Last updated: June 1, 2023

Summarytoggle arrow icon

Photodermatoses (photosensitivity disorders) are a group of skin conditions that result from an abnormal reaction to UV light and can be categorized as either primary or secondary photodermatoses depending on the specific cause. Primary photodermatoses are induced by immune-mediated reactions (e.g., as in polymorphous light eruption) or stem from chemical/drug exposure. Secondary photodermatoses result from underlying disorders (e.g., genetic diseases, photoaggravated dermatoses) that increase an individual's susceptibility to adverse UV reactions. Most photodermatoses present as an erythematous rash on areas of sun-exposed skin. A careful history and full skin examination are required to differentiate between the types. In the case of diagnostic uncertainty, further workup includes laboratory studies for underlying causes, skin biopsy, and phototesting. The general management of photodermatoses for both adults and children involves supportive therapy for symptom relief, photoprotective measures, and avoidance of triggers (e.g., phototoxic agents). Further treatment, if required, is usually overseen by a specialist and may include phototherapy and immunosuppressive therapy.

The diagnosis and management of sunburn are discussed in a separate article.

Approach to suspected photodermatosestoggle arrow icon

General principles

Clinical evaluation

The rash in photodermatoses usually spares skin folds and areas covered with jewelry or clothes. [2]

Diagnostics of photodermatoses [2][4][5]

Phototesting [2][5]

  • Definition: a collection of studies that assess the reaction of the skin when exposed to UV radiation
  • Indication: diagnostic confirmation for patients with suspected primary photodermatoses
  • Methods
    • Minimal erythema dose (MED) testing
      • Different skin fields are exposed to increasing UV doses to determine the threshold dose to trigger.
      • Serial readings of the erythema are indicated every few hours.
    • Photoprovocation test
      • A test that aims to reproduce photodermatoses
      • Performed by repeatedly exposing a patient to fixed doses of UV radiation for a period of at least 3 days
    • Photopatch testing
      • A study used to identify photoallergens
      • Suspected agents are applied to the skin in duplicate sets, with one set being exposed to UV radiation and the other not exposed and used for control.

Phototesting is not always available and challenge-rechallenge testing may be required as an alternative. [2]

General management of photodermatoses

  • Start supportive therapy for photodermatoses. [4][6]
  • Advise patients to avoid UV radiation; when possible and use photoprotective measures if exposure is unavoidable. [5][7][8]
  • When possible, stop medications that may be contributing to phototoxic or photoallergic reactions.
  • Refer patients to a specialist (e.g., dermatologist, immunologist) if symptoms persist.

Immune-mediated photodermatosestoggle arrow icon

Immune-mediated (idiopathic) photodermatoses result from an abnormal immune response to UVR exposure. Polymorphous light eruption is the most common type of immune-mediated photodermatosis and the most ubiquitous photodermatosis overall; other forms of immune-mediated photodermatoses are comparatively rare. [2]

Polymorphous light eruptiontoggle arrow icon

Etiology [5]

An acquired photodermatosis characterized by a pathological response to UV exposure


  • Most common type of photodermatoses in both adults and children [1][2]
  • Predominantly affects genetically-predisposed individuals and those with a darker skin tone [2][3][4]
  • Typically worse during the spring and summer [5]

Pathophysiology [2]

Clinical features [2]

  • Erythematous rash
  • Common sites involved:
    • Sun-exposed areas
    • Ears in children; this variant is known as juvenile spring eruption.
  • Develops minutes to hours (can be days) after the first high-intensity UV exposure in the spring or the summer
  • Without continuous sun exposure: resolves within a week
  • Symptoms usually:
    • Improve over the summer because of UVR-induced immunologic tolerance (photohardening)
    • Recur annually (always at the same anatomical sites and after the first sun exposure)

Diagnostics [2][5]

Management [5]

Starting phototherapy in the spring can help prevent symptoms during the summer. [4]

Chronic actinic dermatitistoggle arrow icon

Actinic prurigotoggle arrow icon

Solar urticariatoggle arrow icon

Chemical sunscreen does not block long-wavelength UV light or visible light, both of which may trigger solar urticaria. Mineral sunscreen should be used instead. [5]

