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HYPERPIGMENTATION

Systemic causes of hyperpigmentation

Hyperpigmentation occurs in many situations. It may occur in many systemic disorders (Table 21.2), with either a diffuse pattern or an addisonian distribution (i.e. reminiscent of Addison disease: accentuated at sun-exposed sites, at pressure or friction sites, on palms and soles, and at sites that are normally hyperpigmented such as areolae and genitalia).
    Management of most of these conditions is not the province of the dermatologist, and they are not considered in detail here.

Postinflammatory hyperpigmentation

Etiology and pathogenesis

A variety of inflammatory conditions may intensify the pigment of the skin. Some of this results from ‘pigmentary’ incontinence (i.e. epidermal pigment deposited in the dermis, typically due to inflammatory processes that disrupt the basal layer of the epidermis) and the rest from increased epidermal pigmentation. Why the body responds to injury with
increased pigmentation is not clear, but it may be a protective response (i.e. shielding the rejuvenating cells from potentially damaging UV rays). When pigmentary incontinence has occurred, the pigment granules are gradually engulfed by tissue macrophages (which may then be termed melanophages).

Clinical

A hyperpigmented patch at the exact site of a prior inflammatory condition is typical. The exact shape of the prior lesion is usually formed by the dark spot. Any part of the body, including the face, trunk, and extremities, may be affected. Patients may have one spot or many, depending on the extent of the inciting process. This sort of hyperpigmentation is classically the main manifestation of photocontact dermatitis (Fig. 21.18), but it is common in the resolving phase of lichen planus or fixed drug eruption (Ch.18); in the latter, it may become permanent due to repeated episodes at the same site. Postinflammatory hyperpigmentation is less commonly seen in nummular eczema (Fig.21.18) and in a variety of other inflammatory dermatoses (Fig. 21.19).

Differential diagnosis

This is usually not in doubt, although the nature of the inflammatory stimulus may be, if it has already resolved. The pattern and site of lesions may suggest the diagnosis even in retrospect, for example multiple small spots on the volar wrists suggests lichen planus, and a solitary postinflammatory pigmented area on the glans penis suggests fixed drug eruption.

Treatment

Preventing further trauma and inflammation is critically important in the treatment of postinflammatory hyperpigmentation. Thus patients with acne desperately need their acne controlled as much as they need active treatment of the postinflammatory hyperpigmentation. It is easier to prevent postinflammatory hyperpigmentation than it is to remove it once it has formed.
    If the inciting inflammatory process is controlled, observation is often the only other course of action; active interventions, especially for dermal pigmentation, are often of limited benefit, as such pigmentation is relatively inaccessible to therapy. Even use of the laser has met with variable and often disappointing results. If further intervention is desired, a biopsy may be indicated. Patients should be told that the time it takes for lesions to fade is highly variable. It may be months, years, or possibly never happen. There are more potentially helpful treatment options for epidermal than for dermal postinflammatory hyperpigmentation. Photoprotection with a broad-spectrum sunscreen (UVA and UVB), protective clothing, and avoidance of peak UV exposure times are all important. In addition, topical hydroquinone, tretinoin, or azelaic acid may be tried.

Phytophotodermatitis and berloque dermatitis

Burning, erythema, and bulla formation followed by dark postinflammatory hyperpigmentation distributed in bizarre linear arrangements are characteristic (Fig.21.20 and see also Fig.16.14). Phytophotodermatitis is caused by furocoumarins, such as psoralens or angelicins in plants or fruit, which, when inadvertently placed in contact with the skin, make it photosensitive. Common offenders include oranges, limes, lemons, celery, figs, dill, carrots, and parsley, as well as a number of hedgerow plants, such as hogweed (see also Ch.17, and Ch.5 for therapeutic uses of psoralens).
    The same types of agent are found in perfumes based on bergamot oil, and cause exactly the same photosensitization process; the classic variety on the upper chest was named berloque dermatitis (from the French for pendant), but the term is now used for any body site affected by this process when a psoralen-containing perfume is the cause.

Melasma (chloasma)

Etiology and pathogenesis

Melasma, also called chloasma, is a common, acquired, benign, symmetric form of facial hyperpigmentation found primarily in adult women. The exact cause of melasma is unknown, but sunlight exposure seems to be relevant, and its onset is often related to pregnancy or the use of oral contraceptives. However, it is a mistake to assume that all, or even most, are so exposed. A woman not on oral contraceptives or pregnant may develop melasma in the setting of significant repeated sun exposure, and especially if she is dark-skinned. Of note, the use of estrogen in postmenopausal women is not a typical trigger factor. Men occasionally develop melasma, and their clinical presentation seems similar to that in pale-skinned women.

Clinical

Symmetric, uniformly hyperpigmented, sharply defined macules and patches on the face in the sun-exposed areas of a woman are characteristic of melasma (Fig.21.21a). They may appear as large patches or as confetti-like pigmented macules. Melasma commonly affects the upper lip, cheeks, and forehead. Some women complain of a mustache appearance due to melasma (Fig.21.21b). Inflammation is absent. Other places besides the face may occasionally be affected (e.g. the anterior chest, the upper back, and the photoexposed side of the arms). Onset is usually in the summer months when UV exposure is high.

