Phytophotodermatitis (PPD) is a cutaneous phototoxic inflammatory eruption resulting from contact with light-sensitizing botanical substances and long-wave ultraviolet A (UV-A, 320-380 nm) radiation. Certain types of chemical compounds called furocoumarins, which are present in some plants, parsley, celery, carrots, and limes, react using their parent compound, psoralen, with the UV radiation, which forms the eruptions on the skin.  The eruption usually begins approximately 24 hours after exposure and peaks at 48-72 hours.  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.
See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and poisonings.
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. In other words, 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.
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.
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.
Any race may be affected, but phytophotodermatitis is most easily recognized in fair-skinned patients.
Both sexes may be affected.
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.
The prognosis is good with identification and avoidance of the offending agent. 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.
Reassure the patient that phytophotodermatitis is a self-limited problem that resolves with removal of the offending agent.
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