Hydroa vacciniformetoggle arrow icon

Drug or chemical-induced photodermatosestoggle arrow icon


  • Drug or chemical-induced photodermatoses are those caused by exposure (either topical or oral) to a photosensitizer
  • Photosensitizers may be either phototoxic agents or photoallergens
  • While the etiology, pathophysiology, and clinical features vary between the conditions, the diagnostics and management are the same.
Overview of drug or chemical-induced photodermatoses
Etiology Pathophysiology Clinical features
Phototoxic reactions [2] Drug-induced phototoxic reactions [2]
  • Drug metabolites interact with UV light (usually triggered by UVA) → free radical release → direct tissue or cell injury → severe rash
  • Occurs without pre-sensitization to the drug
  • Severe sunburn-like rash, possibly with vesicles or bullae
  • Occurs within minutes to hours of sun exposure
  • Localization: sun-exposed areas of the skin
  • Exposure to phototoxic agents, i.e.: plant compounds furocoumarin (e.g., psoralen)
    • Direct skin contact with the plant [1][8][13]
    • Berloque dermatitis: a type of photodermatitis elicited by the use of perfume or products with bergamot oils (aromatherapy) [13]
  • Skin contact with photosensitizing agents (psoralen) from a plant → phototoxic reaction upon UVA exposure
  • Localization: sun-exposed areas of the skin (most often the extremities)
  • Rash
    • Stripe-like or reticulate rash; usually correlates to plant shape or forms a brush pattern resembling handprints or fingerprints
    • 24–48 hours after contact: redness and blistering; most severe after three days
    • Resolution after 2–4 weeks with hyperpigmentation that may be visible for months
  • Itching, burning pain
Photoallergic reaction [2]
  • The skin changes are limited to areas that were exposed to UVA radiation and were in contact with the photosensitizing agent.
  • Rash: erythema and papules, rarely vesicles

Phytophotodermatitis can typically be differentiated from sunburn by a longer latency period before erythema develops, and the pattern of the rash, which is usually localized rather than generalized.

Diagnostics [2]

Phytophotodermatitis is the most common phototoxic reaction in children. [1]

Management [2][8]

Sunscreen can cause photoallergic reactions; patients should avoid products containing common photoallergens such as oxybenzone and dibenzoylmethanes. [2]

Referencestoggle arrow icon

  1. Chantorn R, Lim HW, Shwayder TA. Photosensitivity disorders in children: part I. J Am Acad Dermatol. 2012; 67 (6): p.1093.e1-1093.e18.doi: 10.1016/j.jaad.2012.07.033 . | Open in Read by QxMD
  2. Guan LL, Lim HW, Mohammad TF. Recognizing photoallergy, phototoxicity, and immune-mediated photodermatoses. J Allergy Clin Immunol. 2022; 149 (4): p.1206-1209.doi: 10.1016/j.jaci.2022.02.013 . | Open in Read by QxMD
  3. Nahhas AF, Oberlin DM, Braunberger TL, Lim HW. Recent Developments in the Diagnosis and Management of Photosensitive Disorders. Am J Clin Dermatol. 2018; 19 (5): p.707-731.doi: 10.1007/s40257-018-0365-6 . | Open in Read by QxMD
  4. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  5. Harshman J, Quan Y, Hsiang D. Phytophotodermatitis: Rash with many faces. Can Fam Physician. 2017; 63 (12): p.938-940.
  6. Robinson JK. Sun Safety. JAMA Dermatol. 2018; 154 (3): p.380.doi: 10.1001/jamadermatol.2017.5256 . | Open in Read by QxMD
  7. Maniam G, Light KM, Wilson J. Margarita Burn: Recognition and Treatment of Phytophotodermatitis. J Am Board Fam Med. 2021; 34 (2): p.398-401.doi: 10.3122/jabfm.2021.02.200382 . | Open in Read by QxMD
  8. Komarow HD, Eisch AR, Young M, Nelson C, Metcalfe DD. Solar Urticaria. J Allergy Clin Immunol Pract. 2015; 3 (5): p.789-790.doi: 10.1016/j.jaip.2015.04.006 . | Open in Read by QxMD
  9. Gutierrez D, Gaulding JV, Motta Beltran AF, Lim HW, Pritchett EN. Photodermatoses in skin of colour. J Eur Acad Dermatol Venereol. 2018; 32 (11): p.1879-1886.doi: 10.1111/jdv.15115 . | Open in Read by QxMD
  10. Valbuena MC, Muvdi S, Lim HW. Actinic Prurigo. Dermatol Clin. 2014; 32 (3): p.335-344.doi: 10.1016/j.det.2014.03.010 . | Open in Read by QxMD
  11. Gruson LM, Chang MW. Berloque Dermatitis Mimicking Child Abuse. Arch Pediatr Adolesc Med. 2002; 156 (11): p.1091.doi: 10.1001/archpedi.156.11.1091 . | Open in Read by QxMD
  12. Balestri R, Neri I. Hydroa vacciniforme. Can Med Assoc J. 2010; 182 (17): p.E796-E796.doi: 10.1503/cmaj.092088 . | Open in Read by QxMD
  13. Chen J, Li H, Zhu H. Successful Treatment of Chronic Actinic Dermatitis with Dupilumab: A Case Report and Review of the Literature. Clin Cosmet Investig Dermatol. 2021; Volume 14: p.1913-1917.doi: 10.2147/ccid.s342401 . | Open in Read by QxMD

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