AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

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

INTRODUCTION

Section 2 of 10  

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

Background

Phytophotodermatitis (PPD) is a cutaneous phototoxic inflammatory eruption resulting from contact with light-sensitizing botanical substances and long-wave ultraviolet (UV-A 320-380 nm) radiation. The eruption usually begins approximately 24 hours after exposure and peaks at 48-72 hours.

PPD typically manifests as a burning erythema that may subsequently blister. Postinflammatory hyperpigmentation lasting weeks to months may ensue. In some patients, the preceding inflammatory reaction may be mild and go unrecognized by the patient. In this case, the patient presents with only pigmentary changes.

Pathophysiology

Cutaneous inflammation produced by plants can be separated into 4 groups based on their specific mechanism of action: urticarial dermatitis, irritant contact dermatitis, allergic contact dermatitis, and phototoxic dermatitis.

PPD is a phototoxic reaction entirely independent of the immune system; that is, PPD can occur in any individual, and prior sensitization or an intact immune system is not required. The ingredients needed to produce PPD include temporal exposure to both a photosensitizing substance, such as psoralens, and ultraviolet radiation. Furocoumarins are photosensitizing chemical components produced by certain plants and consist of psoralens, 5-methoxypsoralens, 8-methoxypsoralens, angelicin, bergaptol, and xanthotal.

The natural sunlight emission spectrum reaching the earth ranges from approximately 270-5000 nm. This electromagnetic radiation consists of photons with a reciprocal relationship between the wavelength and the energy of the photons. Only light that is absorbed into the skin can cause a photochemical reaction. Within the light spectra, UV-A (320-380 nm) is responsible for the vast majority of photoreactions resulting in PPD.

The wavelengths of ultraviolet light that most efficiently produce PPD lie within the UV-A range and have peak activity at 335 nm. When a photon with the appropriate wavelength strikes a furocoumarin, the energy is absorbed, raising this chemical to a triple excited state from the ground state. Upon return to the ground state, energy is released in the form of heat, fluorescence, and/or phosphorescence, and a photoproduct may form.

Two distinct photochemical reactions have been described in PPD, which occur independently from each other. A type I reaction occurs in the absence of oxygen, whereas a type II reaction occurs in the presence of oxygen. These photochemical reactions damage cell membranes and DNA and result in DNA interstrand cross-linking between the psoralen furan ring and the thymines or the cytosines of DNA. This results in activation of arachidonic acid metabolic pathways and in cell death (sunburn cells and apoptotic keratinocytes). Clinically, erythema, blistering, epidermal necrosis, and eventual epidermal desquamation occur.

A postinflammatory pigment alteration may follow the acute phase of this phototoxic reaction. This alteration occurs primarily by 2 mechanisms. First, melanin, which is normally found in the epidermis, "falls" into the dermis and is ingested by melanophages. Secondly, an increased number of functional melanocytes and melanosomes are distributed in the epidermis following PPD and also account for the hyperpigmentation. This hyperpigmentation may serve as a protective mechanism against further UV injury. Clinically, this corresponds with irregular hyperpigmentation (or occasionally hypopigmentation resulting in dyschromia) seen as the end stage of the phototoxic reaction.

Frequency

United States

The frequency of PPD in the general population has not been well established.

International

The overall incidence of PPD is unknown, but it undoubtedly varies according to the population studied and is based on the risk of exposure to psoralen compounds. Because furocoumarins are found in a wide range of wild and domestic plants, a variety of patient groups may become exposed.

Mortality/Morbidity

Most commonly, PPD is a localized cutaneous phenomenon resulting initially in a burning sensation, which may be followed acutely by erythema and blistering. Eventually, the affected sites may desquamate and develop permanent hyperpigmentation or hypopigmentation. However, scarring is rare.

Race

Any race may be affected, but PPD is most easily recognized in fair-skinned patients.

Sex

Both sexes may be affected.

Age

Any age may be affected, but note that PPD occurring on a child may be mistaken for child abuse. Classic examples include a handprint pattern on a child after exposure to a parent cooking with lime juice or a linear drip pattern on a child's hands and arms after eating real juice ice pops.

CLINICAL

Section 3 of 10  

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

History

The history is essential in making the correct diagnosis of PPD. The clinician must be aware that this entity exists and inquire about contact with fruits or plants. This is particularly true if the patient complains of a painful or burning sensation rather than pruritus (which is commonly associated with allergic contact dermatitis). The patient's hobbies, recreational activities, and/or occupation may give essential clues to the most likely culprits.

