Phytophotodermatitis

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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.[1] The phototoxic result may be intensified by wet skin, sweating, and heat.

Phytophotodermatitis typically manifests as a burning erythema that may subsequently blister. Postinflammatory hyperpigmentation lasting weeks to months may ensue (see the images below). 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.


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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 si....


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The 2-month follow-up picture of a patient with a drip-pattern blister formation on the dorsal forearm demonstrates the potential postinflammatory pig....

See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and poisonings.

Also see Berloque Dermatitis and Drug-Induced Photosensitivity.

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.

Phytophotodermatitis is a phototoxic reaction entirely independent of the immune system; that is, phytophotodermatitis can occur in any individual, and prior sensitization or an intact immune system is not required. The ingredients needed to produce phytophotodermatitis 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 (320-400 nm) is responsible for the vast majority of photoreactions resulting in phytophotodermatitis.

The wavelengths of ultraviolet light that most efficiently produce phytophotodermatitis 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 phytophotodermatitis, 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. During the type I oxygen-independent reaction, the RNA and nuclear DNA become fastened to the exposed ultraviolet-activated furocoumarins. Likewise, the oxygen-dependent reactions result in cell membrane damage and edema from activated furocoumarins. 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. See the image below.


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Close-up view of vesicular linear streaks with morphology suggestive of scattered foci of epidermal necrosis.

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 phytophotodermatitis 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.

Epidemiology

Frequency

United States

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

International

The overall incidence of phytophotodermatitis 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. An example of an international greenery known to produce phytophotodermatitis is Ficus carica, also known as a fig tree. This plant is often sought for the fruit it produces, as well as for analgesic folk medicine applications. Ficus pumila can be found worldwide, yet is native to China, Japan, and Taiwan.

Mortality/Morbidity

Most commonly, phytophotodermatitis 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 phytophotodermatitis is most easily recognized in fair-skinned patients.

Sex

Both sexes may be affected.

Age

Any age may be affected, but note that phytophotodermatitis 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.

History

The history is essential in making the correct diagnosis of phytophotodermatitis. 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.

Phytophotodermatitis 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 phytophotodermatitis 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 phytophotodermatitis. Patients are often attracted to this plant by its scented white flower and red berries.

Bartenders and grocers classically develop phytophotodermatitis due to exposure to limes and celery, respectively.[2, 3]

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.[4, 5] 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 phytophotodermatitis.

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 phytophotodermatitis.

One case of iatrogenic phytophotodermatitis resulted from ingestion of an herbal remedy prescribed for chronic hand dermatitis.[6] 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.

One study assessed the potential of a small amount of psoralen in a normal diet to provoke phototoxicity in volunteers with skin types I and II. The study concluded that threshold erythema and phytophotodermatitis was unaffected by ingestion of this normal dietary amount of fresh parsnips.[7]

Another study reports on a 30-year-old man who trimmed the stems of a F pumila shrub while exposing his forearms, antecubital fossae, neck, and forehead. Within the following 3 days, the patient noticed eruptions appearing on the exposed areas. Six weeks following, the patient experienced confettilike hypomelanosis over the prior-unprotected areas of the skin. He was treated with clobetasol propionate cream.

Physical

The primary skin lesion of phytophotodermatitis 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.

Causes

The most common plant family to cause phytophotodermatitis is the Umbelliferae family. See the images below.


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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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Ficus. The common fig contains furocoumarins and should be considered amidst the list of potential offending agents that cause phytophotodermatitis.

Phytophotodermatitis 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,[8] Rutaceae,[9] Moraceae, and Leguminosae.

Table. Common Causes of Phytophotodermatitis


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See Table

Chart modified from Plants and the Skin. 1993:70-71.[11]

Laboratory Studies

Procedures

Histologic Findings

Classic histopathologic features of phytophotodermatitis 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.

Both light microscopy and transmission electron microscopy in animal models show keratinocyte necrosis and vacuolization within 24 hours. Within 72 hours, intraepidermal and subepidermal blistering is visible.[19, 20]

Medical Care

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 Summary

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

Hydrocortisone valerate 0.2% cream (Westcort)

Clinical Context:  Treats inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Clobetasol (Temovate)

Clinical Context:  Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Betamethasone topical (Diprolene, Betatrex)

Clinical Context:  For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Class Summary

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 phytophotodermatitis as well as to reduce the associated postinflammatory hyperpigmentation.

Indomethacin (Indocin)

Clinical Context:  Has anti-inflammatory properties due to inhibition of prostaglandin synthesis and/or leukocyte migration into inflamed areas. Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation.

Class Summary

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.

