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Phytophotodermatitis
Phytophotodermatitis
Phytophotodermatitis
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Phytophotodermatitis
Other namesberloque dermatitis, margarita photodermatitis, lime disease, lime phytodermatitis
Phytophotodermatitis caused by lime juice
SpecialtyDermatology Edit this on Wikidata
Causesphotosensitizer and UV-A light
Differential diagnosisskin burn; allergic contact dermatitis

Phytophotodermatitis, also known as berloque dermatitis,[1][2][3] margarita photodermatitis,[4][5] lime disease[6] or lime phytodermatitis[6] is a cutaneous phototoxic inflammatory reaction resulting from contact with a light-sensitizing botanical agent (such as lime juice) followed by exposure to ultraviolet A (UV-A) light (from the sun, for instance). Symptoms include erythema, edema, blisters (vesicles and/or bullae), and delayed hyperpigmentation. Heat and moisture tend to exacerbate the reaction.

A reaction may be elicited in any person who has been exposed to adequate amounts of both a photosensitizer and UV-A light. Phytophotodermatitis is not an immunologic response; no prior exposure to the photosensitizing agent is required.

The photosensitizing substances found in phototoxic plants belong to a class of chemical compounds called the furanocoumarins, which are activated by long-wavelength ultraviolet (UV-A) light. The most toxic of these organic compounds are the linear furanocoumarins, so called since they exhibit a linear chemical structure. Bergapten and xanthotoxin (also known as methoxsalen), two linear furanocoumarins derived from psoralen, are invariably found in plants associated with phytophotodermatitis.[2]

Symptoms and signs

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A severe case of phytophotodermatitis in an 11-year-old boy.

A reaction typically begins within 24 hours of exposure and peaks at 48–72 hours after exposure.[7] Initially, the skin turns red and starts to itch and burn. Large blisters (or bullae) form within 48 hours.[8] 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 agent can lead to temporary or permanent blindness, the risk of permanent blindness is not supported by existing research.[9]

Phytophotodermatitis can affect people of any age. In children, it has sometimes been mistaken for child abuse.[10]

Phototoxic species

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Plants associated with phytophotodermatitis mainly come from four plant families:[2][11] the carrot family (Apiaceae), the citrus family (Rutaceae), the mulberry family (Moraceae), and the legume family (Fabaceae).

Apiaceae

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The carrot family Apiaceae (or Umbelliferae) is the main family of plants associated with phytophotodermatitis. Of all the plant species that have been reported to induce phytophotodermatitis, approximately half belong to the family Apiaceae.[12]

False bishop's weed (Ammi majus), the world's major source of the linear furanocoumarin xanthotoxin, has been used since antiquity to treat vitiligo[2] but accidental or inappropriate use of this plant can lead to phytophotodermatitis.[13] Despite this danger, A. majus continues to be cultivated for its furanocoumarins,[14] which are still used for the treatment of skin disease.

Numerous species in the family Apiaceae are cultivated as food products, some of which exhibit phototoxic effects. In particular, celery, parsnip, and parsley have been reported to cause phytophotodermatitis among agricultural workers, grocery workers, and other occupational food handlers.[15][16][17][18][19][20][2][excessive citations]

A number of phototoxic plant species in the carrot family have become invasive species, including wild parsnip (Pastinaca sativa)[21][22] and the tall hogweeds of the genus Heracleum,[23][24] namely, Persian hogweed (Heracleum persicum), Sosnowsky's hogweed (Heracleum sosnowskyi), and giant hogweed (Heracleum mantegazzianum). In particular, the public health risks of giant hogweed are well known.[25]

Other plant species in the family Apiaceae that are associated with phytophotodermatitis include blister bush (Notobubon galbanum), cow parsley (Anthriscus sylvestris), wild carrot (Daucus carota), various species of the genus Angelica (e.g., Korean angelica Angelica gigas), and most (if not all) species of the genus Heracleum (esp. the tall invasive hogweeds and the cow parsnips, Heracleum sphondylium and Heracleum maximum).

Rutaceae

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The citrus family Rutaceae is the second most widely distributed family of plants associated with phytophotodermatitis.

Effect of common rue on skin

Numerous citrus fruits in the family Rutaceae exhibit phototoxic effects. Of these, perhaps the best known is lime.[26][27][28][29] Phytophotodermatitis associated with limes is sometimes colloquially referred to as "lime disease,"[30][31] not to be confused with Lyme disease.

In the family Rutaceae, the most severe reactions are caused by the essential oil of the bergamot orange (Citrus bergamia).[2][32] Bergamot essential oil has a higher concentration of bergapten (3000–3600 mg/kg) than any other citrus-based essential oil, even lime oil, which contains 1700–3300 mg/kg of bergapten.[33]

Other plant species in the family Rutaceae that are associated with phytophotodermatitis include burning bush (Dictamnus albus),[34] common rue (Ruta graveolens),[35][36][37][38] and other plants in the genus Ruta.

Moraceae

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The mulberry family Moraceae is often associated with phytophotodermatitis. Multiple species in the genus Ficus are known to exhibit phototoxic effects. Of these, the common fig (Ficus carica) is well known and thoroughly documented.

