Phytophotodermatitis is phototoxic inflammatory eruption of the skin which results from contact with light-sensitizing botanical [from plants] agent, followed by exposure to ultraviolet light [from the sun or otherwise].
Some plants contain chemicals which can sensitize the skin to sunlight. If an individual comes in contact with such a plant and simultaneously gets exposed to sunlight, he/she is likely to develop hyperpigmentation in the areas exposed to the plant and the sunlight.
The name phyto-photo-dermatitis indicates
- phyto- plant
- photo- sunlight
- dermatitis- inflammation of the skin
As phytophotodermatitis is not an immunologic response, the condition can occur without any previous exposure to the photosensitizing agent
It is less common than other types of contact dermatitis.
The symptoms of phytophotodermatitis go away on its own over time.
The light-sensitizing botanical substances are also called furanocoumarins. These contain psoralens and other active particles.
Furanocoumarins are found in plants like parsley, celery, carrots, and limes etc.
The overall incidence of phytophotodermatitis is unknown. It may affect any race but is more readily recognized in fair-skinned patients. There is no sex predilection.
Most of these cases resolve on their own over a period of a few weeks.
Other names for phytophotodermatitis are Berloque dermatitis or margarita photodermatitis
Pathophysiology of Phytophotodermatitis
Phytophotodermatitis is a phototoxic reaction that can occur in any individual, even those without prior exposure as the immune system is not involved.
All it needs is an 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 and other substances.
Ultrviolet A (wavelength: 320-400 nm) is responsible for most of the photoreactions. When a photon with the appropriate wavelength strikes a furocoumarin, the furocoumarin absorbs the energy changes to a triple excited state from the ground state followed by a return to the ground state and release of energy in the form of heat, fluorescence, and/or phosphorescence.
These photochemical reactions damage cell membranes and DNA, and result in cell death.
Clinically, it is manifested by erythema, blistering, epidermal necrosis, and epidermal desquamation.
Pigmentation after inflammation is thought to occur by following mechanisms.
- Melanin falls into the dermis and is ingested by melanophages.
- Increased number of functional melanocytes and melanosomes in the epidermis
This hyperpigmentation is thought to serve as may serve as a protective mechanism against further ultraviolet injury.
Berloque dermatitis is a subtype which is caused by certain substances found in perfume and the symptoms appear at the site of perfume applications.
Berloque dermatitis is caused by a substance called bergapten contained in plants used in perfumes.
Phytophotodermatitis is most commonly caused by topical exposure to psoralens (furanocoumarins) or their ingestion. Four different plant families, namely Umbelliferae, Rutaceae, Moraceae, and Leguminosae are known to produce furanocoumarins.
Common plants in these family are
- Queen Anne’s lace [Wild carrot]
- Bishop’s weed
- Bergamot lime
- Gas plant
- Scurf pea
Phytophotodermatitis most commonly occurs in the spring and the summer [furocoumarins are at their highest concentration in plants and UV exposure is greatest.
Few instances where the exposure could occur are
- Kids playing outdoors come in contact with meadow grass [Umbelliferae family].
- Agricultural workers when picking parsley, parsnips, celery and/or carrots (Daucus carota). Also known as Harvester’s dermatitis and is primarily due to exposure to Umbellifers.
- Grass cutting, usually Giant Hogweed [called Strimmer rash]
- Hikers in southwestern coastal united states getting exposed to Cneoridium dumosumis
- Bartenders and grocers due to exposure to limes and celery, respectively.
- Fig leaf preparations application on skin
- Lime application on skin
The patient often presents with burning erythematous rash that subsequently blisters. The lesions are primarily located on the areas not covered by clothes and there is a history of exposure.
The shapes and the sizes of these macules will depend upon the causative agent.
If the patient is exposed directly to the leaves of the plant as during lying down on grassy plots along the swimming pools or sea-beaches, the pattern of pigmentation may resemble the shapes of the leaves of that plant.
If the exposure is to the perfumes, the lesions may occur as minute punctuate spots if the perfume was used as a spray, or as irregular smudges if the perfume is applied with the hand or cotton balls. Linear streaks with a drop like appearance may be produced if the perfume flows down from the area of application (Berloque dermatitis).
In case the cause is a perfume present in a cosmetic, the pattern of the lesions will correspond to the areas where the cosmetic is applied.
In case a hair oil is responsible, the pigmentation is more around the forehead, ears, sides of the face and the upper central part of the back not covered by the blouse.
Phytophotodermatitis typically manifests as a burning erythema that may subsequently blister. The rash is non-pruritic and in case of itching being present, other diagnoses should be considered.
Postinflammatory hyperpigmentation lasting weeks to months may follow.
Sometimes the initial rash is mild and may be unrecognized In such cases, the patient presents with delayed hyperpigmentation.
On examination, skin lesions are seen 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
Bizarre inflammatory patterns and linear streaks of hyperpigmentation are important clues for diagnosing phytophotodermatitis.
- Allergic Contact Dermatitis
- Drug-Induced Bullous Disorders
- Irritant Contact Dermatitis
- Porphyria Cutanea Tarda
Phytophotodermatitis is mainly diagnosed clinically. Lab studies may be used to support the diagnosis or exclude other diseases in the differential diagnosis.
- Serum psoralen levels – When there is known ingestion of psoralens
- Porphyrin levels- To rule out porphyria cutanea tarda.
- Photopatch test – To distinguish between photoallergic and phototoxic dermatitis
- Skin biopsy – to determine the clinical diagnosis
- Epidermal hyperkeratosis, with or without parakeratosis
- Scattered necrotic keratinocytes (apoptotic cells) are found in the epidermis
- Sunburn cells in epidermis
- Pyknotic nuclei
- Increased volume
- Pale staining cytoplasm
- Slight spongiosis in the epidermis
- Minimal inflammatory cell infiltrate
It is important to find out the causative agent and advise the patient to prevent further exposures to the same as well as other similar agents. In case there is no clue to the causative agent, further exposures to all kinds of plants/perfumes must be stopped and the skin protected from sunlight. These measures should be able to prevent the appearance of new lesions.
The old lesions tend to disappear by themselves in due course, but the time taken for this depends upon the intensity of hyperpigmentation and may take several months.
Cool wet compresses may help acute lesions. Topical steroids like hydrocortisone valerate 0.2% cream, clobetasol ointment, topical betamethasone may be used if the eruption is severe and edematous.
An anti-inflammatory drug like Indomethacin 50-75 mg orally may be used in adult patients to control inflammation and pain.
Very severe exposure resulting > 30% of the surface area of the body should be treated in a burn unit for local wound care.
Regular use of UV-A–blocking sunscreens may help to diminish the cutaneous effects of phytophotodermatitis if contact with plant psoralens occurs.
Patients should avoid the offending agent.
The prognosis is good when the offending agent is identified and the offending agent is avoided in future.
The patient may develop permanent hyperpigmentation or hypopigmentation after an acute episode.
scarring is rare.
- Marcos LA, Kahler R. Phytophotodermatitis. Int J Infect Dis. 2015 Sep. 38:7-8.
- Raam R, DeClerck B, Jhun P, Herbert M. Phytophotodermatitis: The Other “Lime” Disease. Ann Emerg Med. 2016 Apr. 67 (4):554-6
- Tunget CL, Turchen SG, Manoguerra AS, Clark RF, Pudoff DE. Sunlight and the plant: a toxic combination: severe phytophotodermatitis from Cneoridium dumosum. Cutis. 1994 Dec. 54(6):400-2.