Differential diagnosis

The main differential is poikiloderma of Civatte (see later) and occasionally forms of postinflammatory hyperpigmentation that may predominantly affect the face (e.g. a photolichenoid drug eruption).

Treatment

Use of oral contraceptives should be avoided.
    Each patient should be asked, ‘How much time do you spend in the sun?’, and the need for sun protection should be discussed. Morning application of a broad-spectrum sunscreen (at least sun protection factor, SPF, 15) daily is critical. If she is to be out for more than 20 min, an SPF 30 sunscreen or higher is recommended. If patients are to be out all day, reapplication of a waterproof, SPF 30 or higher sunscreen every 2 h is recommended. Hats, shade, etc. are also recommended.
    Sun protection is usually combined with topical therapy (e.g. hydroquinone, 2-4% twice a day). Of course, monobenzylether of hydroquinone, a permanent bleaching agent, should never be used for melasma. Tretinoin (e.g. 0.05% cream, before sleeping, for 6-12 months) is also helpful and is effective for melasma in both dark- and pale-skinned patients if given over 40 weeks in combination with daily sunscreen
use. Azelaic acid is a naturally occurring dicarboxylic acid that has been shown to be effective in treating melasma when given twice daily for 6 months. Finally, various combinations using hydroquinone with or without tretinoin and/or a topical steroid have been tried by individual physicians.
    Chemical peels have been used successfully in darker-skinned patients, but hypopigmentation, hyperpigmentation, and keloid formation are significant risks.

Poikiloderma of Civatte

This is a common, chronic, symmetric, red-brown, and atrophic discoloration of the lateral neck, chest, or cheeks that occurs mainly in middle-aged women (Fig.21.22). Chronic sunlight exposure, possibly interacting with perfume constituents (to explain the sites involved and the female sex predilection), has been implicated as the cause but never proved. The pulsed dye laser has been reported to decrease the redness of the lesion.

PRACTICE POINTS

Confluent and reticulated papillomatosis (Gougerot-Carteaud disease)

Etiology and pathogenesis

For years, this rare condition was considered a manifestation of infection by Pityrosporum yeasts. However, repeated trials of antifungal agents failed to clear the condition. It is now considered a disease of keratinization of unknown cause.

Clinical

Confluent and reticulated papillomatosis results in symmetric pigmented plaques and brown papules of the mid-chest, inframammary area, and axillae in young adults (Fig.21.23). The back and neck may also be involved.

Differential diagnosis

Acanthosis nigricans lacks the reticulate pattern and does not affect the mid-chest or back.
Pityriasis versicolor possesses a pityriasiform scale that may be demonstrated by stroking with a tongue blade; KOH examination shows fungal elements.

Treatment

No treatment is needed. Minocycline (e.g. 100mg twice a day for 1-3 months) has been very effective in many cases and, indeed, should be considered first-line therapy. The response to retinoids may be dramatic but temporary, with the disease returning after therapy. Topical tretinoin or tazarotene may be effective locally, but for widespread clearing, isotretinoin (e.g. up to 2.0mg/kg per day), tacalcitol, or acitretin may be employed. High-potency topical steroid can anecdotally clear the disease, and a topical cream containing 12% urea and 0.03% tretinoin twice daily cleared the condition in two patients.

Dowling-Degos disease

Also known as reticulated pigmented anomaly of the flexures, Dowling- Degos disease presents with reticulated hyperpigmented macules in the axillary, inguinal, and inframammary areas (Fig.21.24). Onset is often in the twenties and thirties; an autosomal dominant inheritance pattern with variable penetrance occurs, as well as sporadic cases. Laser therapy has been beneficial anecdotally.

Tattoos and tattoo reactions

Etiology and pathogenesis

Tattoos have adorned human skin for thousands of years. They may identify the wearer as a member of a social group or, conversely, give the wearer a sense of individuality.
    The pigments used in tattoos include carbon (black), cobalt (blue), chrome (green), cadmium sulfide (yellow), cinnabar (red), and manganese (purple). Cinnabar is much less commonly used now, having been replaced by organic red pigments. Various inks may be used in amateur tattoos; carbon particles may be implanted in the skin accidentally (e.g. in a blast tattoo in coal miners).

Clinical

Patients who see a dermatologist regarding a tattoo do so either because of a local adverse reaction or because they are seeking tattoo removal. Local reactions fall into the following groups.

Treatment

For hypersensitivity and localized sarcoidal reactions, a topical steroid twice a day should be tried, as this has been reported to resolve the inflammation, leaving a normal tattoo. In some cases, intralesional steroids may be more convenient. Some nodular sarcoidal reactions require excision.
    For removal of unwanted tattoos, surgical excision (staged if needed) or laser treatment (e.g. ruby, alexandrite, and neodymium:yttrium- aluminum-garnet [Nd:YAG]) may be done. Irreversible darkening of the tattoo requiring excision has occurred during the treatment with some lasers.
    If allergy has occurred to one of the tattoo pigments (usually mercuric sulfide), laser treatment is not recommended, as it merely turns large allergenic particles into many small allergenic particles.

Hyperpigmented lesions discussed elsewhere

These include:

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.