AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Phytophotodermatitis (PPD) is a photosensitive dermal reaction induced by exposure to certain plants with subsequent exposure to sunlight. Both components (plant and light) are required; neither agent alone can cause PPD.

Pathophysiology

PPD can occur through ingestion of the plant or, more commonly, through topical contact. Furocoumarins (psoralens) are the major photoreactive essential plant oils involved in PPD reaction. Plants are thought to produce furocoumarins for disease resistance.

Members of plant families Apiaceae, Rutaceae, Moraceae, Rosaceae, Asteraceae, Brassicaceae, Clusiaceae, Convolvulaceae, Anacardiaceae, Fabaceae, and Ranunculaceae are noted to cause PPD reaction. Common plants implicated in these families include celery, giant hogweed, angelica, parsnip, fennel, dill, anise, parsley, lime, lemon, rue, fig, mustard, scurf pea, and chrysanthemums.

Oil of bergamot, extracted from the rind of fresh bergamot oranges (Citrus bergamia), is commonly used to scent commercial perfumes and colognes. Perfume-induced berloque dermatitis is a specific form of PPD reaction; areas of skin reaction correspond to areas exposed to perfume.

Exposure to certain wavelengths of ultraviolet A (UV-A) light enables furocoumarin to absorb the energy, thereby altering reactivity of the molecule and causing the molecule to attain a high-energy state. The activated molecules form photoaddition products with DNA pyrimidine bases and result in epidermal cell nucleic acid damage (type I reaction). Activated furocoumarins can also produce oxygen, superoxide, and hydroxy radicals, which cause cellular membrane damage (type II reaction).

Both mechanisms result in cellular dysfunction and tissue destruction. When acute, the process is phototoxic. Chronic presentation of PPD involves a photoallergic response; light-activated plant products act as haptens and produce a cell-mediated hypersensitivity response. Psoralens may not be primarily involved in this mechanism of injury.

Phytophototoxicity is amplified by humidity and perspiration.

The phototoxic inflammatory eruption usually appears 24 hours after exposure and peaks within 48-72 hours. Initial burning erythema is followed by blistering.

Frequency

United States

Incidence varies per population and exposure. Individuals who handle produce or receive significant sunlight exposure (eg, field workers, farmers, gardeners, grocery workers, bartenders, vegetarians, persons who use tanning salons) are at an increased risk. Cases of PPD more commonly occur in late spring and summer when furocoumarins are found in increased concentration in plants and when individuals experience increased UV exposure.

International

No difference exists between US and international occurrence.

Mortality/Morbidity

Significant long-term skin changes (hyperpigmentation, scarring) can occur with chronic exposure.

Race

No racial predisposition is demonstrated. Fair-skinned individuals are more frequently reported.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

PPD often occurs in linear and odd patterns, including "handprints."

• A phototoxic reaction can result from contact with a specific plant via skin exposure, or less commonly, ingestion, followed by exposure to sunlight.
• Symptoms usually occur within 24-48 hours following sunlight exposure.
• Symptoms are frequently described as an initial burning pain and erythema, followed by blistering. Blistering may occur within 10 minutes.
• Pruritus is uncommon, distinguishing PPD from allergic phytodermatitis (eg, toxicodendron dermatitis).

Physical

• A usually sharp demarcation between normal covered and abnormal exposed skin
• Initial nonpruritic erythema of exposed areas
• Development of edema, leading to vesicles and/or bullae
• Possible desquamation
• Resultant dense hyperpigmentation from melanocytic response

Causes

PPD is induced by exposure to certain plants with subsequent exposure to sunlight. PPD can occur through ingestion of the plant or, more commonly, through topical contact.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Actinic prurigo
Allergic contact dermatitis to airborne substances
Hydroa aestivalis and vacciniforme
Chronic actinic dermatitis
Porphyria cutanea tarda
Protoporphyria
Polymorphous light eruption
Solar urticaria

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• PPD is a clinical diagnosis. No serum level for psoralens is available or appropriate. Clinical presentation is delayed and systemic clearance of psoralens is complete.

Other Tests

• With yeast inhibition technique, plant extract is used to evaluate for presence of psoralens.
• In individuals in whom the diagnosis is in question, referral to a dermatologist for photo-patch testing may be warranted. Testing should include sunscreens, pesticides, and plant allergens.

