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.[7]
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 phototesting results.[7]
Skin biopsy reveals prominent papillary dermal edema with a lymphocytic perivascular infiltrate.
Phototoxic dermatitis
SIGNS / SYMPTOMS
Caused by a systemic or topical photosensitizer that, coupled with sunlight, creates a markedly increased sunburn reaction.[7]
Systemic medications associated with phototoxicity include amiodarone, doxycycline, griseofulvin, NSAIDs, and fluoroquinolones, among others.[9]
Furocoumarin is a topical photosensitizer found in a variety of plants, including citrus fruits, figs, celery, and parsley, among others (phytophotodermatitis).
Bergapten, the phototoxic ingredient in oil of bergamot, is found in many fragrances (berloque dermatitis).
Onset within hours; no prior sensitization 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 photosensitizers, which typically demonstrate a patchy or linear distribution.
When the diagnosis is in doubt, phototesting may be performed, which shows erythema at lower than expected doses in the UVA range.[9]
Skin biopsy is generally not helpful, as histologic findings may be difficult to distinguish from acute sunburn.
Photoallergic dermatitis
SIGNS / SYMPTOMS
Typically presents as a pruritic, scaly erythematous eruption in a photodistribution.
May be associated with external or internal triggers, resulting in photoallergic contact dermatitis or photoallergic drug reaction, respectively.
Photoallergic reactions have been associated with the common sunscreen ingredient oxybenzone, as well as oral drugs, including thiazides, sulfonamides, sulfonylureas, and phenothiazines.[9]
Occurs only in previously sensitized individuals and may have delayed onset of up to 14 days.[7]
INVESTIGATIONS
Clinical differentiation is usually sufficient, given the predominant symptom of itching and typical eczematous appearance.
The diagnosis can be confirmed by photopatch testing, showing a positive reaction on the irradiated side only.[9]
Skin biopsy demonstrates histologic 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 phototherapy 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.[21]
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 photodistributed areas.
Duration varies from hours to weeks.
Often poikilodermatous (pigmentary/atrophic changes and mottled appearance) with occasional papules and scale.[9]
Other cutaneous and systemic symptoms typically allow for clinical differentiation.
INVESTIGATIONS
Clinical differentiation is usually sufficient.
Skin biopsy demonstrates a lichenoid reaction pattern characterized 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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