1.3.4 Photodermatoses

Grading & Level of Importance: C






Polymorphous light eruption (PMLE) is the most common photodermatosis (prevalence 10% to 20%), followed in decreasing order of frequency by photoaggravated dermatoses, drug-induced photosensitivity, chronic actinic dermatitis (CAD), porphyrias and solar urticaria (SU). 


Dermatoses caused by electromagnetic radiation in the ultraviolet (UV) or visible light spectrum with or without other co-factors.

Aetiology & Pathogenesis

UV light can cause dermatitis as a single agent (sunburn - see chapter XX) or in combination with phototoxic (furocoumarins such as psoralens) or photoallergic substances (medications such as sulphones, promethazine). Ultraviolet B (UVB) is the main spectrum responsible for skin erythema, whereas ultraviolet A (UVA) is mostly involved in the drug-induced photosensitivity reactions. In all instances, oxygen free radicals trigger the release of pro-inflammatory cytokines (acute dermatitis) or cause permanent skin damage (chronic actinic damage). In addition, some skin disorders are negatively influenced by light; e.g. lupus erythematosus and herpes simplex.

Signs & Symptoms

Depends on disorder.
The most relevant idiopathic immune-mediated or drug-induced photodermatoses include:
Polymorphic light eruption (PMLE): Variable skin appearance with itch affecting exposed skin (occasionally sparing the face) developing minutes to hours after sun exposure.Tends to resolve in hours, days or rarely weeks.


Chronic actinic dermatitis (CAD) is a rare, persistent chronic, usually lichenified (UV- and rarely visible) light-induced dermatosis. CAD occurs most commonly in elderly men. Tends to persist over many years.


Solar urticaria (SU). UVB, UVA and visible light chronic Inducible urticaria. Wheals confined to sunlight-exposed skin appear a few minutes after visible radiation exposure.


Drug- and exogenous chemical-induced photosensitivity include:

Phototoxic (non-immunologically mediated) reactions are the result of direct tissue injury caused by a phototoxic agent and radiation. Clinically may resemble acute sunburn. May be induced by either topical or systemic medications, as well as systemic/topical agents (e.g. food ingredients).


Photoallergic reactions are type IV delayed hypersensitivity responses that occur only in pre-sensitized individuals, and requires only a minimal concentration of the photoallergen. Clinically resembles eczematous dermatitis. Induced mostly by systemic medications.


In phototoxic reactions, usually restricted to area(s) of light exposure, in photoallergic reactions distant spread common.


Photosensitive cutaneous disorders can be classified into four main categories:

1. Idiopathic photodermatoses, immunologically mediated where light alone triggers the disease e.g. polymorphic light eruption, solar urticaria, hydroa vacciniforme.
2. - Drug- and chemical-induced photosensibility, including a subgroup of phototoxic or photoallergic dermatoses triggered by exogenous topical or systemic substances, and a second subgroup of metabolic disorders in which there is endogenous accumulation of phototoxic substances because of enzymatic defects, e.g. cutaneous porphyrias.
3. Genodermatoses characterized by a defective DNA repair, in which there is increased sensitivity to light e.g. xeroderma pigmentosum secondary to a defect in DNA-repair enzymes.
4. Photoaggravated dermatoses. Include a heterogeneous group of disorders.

Laboratory & other workups

In cases of photodistributed eruption of unknown etiology, consider a complete blood cell count, biochemical evaluation (liver function tests), autoantibody screening (ANA, anti-dsDNA, anti-Ro) to exclude connective tissue diseases, and porphyrins in blood, urine and stool may be useful for a definite diagnosis. Genetic testing in rare situations.


Histological changes are often non-specific. May be helpful in some cases of PMLE or CAD to rule out other possible diagnoses.


Variable. Depending on the different subtypes.


In severe SU, anaphylactic shock may occur after whole-body exposure. 


History is often most helpful. Questioning regarding possible exposure to various photosensitizers, such as topical and systemic medications, cosmetics, fragrances and plant extracts may suggest a diagnosis of phototoxicity or photoallergy. Light testing: monochromatic UVA and UVB sensitivity testing, photo patch testing, provocation challenge with UV and/ or visible light. In some cases patch testing should be recommended to rule out associated allergic contact dermatitis.

Differential diagnosis

Depending on the different entities. In PMLE the differential diagnosis should be established with photoallergic eczemas, solar urticaria, erythema multiforme and even lupus erythematosus (LE), malabsorption etc. SU lesions should be distinguished from erythropoietic protoporphyria, urticarial phototoxic reactions, other forms of physical urticaria, and PMLE (urticarial lesions), whereas in patients with CAD, the diagnoses of photoallergic reaction, airborne contact dermatitis, mycosis fungoides, and chronic atopic eczema should be ruled out.

Prevention & Therapy

Light protection: Appropriate clothing; appropriate environmental UV exposure modification (e.g. at workplace). Appropriate sunscreens with SPF 50/UVA filters. Treatment of any underlying disorder.

Topical steroids and antihistamines can be used for symptomatic relief. Possible systemic treatments for chronic, refractory cases: antimalarials or immunosuppressive drugs (azathioprine, ciclosporin, mycophenolate mofetil) or thalidomide. Avoid potential photosensitizing agents.

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