Disorders of Hyperpigmentation

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Disorders of Hyperpigmentation

Approach to Disorders of Hyperpigmentation

Circumscribed Hyperpigmentation

Melasma

A very common, acquired disorder characterized by symmetric, hyperpigmented patches with irregular borders, resulting from an increase in epidermal and/or dermal melanin; favors the face (see below) > mid-upper chest and extensor forearms.

Seen primarily in women; increased prevalence in individuals with skin phototypes III–IV.

Pathogenesis thought to be related to hyperfunctional melanocytes that are stimulated by exacerbating factors, such as sun exposure and hormones (e.g. pregnancy, oral contraceptives).

Three classic clinical patterns based on distribution: centrofacial (most common), malar, and mandibular (Fig. 55.2).

Classically, melasma was also classified based on findings from Wood’s lamp examination: lesions that enhance imply an increase in epidermal melanin and lesions that do not enhance imply an increase in dermal melanin; however, mixed epidermal and dermal melasma patterns are common.

In northern latitudes, lesions tend to fade during the winter months; melasma tends to be more persistent in darkly pigmented individuals.

DDx: postinflammatory hyperpigmentation, drug-induced (e.g. minocycline, amiodarone), acquired bilateral nevus of Ota-like macules (especially in Asian women), actinic lichen planus, pigmented contact dermatitis, exogenous ochronosis due to the application of hydroquinone-containing bleaching agents, erythromelanosis faciei.

These other disorders are distinguished from melasma based on historical aspects (e.g. drug ingestion, application of topical medications or cosmetics, previous inflammation), color (e.g. clusters of nevus of Ota-like macules are typically blue-gray in color), distribution pattern, histologic features, and primary lesions, if present.

Treatment options are outlined in Table 55.1; typically epidermal hyperpigmentation responds best to treatment.

Drug-Induced Circumscribed Hyperpigmentation and Discoloration

A wide range of medications and chemicals can cause hyperpigmentation or discoloration in circumscribed, diffuse, and even linear patterns; longitudinal or horizontal melanonychia may also be present.

The most common culprits of drug-induced circumscribed hyperpigmentation and discoloration are minocycline and the antimalarials (Table 55.2; Figs. 55.355.6).

The pathogenesis involves varying mechanisms, from increased melanin production to deposition of drug complexes or heavy metals within the dermis.

The hyperpigmentation or discoloration typically resolves upon discontinuation of the offending drug, but the course may be prolonged.

Postinflammatory Hyperpigmentation

Represents an acquired excess of melanin pigment following cutaneous inflammation (e.g. acne, psoriasis) or injury (e.g. burns or friction).

Depending on the disorder, postinflammatory hypopigmentation may also occur and is discussed in Chapter 54.

Can occur anywhere on the body, including the mucosae or nail unit; increased pigmentation is localized to areas of inflammation and becomes more apparent once the associated erythema resolves (likened to ‘a shadow left behind’).

The preceding inflammation may be obvious, transient, or subclinical (Table 55.3; Fig. 55.7).

The hyperpigmented macules and patches can range in color from light brown to dark brown (epidermal melanin) or gray-blue to gray-brown (dermal melanin).

In general, postinflammatory epidermal pigmentation eventually resolves as long as the underlying disorder is treated effectively, but this may take months or even years; postinflammatory dermal pigmentation can be persistent.

May also be exacerbated by UVR exposure, and photoprotection is an important part of treatment.

DDx: see Table 55.3; occasionally a skin biopsy will assist in establishing the diagnosis.

Causes of postinflammatory hyperpigmentation that often present without obvious prior inflammation.

Primary (localized) cutaneous amyloidosis (see Chapter 39 and Figs. 39.6 and 39.7).

Erythema dyschromicum perstans (EDP or ashy dermatosis) (see Chapter 9 and Figs. 9.9 and 55.8A).

Lichen planus pigmentosus (LPP) (see Chapter 9, Table 9.1, and Figs. 9.4G and 55.8B).

Mastocytosis (see Chapter 96 and Fig. 96.4).

Tinea (pityriasis) versicolor (see Chapters 54 and 64 and Fig. 64.1).

Atrophoderma of Pasini and Pierini (see Chapter 36).