• PPD most commonly occurs in the spring and the summer when furocoumarins are at their highest concentration in plants and when UV exposure is greatest for patients. For instance, children playing outdoors may come in contact with meadow grass of the Umbelliferae family.
• Agricultural workers may develop PPD when picking parsley (Cymopteris watsonii), parsnips (Pastinaca sativa), celery (Apium graveolens), and/or carrots (Daucus carota). The resulting photocutaneous reaction in this group has been called harvester's dermatitis and is primarily due to exposure to Umbellifers. Another report describes an outbreak of "strimmer rash" in several grounds operatives who had all undertaken grass-cutting duties. The affecting agent was likely giant hogweed, also from the Umbellifers.
• Cneoridium dumosum is a plant found along the southwestern coastal United States to which hikers may be exposed, resulting in PPD. Patients are often attracted to this plant by its scented white flower and red berries.
• Bartenders and grocers classically develop PPD due to exposure to limes and celery, respectively.
• Several reports describe patients creating fig leaf decoctions to use as "tanning lotions" or "suntan promoters." Fig leaves (Ficus carica or Ficus benjamina) are either ground up, boiled, or mixed with oil and then applied on the skin. Patients reported having found these decoction recipes from magazines and/or friends.
• One report describes a patient rubbing the juice of medicinal limes (Citrus hystrix) onto the skin as a treatment for insect bites and as an insect repellent, which subsequently resulted in PPD.
• Another report describes a patient rubbing the juice of medicinal lime (C hystrix) onto the scalp hair to dye his hair. The juice trickled in between his fingers onto the back of his hands and down the arms to the elbows, where the patient developed PPD.
• One case of iatrogenic phytophotodermatitis resulted from ingestion of an herbal remedy prescribed for chronic hand dermatitis. Plant fragments contained in the herbal mix included extracts from Compositae, a member of the daisy family. No reports describe phytophotodermatitis after contact with members of the Compositae family. However, the action of boiling the plant mix may have possibly released high concentrations of intracellular furocoumarins.

Physical

The primary skin lesion of PPD may range from delayed erythema (24-48 h) to frank blisters. The skin lesions are limited to the areas in contact with furocoumarin and with sunlight exposure. The primary lesion is often not seen by the physician because of the transient nature of the reaction. Rather, the patient presents with late skin changes that become apparent after 72 hours.

• Late skin lesions
• • Bizarre inflammatory patterns and linear streaks of hyperpigmentation are key clues to diagnosing PPD. These patterns often result from brushing against a plant's stems or leaves while outdoors or from the liquid spread of lime juice over the hand or down the forearm. A handprint pattern from lime juice contact is not uncommon.
  • Furthermore, a buckshot spray over exposed surfaces is commonly seen in association with the use of string trimmers (weed-whackers) when unwanted weeds possessing furocoumarins are cleared from a field or a yard.
• Skin - distribution: PPD is most commonly found on skin sites exposed to plants and sunlight; these include such areas as the arms and the legs, but it may occur anywhere.
• Skin - color: Skin color varies depending on the patient's underlying skin tone and the degree of the reaction. However, as previously stated, the acute phase of PPD manifests as erythema, and the end stage manifests as postinflammatory hyperpigmentation.

Causes

The most common plant family to cause PPD is the Umbelliferae family.

PPD is most commonly caused by ingestion of or topical exposure to psoralens (furocoumarins). Psoralens have been isolated from at least 4 different plant families: Umbelliferae, Rutaceae, Moraceae, and Leguminosae.

DIFFERENTIALS

Section 4 of 10  

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

Other Problems to be Considered

Child abuse
Cutaneous larva migrans
Factitious dermatitis
Folk medicine
Marine envenomations
Phototoxic eruption
Phototoxic drug reaction
Straw mite or grocer's mite dermatitis
Superficial lymphangitis
Sunburn

WORKUP

Section 5 of 10  

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

Lab Studies

• PPD is a clinical diagnosis. All laboratory data obtained are used to support the diagnosis and to exclude other diseases in the differential diagnosis.
• Serum psoralen levels may be checked if unknown ingestion of psoralens is suspected.
• Porphyrin levels may be obtained to rule out porphyria cutanea tarda.
• If the clinical picture does not clearly distinguish between photoallergic and phototoxic dermatitis, performing a photopatch test may be prudent. The photopatch test should include testing for sunscreens because they may be a cause of allergic contact dermatitis associated with sun exposure.

Procedures

• A skin biopsy may be performed to determine the clinical diagnosis if it remains in question and to help distinguish between allergic contact, photoallergic, and photodrug reactions.

