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Light-Related Diseases and Disorders of Pigmentation


Sun-Damaged Skin, Actinic-Damaged Skin, and Photoaging

Description

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    Sun-damaged skin is easily recognizable and shows specific skin findings, resulting from damage due to ultraviolet radiation (UVR).

History

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    Acute exposure to UVR results in sunburn and is especially caused by ultraviolet B (UVB) radiation.

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    Chronic UVR exposure results in photoaging and skin cancer.

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    Light-colored skin, genetic disorders (e.g., xeroderma pigmentosum), and certain medications (e.g., doxycycline and sulfa-based medications) predispose to sunburn and photoaging.

Skin Findings

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    Sunburn results from acute UVR and produces pain, redness, and peeling.

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    Immediate pigment darkening occurs minutes after ultraviolet A (UVA) radiation and fades in 6 to 8 hours.

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    Delayed tanning occurs 48 to 72 hours after exposure to UVB and UVA radiation and is due to new pigment production.

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    Chronic UVR exposure results in hyperpigmentation, hypopigmentation, telangiectasia, rhytides (e.g., fine lines and furrows), large sebaceous glands, comedones, milia, bruises, and atrophy of the skin.

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    Certain cutaneous sites develop characteristic patterns, such as deep furrows on the back of the neck (cutis nuchae rhomboidalis) and red-brown discoloration on the sides of the neck (poikiloderma of Civatte)

Laboratory

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    No testing if necessary to diagnose sun-damaged skin.

Fig. 15.1, Sun-damaged skin, actinic-damaged skin, photoaging distribution diagram.

Fig. 15.2, Cutaneous blood vessels are easily damaged by trivial external trauma to sun-damaged skin resulting in asymptomatic but unsightly ecchymosis. Aspirin therapy worsens solar purpura. Regular use of sunscreen and alpha-hydroxy acid moisturizer are of some benefit.

Fig. 15.3, Course wrinkling occurs after loss of elastic tissue and collagen. The skin surface is firm, smooth, and yellow.

Fig. 15.4, Solar elastosis is a sign highly characteristic of severe sun damage. There is coarsening and yellow discoloration of the skin.

Differential Diagnosis

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    Sunburn differential diagnosis: phototoxic medication reaction, toxin-mediated erythema, underlying genetic skin disorder (e.g., xeroderma pigmentosum)

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    Chronic sun exposure differential diagnosis: rosacea, premature aging syndrome

Course and Prognosis

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    With proper sun precautions, use of sunscreen, and sun-protective clothing, photoaging can be minimized.

Treatment

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    Sunburns should be treated with cool compresses, soothing creams (e.g., aloe vera or soy-based creams), nonsteroidal anti-inflammatory medicine (e.g., ibuprofen), and oral hydration.

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    Effects of chronic sun exposure, such as wrinkles, can be treated with topical “antiaging” creams containing retinol and alpha-hydroxy acids, heat-based therapies (e.g., radiofrequency, laser and ultrasound), nonablative and ablative lasers, surgical face-lift, and lightening creams containing hydroquinone.

Fig. 15.5, Sun-damaged skin. White, round, 2- to 3-mm papules (milia) and telangiectasia occur on the face in predisposed individuals with severely sun-damaged skin.

Fig. 15.6, Sun-damaged skin. Coarse, deep wrinkles radiate from the lateral margin of the eye. Degraded collagen cannot support hair follicles. The follicles expand, accumulate sebum, and form comedones.

Pearls

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    Sun-protective measures improve photoaging and prevent further damage.

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    Patients seeking treatment for photodamage and cosmesis should commit to daily sunscreen use.

Fig. 15.7, Sun-damaged skin. Bleeding occurs with the slightest trauma to the sun-damaged surfaces of the forearms and hands. The fragile skin tears easily and heals with crisscrossed scars.

Fig. 15.8, Sun-damaged skin. Sun-induced wrinkling on the back of the neck shows a series of crisscrossed lines. Reactive hyperplasia of melanocytes causes lentigines. Diffuse persistent erythema is prominent in fair-skinned people.

Fig. 15.9, Poikiloderma of Civatte. Chronic sun exposure may cause red-brown pigmentation with telangiectasia and atrophy on the sides of the neck in predisposed individuals. The shaded area under the chin is spared.

Fig. 15.10, Actinic comedones. Extensive sun exposure results in open and closed comedones.

Fig. 15.11, This photo-distributed rash is due to a quinolone antibiotic.

