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Sun-damaged skin is easily recognizable and shows specific skin findings, resulting from damage due to ultraviolet radiation (UVR).
Acute exposure to UVR results in sunburn and is especially caused by ultraviolet B (UVB) radiation.
Chronic UVR exposure results in photoaging and skin cancer.
Light-colored skin, genetic disorders (e.g., xeroderma pigmentosum), and certain medications (e.g., doxycycline and sulfa-based medications) predispose to sunburn and photoaging.
Sunburn results from acute UVR and produces pain, redness, and peeling.
Immediate pigment darkening occurs minutes after ultraviolet A (UVA) radiation and fades in 6 to 8 hours.
Delayed tanning occurs 48 to 72 hours after exposure to UVB and UVA radiation and is due to new pigment production.
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.
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)
No testing if necessary to diagnose sun-damaged skin.
Sunburn differential diagnosis: phototoxic medication reaction, toxin-mediated erythema, underlying genetic skin disorder (e.g., xeroderma pigmentosum)
Chronic sun exposure differential diagnosis: rosacea, premature aging syndrome
With proper sun precautions, use of sunscreen, and sun-protective clothing, photoaging can be minimized.
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.
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.
Sun-protective measures improve photoaging and prevent further damage.
Patients seeking treatment for photodamage and cosmesis should commit to daily sunscreen use.
Polymorphous light eruption (PMLE) is an idiopathic, recurrent rash, occurring on sun-exposed sites, especially in the spring or with first sun exposure.
PMLE is commonly referred to as sun poisoning or sun allergy.
PMLE occurs in all races, at any age, but is most common in young women.
Up to 10% of the population is affected, and it is considered the most common photodermatosis.
Hereditary PMLE occurs in Inuit and people of Native American descent.
Autosomal dominant inheritance with incomplete penetrance and variable expressivity has been described.
Symptoms may include pruritus, malaise, chills, headache, and nausea.
The rash tends to improve with increasing sun exposure (“hardening”).
The underlying pathogenesis is unknown, but it is thought to involve a delayed-type hypersensitivity reaction to an unknown antigen.
Pink pruritic papules, vesicles, and plaques appear minutes to days (up to 5 days) after sun exposure and fade over days to weeks.
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.
PMLE tends to spare the face (except in hereditary form).
Skin biopsy is helpful to rule out other photo-distributed rashes, such as lupus and porphyria.
Serologic tests for lupus and porphyria should be ordered.
Lupus erythematosus
Photo-exacerbated rash (seborrheic dermatitis, rosacea)
Phytophotodermatitis
Erythropoietic protoporphyria
PMLE is persistent but may improve over the years.
UVA is the trigger in most cases, although the amount of exposure needed to trigger a flare varies.
Minimize sun exposure, especially between 10 am and 2 pm .
Sun-protective clothing should be encouraged.
Apply broad-spectrum, UVA-blocking sunscreens, especially those containing avobenzone, titanium dioxide, and zinc oxide.
Groups II to V topical steroids may relieve itch and fade the rash.
Oral steroids tapered over 2 weeks are useful in severe cases.
Gradual increase in sunlight or UVR before intense sun exposure lessens the severity of PMLE.
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 (PCT) is a disorder of the porphyrin−heme biosynthetic pathway (decreased catalytic activity of uroporphyrinogen decarboxylase), resulting in photosensitivity and skin fragility.
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.
Precipitating factors include alcohol, estrogen, dialysis, iron, hepatitis C, and HIV.
PCT patients have an increased risk for hepatocellular carcinoma.
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