There is some debate as to whether this represents a distinct entity or is an end-stage (i.e. ‘burned-out’ stage) of morphea.

Typically seen in young healthy adults as several 3- to 6-cm, oval, hyperpigmented, minimally depressed patches on the posterior trunk.

Lacks an inflammatory phase.

Rx: In addition to treating the underlying inflammatory disorder and photoprotection, the following topical agents may be used: hydroquinone 2–4%; a combination of hydroquinone, tretinoin, and a low-strength CS; azelaic acid 15%; α-hydroxy acids (e.g. glycolic acid).

Linear Hyperpigmentation

Linear hyperpigmentation, like linear hypopigmentation (see Chapter 54), can result from multiple etiologies; one of the initial steps is determining if the lesions do or do not follow Blaschko’s lines (see Chapter 51).

The differential diagnosis of linear hyperpigmentation is presented in Table 55.4 (Figs. 55.1055.16).

Linear Hyperpigmentation that is Not Along Blaschko’s Lines

Pigmentary demarcation lines.

In humans, the dorsal skin surfaces are relatively hyperpigmented compared to the ventral surfaces.

In patients with darker pigmentation, visible lines of demarcation between dorsal and ventral surfaces are more apparent.

These demarcation lines are present from infancy and persist throughout life; they are most prevalent on the anterolateral upper arm and posteromedial thigh (Fig. 55.13).

Several forms of pigmentary demarcation lines exist and are presented in Table 55.5 and Fig. 55.14.

Flagellate pigmentation from bleomycin.

Occurs in ~10–20% of patients treated with systemic bleomycin.

Pathogenesis is not well understood.

Presents as linear hyperpigmented streaks on the chest, back, and occasionally extremities (Fig. 55.15); typically in a configuration that suggests a relationship to scratching, but attempts to reproduce lesions by scratching have in general been unsuccessful; an erythematous phase, which is typically pink in light-skinned individuals, can precede the hyperpigmentation.

The hyperpigmentation is usually reversible once the bleomycin is discontinued, but may take 3–4 months to fade.

Other skin findings can include circumscribed hyperpigmentation overlying the small joints of the hands as well as sclerodermoid changes.

Flagellate mushroom dermatitis.

Occurs after eating large amounts of raw or partially cooked shiitake mushrooms.

A second form occurs in persons who cultivate shiitake mushrooms.

Presents initially with pruritic papules and vesicles that develop on the face, scalp, trunk, and proximal extremities; scratching of these lesions then leads to long, flagellate streaks composed of petechiae or papules, followed finally by linear patterns of discoloration (due to hemosiderin) or postinflammatory hyperpigmentation.

Linear Hyperpigmentation That May or May Not be Along Blaschko’s Lines

Linear postinflammatory hyperpig­mentation.

More common in individuals with darkly pigmented skin.

Occurs after linear trauma (e.g. burn, abrasion, dermatitis artefacta [Fig. 55.16]) and along veins (e.g. phlebitis, intravenous drug abuse, systemic sclerosis); also follows linear inflammatory dermatoses, most often allergic contact dermatitis due to plants (e.g. poison ivy/oak dermatitis) or phytophotodermatitis, which requires both plant exposure and UVR (see Fig. 55.7E).

Occasionally, postinflammatory hyperpigmentation may follow Blaschko’s lines due to the configuration of the antecedent inflammatory dermatosis (e.g. linear lichen planus, Blaschkitis).

Reticulated Hyperpigmentation

Disorders characterized by true reticulated macular hyperpigmentation are unusual and are primarily rare genodermatoses (Table 55.6; Figs. 55.1755.20).

It is more common to encounter disorders where the reticulated hyperpigmentation represents just one of several components; as an example, confluent and reticulated papillomatosis (CARP) of Gougerot and Carteaud also has papillomatosis and slight hyperkeratosis.

In addition, it is necessary to exclude cutaneous disorders characterized by reticulated erythema (e.g. livedo reticularis) or poikiloderma (e.g. poikiloderma of Civatte).

Reticulated hyperpigmentation can also correspond to the pattern of the venous plexus (e.g. later stage of erythema ab igne); the clinical clue is a wider spacing than in genodermatoses.

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