Here Comes the Sun Exposure: Photodermatoses

Unless otherwise stated, all treatments and doses are for adults and not weight based for the pediatric population.

What are photodermatoses?

Photodermatoses are a collection of skin disorders that are provoked by exposure to specific wavelengths of electromagnetic radiation due the presence of an underlying autoimmune process, a concurrent medication, photo-aggravation, or inherited abnormalities in DNA repair.¹

Dark- and light-colored skin phototypes have different properties in response to UV radiation based on melanin content (see Table 1).²

Immune-mediated photodermatoses are divided into polymorphous light eruptions, actinic dermatitis, actinic prurigo, and solar urticaria.

Chemical- and medication-induced (also called photoaggravated)  photosensitivities are from either an ingested medication or porphyria.

See Table 2 for a list of photodermatoses, including some not specifically discussed below.

More than you ever wanted to know about sun rays

Radiant energy emitted by the sun is composed of three different ultraviolet wavelengths: A, B, and C.³ UVA represents long wavelengths, UVB is intermediate, and UVC is considered short. Our ozone absorbs UVC, but UVA and UVB can get through, eventually making contact with our skin. 99% of the wavelengths that make it to the Earth’s surface are visible or infrared, with only 1% made up of UVA and UVB. UVA is present consistently throughout the day, whereas UVB is predominately present during midday.⁴ Of the two, UVA (associated with photoaging and skin cancer) is seen in quantities 20 times larger than UVB. Upon contact with our skin, the rays are either reflected, transmitted, scattered, or absorbed. The portion that is absorbed leads to the pathologic effects we will discuss below.

A clinical approach to suspected photodermatosis

A thorough history and physical are paramount. Ask about the onset of the skin condition around the time of sun exposure, including the use of tanning beds. Examine areas such as the upper arms, torso, and thighs that may be covered by clothing and, conversely, areas that are commonly exposed to the sun, such as the forearms, scalp, neck, and lower legs. Because one of the four classifications of photodermatoses has a genetic component, ask about a family history of similar skin conditions. Perform a through medication reconciliation to reveal any medications that may have been associated with photodermatoses.

Diagnostic evaluation should include antinuclear antibody (ANA) titers to rule out an autoimmune process. Consider a skin biopsy and/or photopatch testing for further clarification, as up to 10% of patients will have a positive photopatch test.⁵ Photopatch testing involves exposing an area of skin to escalating doses of UVA, UVB, and visible light for an immediate reaction (commonly seen in solar urticaria) as well as a delayed reaction (patient returns to the clinic after 24 hours and then seven days later).⁵ If you suspect porphyria, porphyrin levels should be tested to support your diagnosis.

Immune-mediated photodermatoses

Polymorphous light eruption

Polymorphous light eruption (PLE) is a condition that occurs within hours of sun exposure. It manifests as erythematous, mildly pruritic papules, plaques, and/or nodules most commonly on the hands, lower neck, and cheeks. If patients present with lesions localized to the cheeks, then cutaneous lupus erythematosus should be ruled out through ANA and anti-SSA Ab testing. PLE is most commonly diagnosed in patients residing in temperate climates.⁵ Interestingly, the eruptions are worse in the early spring and may improve as the summer season progresses, termed the “hardening” effect.⁶ Phototesting can be performed to confirm the diagnosis, with patients typically being more sensitive to UVA than the UVB spectrum. Therapy involves treatment with narrow-band UVB early in the spring in repeated sessions (eg, 2 times a week for 4 weeks) with consideration of oral steroids during initiation of treatment.^5,7

Chronic actinic dermatitis

This is a delayed-type hypersensitivity dermatitis that is most commonly seen in those 50-70 years of age, with a predilection toward those with darker skin along the scalp, face, chest, and dorsal extremities.¹ It presents with pruritic patches or plaques that may lichenify. Chronic actinic dermatitis can be difficult to distinguish from allergic dermatitis caused by sunscreen and certain hair products with para-phenylenediamine, as the lesions often occur in similar places of sun exposure.⁸

Solar urticaria

Less common than other immune-mediated conditions, solar urticaria characteristically appears with burning, pruritus, erythema, and wheals within 30 minutes of UV radiation exposure and spontaneously resolves 24 hours after onset.⁵ This differs from PLE, which takes 2-3 days after UV exposure before lesions appear. As above, common locations include the V of the neck and dorsal arms, but lesions can occur on skin under clothes if the clothing does not provide UV protection.⁹ Diagnosis can be made with phototesting through increasing exposure to UV radiation. Solar urticaria may not last a lifetime; various studies have shown that more than half of patients with the condition report resolution approximately 5 years after onset. Treatment with antihistamines, topical steroids, and compresses can be used short term, with protective measures detailed below being better for long-term management.

Chemical- and medication-induced photosensitivity

Medications that cause skin eruptions are more common in White individuals than in people of color (except for diltiazem-induced eruptions, which are more common in people of color).¹ The eruptions can be caused by exogenous exposure to the medication itself (see Table 3) or by endogenous substrates that accumulate internally, causing tense blisters and vesicles that break easily and leave the fragile skin to heal slowly thereafter.⁵ Photosensitivities from endogenous accumulation are termed porphyrias, the most common of which are porphyria cutanea tarda and erythropoietic protoporphyria, and they are more prevalent in White individuals.¹⁰ Porphyrias are defined pathologically as a metabolic disorder caused by abnormal heme synthesis leading to the accumulation of porphyrins that react to UV light, producing reactive oxygen species and resulting in skin damage. Individuals with hepatitis C and HIV, along with those with a known HFE gene mutation suggestive of hereditary hemochromatosis, are at highest risk for porphyrias such as porphyria cutanea tarda. Given these factors, avoidance is first-line treatment. Sunscreens should be opaque in nature, rather than ultraviolet, to block the visible light spectrum.