Procedures

• In individuals in whom the diagnosis is in question, referral to a dermatologist for a skin biopsy may be warranted. A skin biopsy may demonstrate epidermal hyperkeratosis, "sunburn cells," and an inflammatory cell infiltrate. An increase in melanocytes is seen.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Emergency Department Care

• Limit or avoid contact with the specific plant.
• Avoid sun exposure.
• In most cases, history identifies plant exposure.
• Treat inflammatory condition based on severity of symptoms.
• • Treat mild reactions with cool wet dressings, topical steroids, and nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Severe reactions may require systemic steroids.
  • Topical application of 4% hydroquinone cream once or twice daily for several weeks may lessen hyperpigmentation. This is best done in conjunction with a dermatologist.

Consultations

Consultation with a dermatologist may be helpful.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Depigmenting agents

These agents have been shown to be useful in the treatment of phytophototoxins plant poisoning.

Drug Category: Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Drug Name	Prednisone (Deltasone, Meticorten, Orasone)
Description	Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocyte and antibody production.
Adult Dose	0.5-2 mg/kg/d PO; taper as condition improves; single morning dose is safer for long-term use, but divided doses have more anti-inflammatory effect
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; viral, fungal, connective tissue, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration
Interactions	Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Drug Category: Nonsteroidal anti-inflammatory agents

Although most NSAIDs are used primarily for their anti-inflammatory effects, they are effective analgesics and are useful for the relief of mild to moderate pain.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• In general, a phototoxic exposure is self-limited and subsides within a week if further insult is avoided.
• If symptoms persist or worsen instead of improving, other illnesses, such as the primary light disorders, should be considered and further evaluation is warranted by a dermatologist.

Deterrence/Prevention

• Limit or avoid contact with the specific plant.
• Limit sun exposure.

Complications

• Long-term exposure and severe reactions may result in hyperpigmentation requiring continued topical steroid treatment.

Prognosis

• Significant long-term skin changes (hyperpigmentation, scarring) can occur with chronic exposure.

Patient Education

• Patients should be educated regarding plants that produce phytophototoxicity in order to avoid skin exposure. Patients may be counseled to wear gloves and skin coverings when their work necessitates ongoing exposure to these plant oils and to the sun.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to recognize systemic photosensitization caused by exposure to plant furocoumarins and the use of common drugs (eg, tetracycline, minocycline, doxycycline, chlorpromazine, chlorothiazide diuretics, sulfonamides, nalidixic acid, griseofulvin, sulfonylureas)
• Once possibility of an exogenous light photosensitizer has been ruled out, failure to consider primary light disorders such as porphyria and collagen vascular disorders with polymorphous light eruption

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Bansal I, Kerr H, Janiga JJ, Qureshi HS, Chaffins M, Lim HW. Pinpoint papular variant of polymorphous light eruption: clinical and pathological correlation. J Eur Acad Dermatol Venereol. Apr 2006;20(4):406-10. [Medline].
• Berkley SF, Hightower AW, Beier RC, et al. Dermatitis in grocery workers associated with high natural concentrations of furanocoumarins in celery. Ann Intern Med. Sep 1986;105(3):351-5. [Medline].
• Epstein WL, Epstein JH. Plant induced dermatitis. In: Wilderness Medicine. 3^rd ed. 1995:843-61.
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• Sasseville D. Phytodermatitis. J Cutan Med Surg. Jul 1999;3(5):263-79. [Medline].
• Sharma A, Goel HC. Some naturally occurring phytophototoxins for mosquito control. Indian J Exp Biol. Oct 1994;32(10):745-51. [Medline].
• Tunget CL, Turchen SG, Manoguerra AS, et al. Sunlight and the plant: a toxic combination: severe phytophotodermatitis from Cneoridium dumosum. Cutis. Dec 1994;54(6):400-2. [Medline].
• White W. Club Med dermatitis. N Engl J Med. Jan 30 1986;314(5):319-20. [Medline].
• Wolf R, Oumeish OY. Photodermatoses. Clin Dermatol. Jan-Feb 1998;16(1):41-57. [Medline].
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Article Last Updated: Feb 29, 2008