Fig. 15.12, Photodermatitis due to loratadine. Common over-the-counter medicines, such as loratadine, may cause photosensitivity.

Polymorphous Light Eruption

Description

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    Polymorphous light eruption (PMLE) is an idiopathic, recurrent rash, occurring on sun-exposed sites, especially in the spring or with first sun exposure.

History

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    PMLE is commonly referred to as sun poisoning or sun allergy.

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    PMLE occurs in all races, at any age, but is most common in young women.

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    Up to 10% of the population is affected, and it is considered the most common photodermatosis.

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    Hereditary PMLE occurs in Inuit and people of Native American descent.

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    Autosomal dominant inheritance with incomplete penetrance and variable expressivity has been described.

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    Symptoms may include pruritus, malaise, chills, headache, and nausea.

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    The rash tends to improve with increasing sun exposure (“hardening”).

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    The underlying pathogenesis is unknown, but it is thought to involve a delayed-type hypersensitivity reaction to an unknown antigen.

Skin Findings

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    Pink pruritic papules, vesicles, and plaques appear minutes to days (up to 5 days) after sun exposure and fade over days to weeks.

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    Initial symptoms are burning, itching, and erythema on exposed skin, such as the upper chest, back of the hands, extensor aspects of the forearms, and lower legs.

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    PMLE tends to spare the face (except in hereditary form).

Laboratory

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    Skin biopsy is helpful to rule out other photo-distributed rashes, such as lupus and porphyria.

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    Serologic tests for lupus and porphyria should be ordered.

Differential Diagnosis

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    Lupus erythematosus

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    Photo-exacerbated rash (seborrheic dermatitis, rosacea)

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    Phytophotodermatitis

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    Erythropoietic protoporphyria

Course and Prognosis

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    PMLE is persistent but may improve over the years.

Discussion

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    UVA is the trigger in most cases, although the amount of exposure needed to trigger a flare varies.

Treatment

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    Minimize sun exposure, especially between 10 am and 2 pm .

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    Sun-protective clothing should be encouraged.

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    Apply broad-spectrum, UVA-blocking sunscreens, especially those containing avobenzone, titanium dioxide, and zinc oxide.

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    Groups II to V topical steroids may relieve itch and fade the rash.

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    Oral steroids tapered over 2 weeks are useful in severe cases.

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    Gradual increase in sunlight or UVR before intense sun exposure lessens the severity of PMLE.

Fig. 15.13, Polymorphous light eruption distribution diagram.

Fig. 15.14, Polymorphous light eruption. The papular type is the most common form. Small papules are densely aggregated. The back of the hands is a common site. The rash itches and is sometimes painful. Lesions persist for 7 to 10 days.

Fig. 15.15, Polymorphous light eruption. The papulovesicular type begins with urticarial plaques from which groups of vesicles arise.

Fig. 15.16, Polymorphous light eruption. Small papules are disseminated or densely aggregated on a patchy erythema.

Fig. 15.17, Polymorphous light eruption. The papulovesicular type occurs primarily on the arms, lower limbs, and the V area of the chest.

Fig. 15.18, Polymorphous light eruption. Papules are localized and symmetrically distributed. They do not occur on the entire sun-exposed areas. Itching is not a constant feature.

Fig. 15.19, Polymorphous light eruption. Acute flare on the arms is coincident with the patient's first prolonged sun exposure of the spring.

Fig. 15.20, Polymorphous light eruption. Discrete monomorphic pruritic papules limited to sun-exposed skin.

Fig. 15.21, Polymorphous light eruption. Urticarial plaques on the legs with papules on the arms.

Fig. 15.22, Polymorphous light eruption. Patients who are highly sensitive to the sun may develop vesicles. A short course of low-dose prednisone may abate a severe reaction.

Pearls

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    Patients may be treated with UVB therapy in the spring to “harden” the skin before intense summer sunlight. UVB therapy is also effective to prevent PMLE before vacations in sunny climates.

Porphyria Cutanea Tarda

Description

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    Porphyria cutanea tarda (PCT) is a disorder of the porphyrin−heme biosynthetic pathway (decreased catalytic activity of uroporphyrinogen decarboxylase), resulting in photosensitivity and skin fragility.

History

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    There are two types of PCT: acquired (more common), due to decreased enzyme function in the liver; and inherited (autosomal dominant), due to decreased enzyme function in all tissues.

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    Precipitating factors include alcohol, estrogen, dialysis, iron, hepatitis C, and HIV.

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    PCT patients have an increased risk for hepatocellular carcinoma.

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