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Gary M. White & Neil H. Cox
Diseases of the Skin


17

Photodermatology and Photodermotosess


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ADVERSE EFFECTS OF UV RADIATION

The UV part of the spectrum from 280 to 400nm is the most important wavelength range in dermatology. It has important physiologic effects on the skin and useful therapeutic effects for some dermatoses, but also has adverse effects, including carcinogenesis and provocation of several specific dermatoses. These effects are summarized in Table 17.2. Aspects of carcinogenesis are discussed in Chapter 32.

Table 17.2  EFFECTS OF ULTRAVIOLET RADIATION

Beneficial effects Adverse effects

Physiologic

Production of vitamin D

Feeling of well-being

Protective

Tanning*

Production and dispersal of melanins (tanning)

Epidermal proliferation

Production of urocanic acid

Therapeutic

Beneficial for several dermatoses

Therapeutic photosensitization, for

example psoralen plus UVA (PUVA)

Short-term dose-related

Erythema (sunburn)

Tanning*

Long-term dose-related

Carcinogenesis

Wrinkling and other photodamage

Photodermatoses

Drug-related

Idiopathic

Photoaggravation of other dermatoses

*tanning is included both as beneficial and adverse. It does have some (beneficial) protective effect but this is very minor, and others would view any tanning as being a marker of (damaging) sun exposure.

Short-term (sunburn and tanning)

Excessive exposure to UVB causes erythema, which is initially visible about 4–6h after exposure, peaks at about 24h, and fades over a few days unless there is further exposure (Figs 17.7 and 17.8). At higher doses, the erythema is accompanied by edema and pain. A dose of several times the MED can be obtained from natural sunlight before erythema becomes visible or any discomfort is felt. This is particularly likely if there is cloud cover, which induces a false sense of security, because it reduces infrared radiation (heat) and visible sunlight but is not an effective barrier against UVB or UVA.

 

Figure 17.7 (a,b) Sunburn on the upper back. Note the sharp cut-off at the line of clothing, and also the relative sparing further up the neck due to shielding by the hair.

 

Figure 17.8 Sunburn producing superficial blistering. Sunburn typically causes peeling and patchy pigmentation as it resolves, even if frank blistering has not been an early feature.

The inflammatory mediators that are most important in sunburn and UVB-induced erythema are arachidonic acid metabolites, particularly prostaglandins PGD2, PGE2, PGF2 a , and PGI2, and the monohydroxyeicosatetraenoic acid 12-HETE. The clinical importance of this is that inhibitors of these chemicals, such as indomethacin, are therapeutically useful in reducing the intensity of sunburn. The best results are obtained by early treatment within about the first 12 h after exposure.

Tanning is viewed by many as a desired effect of sun exposure. Melanin dispersal is an early effect after UV exposure, before new melanin production is clinically manifest. It has a protective effect but must nonetheless be viewed as an indicator that solar exposure (and therefore solar damage) has occurred. Darkening of freckles occurs (Fig. 17.9) and is seasonal; new freckle-like lesions on the trunk after sunburn are often permanent (Fig. 17.10).

 

Figure 17.9Skin type I–II (red hair and freckles). Freckling affecting predominantly the right side of the forehead, provoked by an episode of sunburn.

 

Figure 17.10 Stellate freckles on the upper back. This pattern is common in young men after episodes of sunburn, and is common in pale-skinned individuals who live in sunny climates.

(Long-term) photoaging

The chronic effects of photodamage are well known and include atrophy and elastic tissue damage (solar elastosis), which are manifest in the skin as wrinkling, cutis rhomboidalis nuchae, solar purpura, pseudoscars, and colloid milium (Figs 17.11 17.18). Therapeutic aspects of photoaging are discussed in Chapter 5.

 

Figure 17.11 Elastosis, a form of solar aging, is clinically apparent as semiconfluent yellowish papules that are usually most prominent on the lateral aspects of the forehead, cheeks, and nape of neck.

 

Figure 17.12 Elastoma, a localized nodule of solar-induced elastotic material.

 

Figure 17.13 Solar aging on the exposed dorsal forearms causes skin atrophy and flattening of the rete ridges. Minor shearing injuries in this thinned skin commonly cause macular areas of purpura.

 

Figure 17.14 Solar aging may cause easy tearing and stellate-shaped ‘solar pseudoscars’, as well as purpuric areas; all are shown here.

 

Figure 17.15 Nodular elastosis is a photoaging disorder that is most apparent around the eyes (a), although it may also occur at other sites (b). The elastotic nodules may be accompanied by comedones and cysts (also termed the Favre–Racouchot syndrome), and are occasionally confused with skin malignancies.

 

Figure 17.16 Colloid milium. Amorphous material, probably actinically damaged elastic fibers, is deposited in the dermis to produce translucent papules on sun-exposed skin. There are also juvenile and nodular forms of this disorder, and a type that is induced by topical hydroquinone (a depigmenting agent).

 

Figure 17.17 Colloid milium: another example of this unusual form of actinic damage.

 

Figure 17.18 Cutis rhomboidalis nuchae. A pattern of photoaging that is apparent at the nape of the neck, usually in men who have worked outdoors. The diamond-shaped (rhomboid) patterning of skin creases is characteristic.

Photodermatoses and photosensitivity reactions

A classification of photodermatoses is given in Table 17.3. These constitute the remainder of the discussion in this chapter.

Table 17.3  CLASSIFICATION OF PHOTODERMATOSES AND PHOTOSENSITIVITY DISORDERS

Classification Disorder
Genetic or inherited

Xeroderma pigmentosum

Bloom syndrome, Rothmund–Thomson syndrome

Albinism

Porphyrias

Reactions to exogenous agents

Drug phototoxicity or photoallergy (internal)

Reactions to external photosensitizers or plants

Porphyria cutanea tarda, (many cases are caused by alcohol, less commonly, estrogen intake); pseudoporphyria (diuretics, naproxen, high dose UVB)

Idiopathic photodermatoses

Solar urticaria

Polymorphic light eruption and variants

Hydroa vacciniforme

Actinic prurigo

Photosensitivity dermatitis or actinic reticuloid

Dermatoses associated with photoaggravation

See Table 17.10


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