Deterrence/Prevention

Prognosis

Author

William P Baugh, MD, Assistant Clinical Professor of Dermatology, Western University of Health Sciences; Medical Director, Full Spectrum Dermatology; Consulting Staff, Department of Dermatology, St Jude Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia L Chen DO, Intern, Pacific Hospital of Long Beach, California

Disclosure: Nothing to disclose.

David Barnette Jr, MD, Voluntary Associate Clinical Professor, University of California San Diego School of Medicine

Disclosure: Nothing to disclose.

Walter D Kucaba, DO, Private Family Practice, Simpsonville, South Carolina

Disclosure: Nothing to disclose.

Specialty Editors

Craig A Elmets, MD, Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Disclosure: Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; UpToDate Salary Employment

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD, Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

References

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  2. 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. [View Abstract]
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  10. Izumi AK, Dawson KL. Zabon phytophotodermatitis: first case reports due to Citrus maxima. J Am Acad Dermatol. May 2002;46(5 Suppl):S146-7. [View Abstract]
  11. Lovell CR. Plants and the Skin. London, England: Blackwell Science; 1993:64-95.
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  15. Koh D, Ong CN. Phytophotodermatitis due to the application of citrus hystrix as a folk remedy. Br J Dermatol. Apr 1999;140(4):737-8. [View Abstract]
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  19. Almeida HL Jr, Sotto MN, Castro LA, Rocha NM. Transmission electron microscopy of the preclinical phase of experimental phytophotodermatitis. Clinics (Sao Paulo). Jun 2008;63(3):371-4. [View Abstract]
  20. Jorge VM, de Almeida HL Jr, Amado M. Serial light microscopy of experimental phytophotodermatitis in animal model. J Cutan Pathol. Mar 2009;36(3):338-41. [View Abstract]
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  32. Wang L, Sterling B, Don P. Berloque dermatitis induced by "Florida water". Cutis. Jul 2002;70(1):29-30. [View Abstract]
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  34. Young AR, Magnus IA. An action spectrum for 8-MOP induced sunburn cells in mammalian epidermis. Br J Dermatol. May 1981;104(5):541-8. [View Abstract]
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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.

The 2-month follow-up picture of a patient with a drip-pattern blister formation on the dorsal forearm demonstrates the potential postinflammatory pigmentation changes and scarring that may occur with severe blistering of phytophotodermatitis.

Close-up view of vesicular linear streaks with morphology suggestive of scattered foci of epidermal necrosis.

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.

Closer clinical view of bizarre angulated vesicular streaks, which occurred after contact with a plant and ultraviolet light exposure.

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.

The 2-month follow-up picture of a patient with a drip-pattern blister formation on the dorsal forearm demonstrates the potential postinflammatory pigmentation changes and scarring that may occur with severe blistering of phytophotodermatitis.

Queen Anne's lace, a member of the Umbelliferae family of plants, is well known to produce a furocoumarin-induced phototoxic eruption.

Ficus. The common fig contains furocoumarins and should be considered amidst the list of potential offending agents that cause phytophotodermatitis.

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.

Closer clinical view of bizarre angulated vesicular streaks, which occurred after contact with a plant and ultraviolet light exposure.

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.

The 2-month follow-up picture of a patient with a drip-pattern blister formation on the dorsal forearm demonstrates the potential postinflammatory pigmentation changes and scarring that may occur with severe blistering of phytophotodermatitis.

Close-up view of vesicular linear streaks with morphology suggestive of scattered foci of epidermal necrosis.

Queen Anne's lace, a member of the Umbelliferae family of plants, is well known to produce a furocoumarin-induced phototoxic eruption.

Ficus. The common fig contains furocoumarins and should be considered amidst the list of potential offending agents that cause phytophotodermatitis.

FamilyGenusSpeciesCommon NamesMain Compounds
UmbelliferaeAmnimajusQueen Anne's lace, Bishop's weed8-methoxypsoralen (8-MOP), 5-methoxypsoralen (5-MOP), imperatorin
HeracleumsphondyliumCow parsnip8-MOP, 5-MOP, imperatorin, phellopterin
HeracleummantegazzianumGiant hogweed, Cartwheel flower8-MOP, 5-MOP, imperatorin, phellopterin
PastinacasativaParsnip8-MOP, 5-MOP, imperatorin, isopimpinellin
ApiumgraveolensCeleryPsoralens, 8-MOP, 5-MOP
RutaceaeCitrusbergamiaBergamot lime5-MOP
CitrusmaximaZabon[10] 5-MOP
DictamnusalbusGas plant, “Burning bush of Moses”8-MOP, 5-MOP
MoraceaFicuscaricaFigPsoralens, 5-MOP
LeguminosaePsoraleacorylifoliaBavchi, Scurf peaPsoralens