Differentials
Polymorphous light eruption (PMLE)
SIGNS / SYMPTOMS
Classically presents with pruritic papules, plaques, vesicles, or erythema, occurring after the first sun exposure of the season.
Usually appears 1 to 4 days after ultraviolet (UV) exposure but can sometimes be seen within minutes. The skin typically demonstrates 'hardening' (diminishing signs and symptoms) with subsequent ultraviolet (UV) exposure.[12]
INVESTIGATIONS
Clinical differentiation is usually sufficient given the pattern of onset and the polymorphous nature of lesions, although bullous PMLE eruptions may be confused with acute sunburn.
A substantial percentage of those affected may have negative photo-testing results.[12]
Skin biopsy reveals prominent papillary dermal oedema with a lymphocytic perivascular infiltrate.
Photo-toxic dermatitis
SIGNS / SYMPTOMS
Caused by a systemic or topical photo-sensitiser that, coupled with sunlight, creates a markedly increased sunburn reaction.[12]
Systemic medications associated with photo-toxicity include amiodarone, doxycycline, griseofulvin, NSAIDs, and fluoroquinolones, among others.[14]
Furocoumarin is a topical photo-sensitiser found in a variety of plants, including citrus fruits, figs, celery, and parsley, among others (phytophotodermatitis).
Bergapten, the photo-toxic ingredient in oil of bergamot, is found in many fragrances (berloque dermatitis).
Onset within hours; no prior sensitisation is required.
Induced by radiation in UVA range.
UVA, unlike UVB, can penetrate window glass.
INVESTIGATIONS
Clinical differentiation is usually possible, especially in cases due to external photo-sensitisers, which typically demonstrate a patchy or linear distribution.
When the diagnosis is in doubt, photo-testing may be performed, which shows erythema at lower than expected doses in the UVA range.[14]
Skin biopsy is generally not helpful, as histological findings may be difficult to distinguish from acute sunburn.
Photo-allergic dermatitis
SIGNS / SYMPTOMS
Typically presents as a pruritic, scaly erythematous eruption in a photo-distribution.
May be associated with external or internal triggers, resulting in photo-allergic contact dermatitis or photo-allergic drug reaction, respectively.
Photo-allergic reactions have been associated with the common sunscreen ingredient oxybenzone, as well as oral drugs, including thiazides, sulphonamides, sulphonylureas, and phenothiazines.[14]
Occurs only in previously sensitised individuals and may have delayed onset of up to 14 days.[12]
INVESTIGATIONS
Clinical differentiation is usually sufficient, given the predominant symptom of itching and typical eczematous appearance.
The diagnosis can be confirmed by photo-patch testing, showing a positive reaction on the irradiated side only.[14]
Skin biopsy demonstrates histological features similar to allergic contact dermatitis, including spongiosis and a dermal lymphohistiocytic infiltrate.
Ultraviolet (UV) recall reaction
SIGNS / SYMPTOMS
Occurs in areas of prior sunburn or UV photo-therapy after the administration of chemotherapy or antibiotics (most notably methotrexate).
Recall reactions may not appear for days to weeks or, in some cases, years after exposure to inciting medication.[26]
May have similar presentation with erythema and vesicles/bullae.
INVESTIGATIONS
Clinical differentiation is usually sufficient, as UV recall and enhancement reactions are not associated with acute sun exposure.
Skin biopsy reveals apoptotic keratinocytes similar to sunburn.
SLE
SIGNS / SYMPTOMS
Classic malar erythema ('butterfly rash') often following sun exposure.
Can also present in other, typically photo-distributed areas.
Duration varies from hours to weeks.
Often poikilodermatous (pigmentary/atrophic changes and mottled appearance) with occasional papules and scale.[14]
Other cutaneous and systemic symptoms typically allow for clinical differentiation.
INVESTIGATIONS
Clinical differentiation is usually sufficient.
Skin biopsy demonstrates a lichenoid reaction pattern characterised by colloid bodies, vacuolar changes in basal keratinocytes, a thickened basement membrane, perivascular and periadnexal lymphocytic infiltrates, and dermal deposition of acid mucopolysaccharide. Immunofluorescence studies may reveal granular deposits of C3, IgG, and IgM at the dermal-epidermal junction.
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