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.

Table 1 | Dark and light skin characteristics


DNA damage with UV exposure
Results from UV exposure
Size of melanosomes

Dark skin

High amount
Discrete, but large in epidermis

Light skin

Low amount
Small and clustered in lower layers

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.

Table 2 | Photodermatoses summarized


Polymorphic light eruptions
Actinic folliculitis
Solar urticaria
Photosensitivity dermatitis
Hydroa vacciniforme

Chemical- and medication-induced photosensitivity

Porphyria cutanea tarda
Erythropoietic protoporphyria

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.

TABLE 3 | Common medications that can induce a photodermatosis



Patients with underlying diseases can present with unique dermatoses that, while not caused by UV radiation, may be exacerbated upon this specific exposure leading to a flare in disease. We will focus on two of the most commonly encountered conditions in primary care that are exacerbated by UV radiation: cutaneous lupus erythematosus and lichen planus. Interestingly, keep in mind that there are also conditions that are treated with UV radiation exposure such as atopic dermatitis and psoriasis (see Table 4).

Cutaneous lupus erythematosus

This is an autoimmune disorder that primarily affects the skin, although some patients may demonstrate systemic involvement or go on to develop systemic disease, which affects multiple organs in the body. Cutaneous lupus erythematosus is more common in women. It manifests as an eruption of confluent, edematous, erythematous lesions. A malar distribution can be a marker of internal disease activity.11 Cutaneous lupus erythematosus worsens through reactive oxygen species generation from UV radiation that triggers autoantibodies and leads to keratinocyte destruction. When healing eventually occurs, pigmentary changes and scars may result.

Lichen planus

Lichen planus is a mucocutaneous condition presenting with the 7 Ps: purple, pruritic, polygonal, planar, papules, and plaques (the 7th being planus).1 Certain medications can cause a lichen planus-like eruption, including but not limited to quinidine, quinine, hydrochlorothiazide, and angiotensin-converting enzyme (ACE) inhibitors.12 Variants include actinicus, which occurs on sun-exposed skin in Middle Eastern and Indian subcontinent populations, and pigmentosus, which is more common in those with darker skin colors (and thought to be related to hepatitis C exposure).

Table 4 | Photo-aggravated conditions

Mild worsening of disease with UV exposure

Cutaneous lupus erythematosus
Lich planus

Moderate to severe worsening of disease with UV exposure

Carcinoid syndrome
Erythema multiforme
Seborrheic dermatitis

Potential improvement in disease / therapeutic with UV exposure

Atopic dermatitis

Do photodermatoses differ in those with darker skin?

When we refer to darker skin colors, this can include skin types of individuals of Asian, Hispanic, African, American Indian, or Alaskan native ancestry. Skin is typed based on Fitzpatrick grading, which ranges from I to VI (see Table 5).13 Melanin, which is seen in higher quantities in those with darker skin, inhibits UVB radiation from penetrating the skin.2

As mentioned above, exogenously mediated drug eruptions caused by exposure to the extended-release formulation of diltiazem (a medication commonly used in rate control for atrial fibrillation) are more common in people of color than in White individuals. While rare in reports, this eruption presents with asymptomatic facial hyperpigmentation manifested in a grayish tone as early as 2 months and as late as 150 months after drug exposure.1,14

Of the photo-aggravated conditions, lichen planus is more common in Black individuals.

Be aware that phototesting may be more difficult to perform in darker skin, as the development of erythema is subjective and may be difficult to ascertain.

TABLE 5 | Fitzpatrick grading of skin phototypes


Eye color

Light blue



Dark brown


Hair color



Dark blonde

Dark brown


Nonexposed skin color


Very pale


Light brown

Dark brown

Freckles in nonexposed areas?






Result when staying in sun too long?

Painful redness, blisters

Blistering then peeling

Occasional burns, peeling

Rare burns

Never had burns

Do you “tan” with sun exposure?

Hardly or not at all

Light color tan

Reasonably tan

Tan very easily

Turn dark brown quickly

Do you turn brown after several hours of sun exposure?






Face reaction to sun exposure

Very sensitive



Very resistant

Never had a problem

When did you last expose your body to sun?

> 3 months ago

2-3 months ago

1-2 months ago

< 1 month ago

< 2 weeks ago

Did you expose the area to be treated to the sun?


Hardly ever




Score interpretation and expected skin reaction
0-7 I Always burn, never tan
8-16 II Usually burn, tan less than average
17-25 III Sometimes mild burn, tan about average
26-30 IV Rarely burn, tan more than average
>30 V or VI Brown skin (VI is black skin)

What should I know about management and sunscreen protection?
Photoprotection with broad-spectrum sunscreen (UVA and UVB coverage) and smoking cessation (smoking can compromise the underlying immune system) are pivotal elements of prevention and management. Physicians may consider checking those patients who do wear sunscreen often for vitamin D deficiency; however, routine screening is not currently endorsed by the United States Preventive Services Task Force.