Histologic Findings

Classic histopathologic features of PPD include the following:

Epidermal hyperkeratosis, with or without parakeratosis, is observed. Scattered necrotic keratinocytes (apoptotic cells) are found in the epidermis. Sunburn cells (cells with pyknotic nuclei, increased volume, and pale staining cytoplasm) are also found in the epidermis. Slight spongiosis is observed in the epidermis. Minimal inflammatory cell infiltrate consisting of neutrophils (predominant cell type early on), lymphocytes (less common), and macrophages and melanophages (late) is present. Subepidermal blistering and extravasation of erythrocytes may or may not be present. Pigment incontinence with melanophages is observed in the papillary dermis. The dermis shows some edema and enlargement of vascular endothelial cells.

TREATMENT

Section 6 of 10  

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

Medical Care

• Patient reassurance is essential once the diagnosis is made. PPD is a self-limited problem that resolves with removal of the offending agent.
• Patients should avoid the offending agent (furocoumarin).
• Cool wet compresses may be used for acute lesions.
• Topical steroids may be used if the eruption is severe and edematous.
• Indomethacin (50-75 mg PO qd) may be used for adults.

Consultations

Referral to a dermatologist may be useful.

Activity

Use of UV-A sunscreens may help prevent further phototoxic reactions from occurring when exposed to sunlight.

MEDICATION

Section 7 of 10  

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

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

Drug Category: Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. Low-to-high potency topical steroids may be applied to affected areas to reduce local inflammation induced by the photoactivated psoralens. They may help to relieve the burning sensation associated with PPD as well as to reduce the associated postinflammatory hyperpigmentation.

Drug Name	Clobetasol (Temovate)
Description	Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.
Adult Dose	Apply bid for up to 2 wk; not to exceed 50 g/wk
Pediatric Dose	Not established; use with caution
Contraindications	Documented hypersensitivity; viral or fungal skin infections
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	May suppress adrenal function in prolonged therapy; not recommended for face or intertriginous areas; can cause atrophy of groin, face, and axillae; if infection develops and is not responsive to antibiotic treatment, discontinue until infection under control

Drug Name	Betamethasone (Diprolene, Betatrex)
Description	For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Adult Dose	Apply thin film bid/qid until response
Pediatric Dose	Not established; use with caution
Contraindications	Documented hypersensitivity; paronychia; cellulitis; impetigo; angular cheilitis; erythrasma; erysipelas; rosacea; perioral dermatitis; acne
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Can cause atrophy of groin, face, and axillae; if infection develops and is not responsive to antibiotic treatment, discontinue until infection under control

Drug Category: Nonsteroidal anti-inflammatory drugs

These agents are most commonly used for relief of mild to moderate pain. Indomethacin is an analgesic and NSAID medication that may offer some protection against acute UV-A–induced epidermal apoptosis as well as provide some relief of skin discomfort.

FOLLOW-UP

Section 8 of 10  

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

Deterrence/Prevention

• Regular use of UV-A–blocking sunscreens may help to diminish the cutaneous effects of PPD if contact with plant psoralens occurs.
• Patients should avoid the offending agent.

Prognosis

• The prognosis is good with identification and avoidance of the offending agent.

Patient Education

• Reassure the patient that PPD is a self-limited problem that resolves with removal of the offending agent.

MULTIMEDIA

Section 9 of 10  

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

Media file 1:  A 37-year-old white woman presented to the clinic complaining of a rash on the medial part of her right thigh and left arm that was acquired after clearing some weeds in her yard. A phototoxic combination of sunlight and a psoralen-containing plant produced this bizarre linear vesicular eruption.
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Media file 2:  Closer clinical view of bizarre angulated vesicular streaks, which occurred after contact with a plant and ultraviolet light exposure (same patient as in Media File 1).
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Media file 3:  A 26-year-old female airline flight attendant exposed to lime while serving drinks en route to the Caribbean. During the Caribbean layover, she had significant sun exposure. The combination of lime juice and sun exposure led to a drip-pattern blister formation on the dorsal forearm consistent with phytophotodermatitis. This picture clearly delineates the potential severity of phytophotodermatitis with extensive blister formation.
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Media type:  Photo

Media file 4:  The 2-month follow-up picture of patient in Image 3 demonstrates the potential postinflammatory pigmentation changes and scarring that may occur with severe blistering of phytophotodermatitis.
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Media file 5:  Close-up view of vesicular linear streaks with morphology suggestive of scattered foci of epidermal necrosis.
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Media file 6:  Queen Anne's lace, a member of the Umbelliferae family of plants, is well known to produce a furocoumarin-induced phototoxic eruption.
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Media file 7:  Ficus. The common fig contains furocoumarins and should be considered amidst the list of potential offending agents that cause phytophotodermatitis.
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Media type:  Photo

REFERENCES

Section 10 of 10

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

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Article Last Updated: Mar 14, 2007