eMedicine Specialties > Dermatology > Photo-Related Diseases

Phytophotodermatitis

Author: William P Baugh, MD, Assistant Clinical Professor of Dermatology, University of California Irvine School of Medicine and Western School of Medicine; Medical Director, Full Spectrum Dermatology; Consulting Staff, Department of Dermatology, St Jude Medical Center
Coauthor(s): Walter D Kucaba, DO, Private Family Practice, Simpsonville, South Carolina; David Barnette, Jr, MD, Chief of Dermatopathology, Departments of Internal Medicine and Dermatology, Naval Medical Center at San Diego; Cynthia L Chen, BA, Clinical Assistant, Full Spectrum Dermatology
Contributor Information and Disclosures

Updated: Mar 14, 2007

Introduction

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

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.

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