CLINICAL HISTORY:

Signs and symptoms:  Two day history of painful, hyperpigmented rash with sparse blisters on trunk, upper extremities bilaterally, and flexor surfaces few hours after sun exposure. No past medical history, no family history, patient otherwise healthy. No systemic symptoms

Previous Treatment:  none

Other information:  13 yo caucasian female had recently arranged a spa day where each individual laid out in the sun after applying lemon juice and other citrus plants/fruits to their body. Few hours after the sun exposure, patient started experiencing pain erythematous rash on sun exposed areas as mentioned with sparse blisters.

PHYSICAL EXAM:

The patient exhibited erythematous and hyperpigmented patches, with sparse blisters and vesicles diffusely on the trunk, bilateral upper extremities and flexor surfaces of the lower extremities. Her trunk displayed areas of mild desquamation.

LABORATORY TESTS:

none

DERMATOHISTOPATHOLOGY:

none

DIFFERENTIAL DIAGNOSIS:

1.   Phytophotodermatitis
2.   contact dermatitis
3.   thermal burn
4.   porphyria cutanea tarda
5.   chemical burn

SCROLL DOWN FOR ANSWER AND DISCUSSION.

CORRECT DIAGNOSIS:

phytophotodermatitis

DISCUSSION:

Phytophotodermatitis, also known as Berloque Dermatitis, is a cutaneous phototoxic eruption as a result of contact with furocoumarin substances and long wave ultraviolet (UVA 320-380 nm) radiation. The cutaneous lesions typically appear approximately 24 hours after exposure, and peaks at 48 to 72 hours. In the acute phase, the affected patches initially range from erythematous macules, patches, plaques, vesicles and or bullae, with tender areas similar to a severe sunburn. In severe cases, systemic symptoms including fever, nausea and vomiting may occur. Post inflammatory hyperpigmentation, characteristically grey-brown in presentation, may ensue following the acute lesions. The hyperpigmentation may however take several weeks to months to completely resolve after cessation of the offending substance.
Bergamont oil is one of the originally described etiologies for this condition, and the oil of Bergamont containing 5-methoxypsoralen found in many commercial products is restricted. However, other psorlens or furocoumarins, such as lemons, limes, figs, parsley and celery also contain psoralens and are well documented to have phototoxic reactions. Other plants associated with phytophotodermatitis include carrots, fennel, dill, buttercup, and mustard. , Limes have a high concentration of psoralens and are often a highly reported culprit of phytophotodermatitis. Additionally, there have been reports of ingestion of psoralen rich foods, such as celery may cause a generalized phototoxicity. The long wave UVA radiation acts on bergapten, a photoactive psoralen component of bergamont oil, resulting in erythema, hyperpigmentation, and in severe cases bullous reactions in the areas exposed. There is documentation that in ancient times, the principles of phototoxic reactions were used as therapy for induction of hyperpigmentation in syndromes such as vitiligo, such as the use of bavachee seeds in India as early as 1400 BC.5
Phytophotodermatitis may clinical present similar to contact dermatitis, chemical burns, and has been mistaken in pediatric patients for child abuse. Other differential diagnosis includes herpes zoster, porphyria cutanea tarda, and thermal burns. Clinical history is important in confirming the diagnosis. The cutaneous findings are commonly unusual, asymmetric patterns in sun-exposed areas with recent exposure to a photosensitizing plant and areas of post-inflammatory hyperpigmentation. As the lesions appear in areas exposed to the citrus fruits in combination with sun exposure, hyperpigmented linear streaks may be one form of clinical presentation. The hands and mouth may be a common involved location as well.
Management in phytophotodermatitis is primarily to stop the offending agent to prevent future recurrences. Further treatment is predominately directed towards symptomatic relief, specifically in diminishing the inflammatory response, which includes cool wet dressings, topical corticosteroids, antipruritic agents, soothing lotions, and potentially systemic corticosteroids if severe or lesions are too extensive.4 Patients must be encouraged to use sunscreen to prevent further or chronic hyperpigmentation.8 Bleaching agents, such as hydroquinone can be used if hyperpigmentation persists and is bothersome to the patient.

TREATMENT:

Our patient was treated with topical corticosteroids and moisturizers, and improved in the subsequent weeks with sun avoidance and sunscreen.

REFERENCES:

Smith E, Kiss F, Porter RM, Anstey AV. A review of UVA-mediated photosensitivity disorders. Photochem Photobiol Sci. Dec 2011; 11(1):199-206.
MacFarlane DF, DeLeo VA. Phtotoxic and photoallergic dermatitis. In: Guin JD, ed. Practical Contact Dermatitis. New York, NY: McGraw-Hill Co; 1995: 83-92.
Pathak MA. Phytophotodermatitis. Clin Dermatol. 1986; 4:102-121.
Gould JW, Mercurio MG, Elmets CA. Cutaneous photosensitivity diseases induced by exogenous agents. J Am Acad Dermatol. 1995; 33:551-73
Lovel CR. Phytophototoxic reactions. In: Lovell CR, ed. Plants and the Skin. Boston: Blackwell Scientifici. 1993;64-95.
Wagner AM, Wu JJ, Hansen RC, et al. Bullous phytophotodermatitis associated with high natural concentrations of furocoumarins in limes. Am J Contact Dermatitis. 2002; 13:10-14.
Lovell CR. Phytodermatitis. Clin Dermatol. 1997;15:607-13.
Marzulli FN, Maibach HI. Perfume phototoxicity. J Soc Cosmet Chem. 1970; 21:695-715.
Solis RR, Dotson DA, Trizna Z. Phytophotodermatitis: a sometimes difficult diagnosis. Arch Fam Med. 2000; 9:1195-1196.
Juckett G. Plant dermatitis. Possible culprits go far beyond poison ivy. Postgrad med. 1996; 100: 159-171.
Weber IC, Davis CP, Greeson DM. Phytophotodermatitis: the other “lime” disease. J Emerg Med. 1999; 17:235-7.

Additional Comment:

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