Broad-spectrum sunscreen, initially developed to minimize sunburn, can inhibit both the acute and chronic deleterious effects of UV radiation exposure. The sun protection factor, or SPF, represents the efficacy of sunscreen and is calculated as the ratio of doses of radiation causing sunburn with sunscreen applied to doses of radiation causing sunburn without it applied (the importance of the amount of sunscreen applied, thin or moderate, has yet to be determined but most experts agree to aim for a “liberal” amount). While international standards are not consistent, in most countries an SPF of 50+ is the maximum allowed; however, a cap has not been set in the United States. In general, an SPF of at least 30 should be applied; higher amounts are helpful in situations where people are less likely to reapply sunscreen.15 Furthermore, be aware of “waterproof” claims, which generally mean that the sunscreen must retain 50% or more of its original SPF level after two 20-minute periods of water immersion. Finally, do not use expired sunscreens.

Individuals with lower Fitzpatrick scale phototypes are more susceptible to sunburns and cancer and should apply and reapply sunscreen more often compared with those at higher Fitzpatrick scale phototypes. However, sensitivity to UV radiation is unique to each individual and can be measured with the minimal erythema dose (MED), typically only done in research settings.

Patients should utilize the published UV index, which is based on the erythema action spectrum that factors in the intensity of erythemal UV radiation, sun elevation, time of day, time of year, latitude, altitude, ozone, cloud cover, and ground reflection.4 In general, people do not apply (and reapply) sunscreen as often as they should. Lastly, clothing is a simple method for sun protection. UV protection factor, or UPF, ratings are given to clothing that protects skin from sun exposure. Clothing with Lycra offers the best photoprotection.15

With the summer upon us, protect your skin and apply sunscreen!


  1. Gutierrez, J.V. Gaulding, A.F. Motta Beltran, H. (2018). Photodermatoses in skin of color. Journal of the European Academy of Dermatology and Venereology, 851-854.
  2. Sharma, V. K., Sahni, K., & Wadhwani, A. R. (2013). Photodermatoses in pigmented skin. Photochemical & Photobiological Sciences, 12-25.
  3. Krutmann, J. (2000). Ultraviolet A radiation-induced biological effects in human skin: relevance for photoaging and photodermatosis. Journal of Dermatological Science, S22-S26.
  4. Young, A. R., Claveau, J., & Beatris Rossi, A. (2016). Ultraviolet radiation and the skin: Photobiology and sunscreen photoprotection. Journal of the American Academy of Dermatology, 038.
  5. Santoro, F. A., & Lim, H. W. (2011). Update on Photodermatoses. Seminars in Cutaneous Medicine and Surgery, 229-238.
  6. Franken, S. M., Genders, R. E., de Gruijl, F. R., Pavel, S., & Rustemeyer, T. (2013). Skin hardening effect in patients with polymorphic light eruption: comparison of UVB hardening in hospital with a novel home UV-hardening device. J Eur Acad Dermatol Venereol, 67-72.
  7. Combalia, A., Fernandez-Sartorio, C., Morgado-Carrasco, D., Podlipnik, S., & Aguilera, P. (2017). Successful Short Desensitization Treatment Protocol with Narrowband UVB Phototherapy (TL-01) in Polymorphic Light Eruption. Actas Dermosifiliogr, 752-757.
  8. Makkana, K. S., Stone, N. M., & Ingram, J. R. (2017). Para-phenylenediamine allergy: current perspectives on diagnosis and management. J Asthma Allergy, 9-15.
  9. Roelandts, R., & Ryckaert, S. (1999). Solar urticare: the annoying photodermatosis. International Journal of Dermatology, 411-418.
  10. Elder, G. H., Gray, C. H., & Nicholson, D. C. (1972). The porphyrias: a review. J Clin Pathol., 1013-1033.
  11. O’Gorman, S. M., & Murphy, G. M. (2014). Photoaggravated Disorders. Dermatologic Clinics, 385-393.
  12. MH, C. (2009). Defining lichenoid photodermatitis. Int J Dermatol 2009, 239.
  13. Gupta, V., & Sharma, V. K. (2019). Skin typing: Fitzpatrick grading and others. Clinics in Dermatology, 1-7.
  14. Blakely, K. M., Drucker, A. M., & Rosen, C. F. (2019). Drug-Induced Photosensitivity-An Update: Culprit Drugs, Prevention and Management. Drug Saf, 827-847.
  15. Li, H., Colantonio, S., Dawson, A., Lin, X., & Beecker, J. (2019). Sunscreen Application, Safety, and Sun Protection: The Evidence. Journal of Cutaneous Medicine and Surgery.

Subscribe to VisualDx Today

Become a VisualDx subscriber today and gain access to clinical information and medical images of thousands of diagnoses. Your first 7 days are FREE.

Learn More

Related Posts