Phytophotodermatitis

Phytophotodermatitis
Phytophotodermatitis caused by lime
Specialty	Dermatology

Phytophotodermatitis, also known as Berloque dermatitis^[1][2] or margarita photodermatitis,^[3][4] is a skin condition caused by a chemical reaction that leaves skin hypersensitive to ultraviolet light. It is frequently mistaken for hereditary conditions such as atopic dermatitis or chemical burns, but in fact, phytophotodermatitis results from contact with certain photosensitizing compounds called furanocoumarins (specifically, psoralen and its derivatives) found naturally in numerous plants, especially in the family Apiaceae.^[5][6] These compounds are also found in the citrus fruits of the Rutaceae family, especially limes,^[7] hence the alternative name "lime disease"^[8] (not to be confused with Lyme disease). Symptoms include burning, itching and large blisters that slowly accumulate over time.^[9]

Historical background

The photosensitizing effects of plants have been known since antiquity. In Egypt around 2000 B.C., the juice of Ammi majus "was rubbed on patches of vitiligo after which patients were encouraged to lie in the sun."^[5] This ancient practice acknowledged the hyperpigmentation effects now known to accompany phytophotodermatitis.

One of the earliest reports of plant-based dermatitis was given by Chaumton in 1815, who noted that the outer rind and root of cow parsnip (a common name for any Heracleum species of plant) contained an acrid sap sufficiently strong to inflame and ulcerate the skin.^[10] Similarly in 1887 Sornevin reported that Heracleum sphondylium caused dermatitis. However, neither of these early reports recognized the crucial role of ultraviolet radiation.

In 1937, dermatitis from Heracleum mantegazzianum was reported by Miescher and Burckhardt who suspected the possibility of light sensitization.^[11] A few years later, Kuske confirmed this hypothesis.^[12][13] In 1942, Klaber introduced the term "phytophotodermatitis" to emphasize that both plants and light were required to affect a reaction.^[14][15]

Darrell Wilkinson, a British dermatologist, gave an accurate description of the disease in the 1950s.^[16] In 1961, Efremov reported 357 cases of phytophotodermatitis from Heracleum dulce (sweet cow parsnip). He "noted the requirement for sunlight in evoking the dermatitis since inunction of the juice of the plant without exposure to sunlight was harmless."^[17] Between 1962 and 1976, numerous reports of phytophotodermatitis from giant hogweed (Heracleum mantegazzianum) were reported. By 1980, the photosensitizing effects of various plant species had become well known (as evidenced by the comprehensive work of Mitchell and Rook^[18]).

Symptoms

Phytophotodermatitis is a cutaneous phototoxic inflammatory reaction resulting from contact with light-sensitizing botanical substances coupled with subsequent exposure to ultraviolet light, usually from the sun. This reaction is caused by the presence of linear derivatives of furanocoumarin in the leaves, roots, stems, flowers, and seeds of certain plants, particularly from the plant families Umbelliferae, Rutaceae, Moraceae, and Leguminosae.

A reaction typically begins within 24 hours of exposure and peaks at 48–72 hours after exposure.^[19] Initially, the skin turns red and starts to itch and burn. Blisters form within 48 hours. The blisters may leave black, brown, or purplish scars that can last for several years. This hyperpigmentation of the skin is caused by the production of melanin triggered by the furanocoumarins.

Although media reports have suggested that eye exposure to the sap can lead to temporary or permanent blindness, the risk of permanent blindness is not supported by existing research.^[20]

Effect of the common rue on skin

A severe case of phytophotodermatitis

Phytophotodermatitis can affect people of any age. In children, it has been mistaken for child abuse.^[21]

Common causes

• The Apiaceae family of plants including carrot,^[22] wild carrot,^[23] parsnip,^[24] parsley, celery,^[5] and giant hogweed^[25]
• Citrus fruits such as lemon,^[15] lime,^[7][8][19] and bergamot orange^[1][2]
• Notobubon galbanum (previously known by the synonym Peucedanum galbanum),^[26] a South African plant also known as "blister bush", "hog's fennel", or locally in Afrikaans as bergseldery (i.e. "mountain celery")^[27]
• Common rue (Ruta graveolens) and other plants in the genus Ruta^{[28][29][30][31]}
• Sclerotinia sclerotiorum, which can infect celery^[32]
• Common fig, its latex contains various furocoumarin isomers such as 8-methoxypsoralen, which induce allergic photodermatitis^[33][34]
• Dictamnus (commonly known as the "burning bush")
• Ambrette Abelmoschus moschatus ^[35]

Prevention

The first and best line of defense against phytophotodermatitis is to avoid contact with phototoxic substances in the first place:

• Avoid contact with the Apiaceae family of plants, citrus fruits, and other biological agents known to have phototoxic effects. Do not incinerate phototoxic plants and agents since this will serve to disperse the phototoxic substances more widely.^[36]
• In outdoor situations where contact with phototoxic plants is likely, wear long pants and a long-sleeve shirt. Wear gloves and protective eyewear before handling such plants.
• If protective clothing is not available, apply sunscreen to exposed areas. This will provide some measure of protection if contact is made.
• After an outdoor activity, take a shower or a bath as soon as possible. Wash your clothing and then wash your hands after handling the dirty clothes.

A second line of defense is to avoid sunlight, so as not to activate a phototoxic substance:

• If you come in contact with a phototoxic substance, immediately wash the affected area with soap and cold water, and avoid any further exposure to sunlight for at least 48 hours. Heat and moisture can worsen the skin reaction,^[25] which is why it’s important to wash the affected area with soap and cold water.
• Stay indoors, if possible. Be sure to avoid light shining through windows.
• If staying indoors is not an option, cover the affected area with sun protective clothing.
• In lieu of sun-protective clothing, apply sunscreen^[37] to the affected areas after washing.

Phytophotodermatitis is triggered by long wavelength ultraviolet light (called UVA) in the range of 320–380 nanometers,^[19] so the best sun-protective clothing and sunscreen products will block these wavelengths of UVA radiation.

In 2011, the U.S. Food and Drug Administration (FDA) established a "broad spectrum" test for determining a sunscreen product's UVA protection.^[38] Sunscreen products that pass the test are allowed to be labeled as "Broad Spectrum" sunscreens, which protect against both UVA and UVB rays.

There is no equivalent test or FDA-approved labeling for sun-protective clothing. Some clothing is labeled with an Ultraviolet Protection Factor (UPF) but test results from Consumer Reports^[39] suggest that UPF is an unreliable indicator of UV protection.

Treatment

Many different topical and oral medications may be used to treat the inflammatory reaction of phytophotodermatitis. A dermatologist may also prescribe a bleaching cream to help treat the hyperpigmentation and return the skin pigmentation back to normal. If the patient does not receive treatment, the affected sites may develop permanent hyperpigmentation or hypopigmentation.^[19]

See also

• List of cutaneous conditions
• Photodermatitis
• Psoralen
• Photosensitivity in humans
• Stinging plant, plants with hairs that inject poisons

References

Wikimedia Commons has media related to Phytophotodermatitis.

External links