lesions, such as those caused by vitiligo, present as milky-white patches due to complete absence of melanocytes. Classification of these disorders may be based on lesion pattern and distribution, underlying cause, or time of lesion onset. In general, hypopigmentation occurs due to alterations in the melanin synthesis pathway, a decrease in melanocytes, or impairment in the melanocyte–melanin transfer system. This chapter briefly discusses common hypopigmented disorders with an overview of treatment options.

Nevus Depigmentosus

This disorder is a non-progressive, congenital form of cutaneous mosaicism affecting melanin synthesis and transfer from melanocyte to keratinocyte. Clinically, lesions present in early childhood as well-defined hypopigmented patches with serrated borders. Three variants have been described (localized, segmental, and linear or whorled) with the localized type being the most common. A negative diascopy test is helpful to rule out nevus anemicus.

Postinflammatory Hypopigmentation

Inflammatory reactions in various dermatoses may lead to hypopigmentation after resolution of the inflammatory phase. Cutaneous injuries, burns, and cosmetic procedures (dermabrasion, chemical peels, cryosurgery) can also lead to pigment loss through postinflammatory changes. Severity of pigment loss and distribution coincides with the distribution of original lesions and the degree of previous inflammation. This disorder is seen most frequently in darker-skinned individuals, due to contrast of the lesions with surrounding skin. The lesional course may vary from spontaneous resolution to permanent hypopigmentation.

Pityriasis Alba

A form of postinflammatory hypopigmentation, this self-limiting, benign disorder is associated with eczema and is especially common among children with a personal or family history of atopy. Lesions present as hypopigmented macules with or without associated scaling, erythema, and/or pruritus. Involvement of the face, neck, shoulders, and upper extremities is common. In contrast with pityriasis versicolor, lesions tend to have more facial involvement, are less numerous, and show no yeast elements on KOH (potassium hydroxide) preparations of overlying scale.

Idiopathic Guttate Hypomelanosis

Idiopathic guttate hypomelanosis (IGH), also called senile depigmented spots , is an acquired leukoderma common among older persons. Lesions present as 1–6 mm hypopigmented to porcelain-white, oval-to-round guttate macules on sun-exposed areas, especially the legs. Although asymptomatic, lesions tend to increase with age and may be of cosmetic concern. Etiology of this disorder is unknown; however, the HLA-DQ3 gene, autoimmunity, trauma, and chronic sun exposure are among suspected culprits. Light microscopy of lesions reveals a hyperkeratotic stratum corneum, an atrophic epidermis, and flattened rete ridges with senescent melanocytes and decreased melanin content.

Chemical Leukoderma

Lesions of chemical leukoderma present as hypo- or depigmented macules at sites of contact with chemicals, especially phenols, catechols, or hydroquinone. A history of onset of lesions after chemical exposure and distribution involving only the exposed sites or similar cases in individuals in the same workplace are needed to establish a diagnosis and distinguish it from vitiligo or other causes of hypo- and depigmentation.

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