Last updated: January 11, 2022

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Photodermatoses consist of a variety of skin conditions that develop as a result of exposure to ultraviolet radiation (UVR) or visible light. The most common photodermatosis in the US is sunburn (dermatitis solaris), an inflammatory reaction that occurs after excessive UV exposure. Other forms of photodermatoses include polymorphous light eruption (PLE) and phototoxic reactions. Polymorphous light eruption (PLE) is a delayed photosensitivity disorder involving pruritic rashes caused by exposure to ultraviolet A (UVA) radiation during the summer months. Lesions may vary from patient to patient; however, spontaneous resolution (on cessation of sun exposure) is often a unifying trait. Phototoxic reactions are patterned, inflamed eruptions of erythema and vesicles caused by contact with photosensitizing agents (like psoralen) and subsequent sun exposure. Diagnosis of these conditions is usually established on the basis of a thorough history and a full skin examination. Additionally, phototesting and/or photopatch testing are often utilized. Measures such as avoiding the sun, sun­ protective clothing, and sunscreen are the mainstay of therapy. Additional symptomatic treatment with cool compresses, emollients, and oral analgesics may be prescribed depending on the severity of symptoms.

  • Definition: acute inflammatory skin response to UVR , which is limited to the area of exposure. Sunburn (or dermatitis solaris) is often classified as a 1st or 2nd-degree burn.
  • Epidemiology: particularly light-skinned individuals
  • Etiology: excessive exposure to UVB radiation
  • Pathophysiology: UV radiation → DNA mutations → apoptosis of keratinocytes in the epidermis and release of inflammatory markers (including chemokines, prostaglandins) → inflammation of the dermis hours after exposure
  • Clinical features
    • Primarily limited to exposed skin
    • Begins a few hours after exposure, with symptoms peaking after 12–24 hours; usually resolves within a week
    • Initially pruritus and pain, then redness and swelling
    • Blisters may occur in severe cases of sunburn; if larger areas are affected, general symptoms (e.g., fever) may arise.
  • Treatment
  • Prognosis
  • Prevention
    • Avoid sun exposure
    • Protective clothing
    • Sunscreen with adequate SPF (a measurement of how much protection a sunscreen provides; SPF values indicate the fraction of ultraviolet rays, specifically UVB, that are absorbed by the sunscreen)
      • Applied at least 30 minutes prior to sun exposure
      • Reapplied after 2–3 hours, exposure to water (swimming), and/or sweating
      • The most effective active ingredients block UVA and UVB radiation
    • Sun-protective measures for infants and children [2]
      • Avoid sun exposure: shade, protective clothing (e.g., lightweight long pants, long-sleeved shirts, brimmed hats shading the neck, sunglasses with UV protection)
      • Avoid the use of sunscreen in infants < 6 months
        • Higher risk of contact dermatitis and photosensitivity in infants
        • If adequate clothing and/or shade are unavailable, a minimal amount of waterproof sunscreen with at least 30 SPF should be applied to small areas (e.g., face, hands).
      • For children, the use of oil-based emulsions of inorganic filters (e.g., zinc oxide, titanium dioxide) is recommended due to low sensitization and irritation potential.

The use of sunscreen is not recommended in infants < 6 months. Avoiding sunlight exposure is the most effective measure to protect children and infants from sunburn.

A severe sunburn with blistering (corresponding to a second-degree burn) that affects over 10% of an adult's body surface (or more than 5% in children) may result in a capillary leak and ultimately lead to hypovolemic shock.

“UVA tAns the skin and UVB Burns it.”


  • Definition: acquired photodermatosis; characterized by a pathological response to UV exposure (also known as a sun allergy)
  • Epidemiology: most frequently occurring idiopathic photodermatosis
  • Pathophysiology
  • Clinical features
    • Symptoms typically present a few hours to days after the first high-intensity UV exposure in the spring or the summer.
    • Rash
    • Without continuous sun exposure: resolves within a week
    • Common sites involved: sun-exposed areas
    • The symptoms usually recur annually (always at the same anatomical sites and after first sun exposure).
  • Diagnostics
  • Treatment


Drug-induced phototoxic reactions

Phytophotodermatitis (dermatitis pratensis)

Berloque dermatitis

  • Occurs with low light exposure and fragrance application (which includes bergamot oil)
  • Direct transition to hyperpigmentation without previous inflammatory phase


  • Description: a specific substance (photosensitizing agent) in combination with UVA exposure causes an allergic reaction after previous sensitization
  • Etiology: Possible photosensitizing agents include fragrances, ingredients in sunscreen products, preservatives, and drugs.
  • Pathophysiology: T-cell mediated delayed hypersensitivity (type IV) after epicutaneous or oral contact with photosensitizing agents
  • Clinical features
    • The skin changes are limited to areas that were exposed to UVA radiation and were in contact with the photosensitizing agent.
    • Efflorescence: erythema and papules, rarely vesicles
  • Diagnostics
    • Patient history
    • Photopatch test
      • Initially, the minimal erythema dose (MED) is determined to establish the patient's general light sensitivity (through UVA and UVB exposure).
      • Then, specific test substances are applied to each side of the back and remain there for 24 hours.
      • The initial reading upon application is recorded, followed by exposure of one side to UVA light. Additional readings occur 24, 48, and 72 hours after exposure.
      • The non-exposed side is used as a control.
      • A visible reaction on the exposed side but not on the control side indicates a photoallergic reaction. If a reaction occurs on both sides for the same test substance, then it is most likely a light-independent allergic contact dermatitis.
  • Management
    • Avoid the specific photosensitizing agent.
    • Sun protection: protective clothing and/or sunscreen
    • During acute phase: topical glucocorticoids
  1. Faurschou A, Wulf HC. Topical corticosteroids in the treatment of acute sunburn: a randomized, double-blind clinical trial. Arch Dermatol. 2008; 144 (5): p.620-624. doi: 10.1001/archderm.144.5.620 . | Open in Read by QxMD
  2. Infant sun protection: How parents can keep their baby safe. Updated: January 1, 2021. Accessed: February 5, 2021.
  3. Lopes DM, McMahon SB. Ultraviolet radiation on the skin: a painful experience?. CNS Neurosci Ther. 2016; 22 (2): p.118-126. doi: 10.1111/cns.12444 . | Open in Read by QxMD
  4. Gies P. Photoprotection by clothing. Photodermatol Photoimmunol Photomed. 2007; 23 (6): p.264-274. doi: 10.1111/j.1600-0781.2007.00309.x . | Open in Read by QxMD
  5. Farina JA Jr, Rosique MJ, Rosique RG. Curbing inflammation in burn patients. Int J Inflam. 2013 . doi: 10.1155/2013/715645 . | Open in Read by QxMD
  6. Guarrera M. Polymorphous Light Eruption. Springer International Publishing ; 2017 : p. 61-70
  7. Zeichner JA. Acneiform Eruptions in Dermatology: A Differential Diagnosis. Springer Science+Business Media ; 2014
  8. Phytophotodermatitis. Updated: September 14, 2014. Accessed: September 9, 2020.
  9. Sunburn Prevalence Among Adults - United States, 1999, 2003, and 2004. Updated: June 1, 2007. Accessed: May 15, 2017.
  10. Boonstra HE, van Weelden H, Toonstra J, van Vloten WA. Polymorphous light eruption: A clinical, photobiologic, and follow-up study of 110 patients. J Am Acad Dermatol. 2000; 42 (2 Pt 1): p.199-207. doi: 10.1016/S0190-9622(00)90126-9 . | Open in Read by QxMD

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