Differential diagnosis
The differential diagnosis for this process includes herpes zoster, atopic dermatitis, allergic contact dermatitis, porphyria cutanea tarda, chemical or thermal burn, and abuse.2,4 While chemical or thermal burn and abuse are suspected with the appropriate history, the remainder of the diagnoses have defining characteristics allowing for proper identification.
Herpes zoster is caused by the reactivation of latent varicella zoster virus. Itching or burning precedes cutaneous eruption of red swollen plaques with vesicles of various sizes, which umbilicate or rupture. These lesions occur in a discreet dermatomal distribution.5
Atopic dermatitis has poorly understood pathophysiology. It typically starts in infancy and causes pruritus, eczematous lesions, xerosis, and lichenification of the skin.5
Allergic contact dermatitis is a delayed hypersensitivity reaction that requires prior sensitization. It is classically described as pruritic papules on an erythematous base.5
Porphyria cutanea tarda is a caused by an inborn enzyme deficiency in the heme biosynthetic pathway that results in mechanical fragility, subepidermal bullae, hypertrichosis, and pigmentation.5
Pathophysiology of phytophotodermatitis
In the presence of ultraviolet A (UVA) irradiation, psoralens cause DNA cross-linkage in the skin. This stimulates increased melanin production with resultant hyper-pigmentation. It may also cause the development of radicals, which damage cell membranes and intracellular contents, resulting in edema, erythema, and the formation of vesicles or bullae.3
Several factors have been implicated in the severity of the phototoxic reaction. Increased humidity, concentration of furocoumarins in plant juice, and UVA intensity all worsened the severity of reactions in one study. The concentration of furocoumarin is variable between species and between different parts of the same plant.2