Like Ammi majus in the family Apiaceae, the common fig has been used since antiquity to treat vitiligo[39] but the milky sap of fig leaves can cause phytophotodermatitis if used accidentally or inappropriately.[40][41][42][43][44][45] A literature search revealed 19 cases of fig leaf-induced phytophotodermatitis reported between 1984 and 2012.[45] In Brazil, several hospitals reported more than 50 cases of fig leaf-induced burn in one summer.[44] In most cases, patients reportedly used the leaves of the fig plant for folk remedies, tanning, or gardening.

Other plant species in the family Moraceae that are associated with phytophotodermatitis include Ficus pumila[46][47] and Brosimum gaudichaudii.[48] Like Ficus carica, the South American species Brosimum gaudichaudii has been shown to contain both psoralen and bergapten.

Prevention

[edit]

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

  • Avoid contact with the plant family Apiaceae, 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.[49]
  • In outdoor situations where contact with phototoxic plants is likely, wear long trousers 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 cold water is required.
  • 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[50] to the affected areas after washing.

Phytophotodermatitis is triggered by long wavelength ultraviolet light (called UVA) in the range of 320–380 nanometers,[7] 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.[51] 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[52] suggest that UPF is an unreliable indicator of UV protection.

Treatment

[edit]

Many different topical and oral medications may be used to treat the inflammatory reaction of phytophotodermatitis. A dermatologist may also prescribe a whitening 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.[7]

History

[edit]

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."[2] In A.D. 50, the Greek physician Dioscorides observed that pigment would return to patches of vitiligo if "cataplasmed with the leaves or the boughes of the Black Figge,"[39] an apparent reference to Ficus carica, the common fig. These ancient practices 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.[53] Similarly in 1887 Sornevin reported that Heracleum sphondylium caused dermatitis. However, neither of these early reports recognized the crucial role of ultraviolet radiation.

"Berloque dermatitis"[3] (from the French word "berloque" meaning trinket or charm) is a term coined by Rosenthal in 1925 to describe the pendant-like streaks of pigmentation observed on the neck, face, and arms of patients.[54][2] He was unaware that, in 1916, Freund had correctly observed that these pigmentation effects were due to sun exposure after the use of Eau de Cologne, a perfume infused with bergamot oil.[55] It is now known that bergamot oil contains a significant amount of bergapten,[2] a linear furanocoumarin that gets its name from the bergamot orange.

In 1937, dermatitis from Heracleum mantegazzianum was reported by Miescher and Burckhardt who suspected the possibility of light sensitization.[56] A few years later, Kuske confirmed this hypothesis.[57][58] In 1942, Klaber introduced the term "phytophotodermatitis" to emphasize that both plants and light were required to affect a reaction.[59][29]

Darrell Wilkinson, a British dermatologist, gave an accurate description of the clinical entity in the 1950s.[60][61] 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."[62] 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[63]).

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Phytophotodermatitis

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from Grokipedia
Phytophotodermatitis, also known as margarita dermatitis when caused by lime juice, is a nonimmunologic phototoxic cutaneous eruption that occurs when the comes into contact with photosensitizing chemicals, primarily furocoumarins such as psoralens found in certain plants and fruits, followed by exposure to A (UVA) radiation from . This reaction damages cells without involving the , leading to and potential long-term pigmentation changes. The condition is self-limited but can mimic burns, infections, or other dermatoses, often presenting as irregular, linear, or drip-like patterns on exposed areas. The mechanism involves furocoumarins penetrating the skin and binding to DNA or cell membranes upon UVA activation, causing oxygen-dependent or independent cell death that manifests clinically within 24 to 72 hours. Common culprits include citrus fruits like limes and lemons, vegetables such as celery, carrots, parsley, and dill, as well as plants like figs, wild parsnip, and hogweed, which release these compounds during handling, consumption, or environmental contact. It frequently affects individuals in occupational settings (e.g., gardeners, chefs, bartenders) or recreational activities (e.g., hiking, citrus squeezing), with children particularly vulnerable due to hand-to-skin transfer from adults. Incidence is underreported but documented in case series from dermatology and pediatrics literature since the 1980s. Symptoms typically begin with burning erythema and tenderness, progressing to vesicles, bullae, or erosions in severe cases, followed by postinflammatory hyperpigmentation that may persist for weeks to months; pruritus is uncommon. Diagnosis relies on clinical history of plant exposure and UVA light, often confirmed by the characteristic morphology, though patch testing or biopsy may rule out differentials like contact dermatitis or cellulitis. Treatment is supportive: mild cases resolve with cool compresses and emollients, while severe blistering may require topical corticosteroids, oral analgesics, or wound care to prevent secondary infection; systemic steroids are reserved for extensive involvement. Prevention emphasizes immediate skin washing after plant contact (ideally within 30-120 minutes) and using UVA-blocking sunscreens or protective clothing in high-risk environments.

Introduction and Pathophysiology

Definition

Phytophotodermatitis is a non-immunologic cutaneous phototoxic inflammatory eruption resulting from contact with light-sensitizing botanical substances, primarily , followed by exposure to A (UVA) . This condition manifests as an acute skin reaction in the areas of contact, typically presenting with , , and sometimes blistering, due to the photochemical activation of the sensitizing agents. The term "phytophotodermatitis" was first introduced in the in 1942 by Robert Klaber to describe this plant- and light-induced dermatosis. Phytophotodermatitis affects individuals of all ages, sexes, and skin types, as it does not require prior or . The acute phase is self-limited, generally resolving within days to weeks with supportive care and avoidance of further exposure, though it often leads to prolonged post-inflammatory that can persist for months due to stimulated activity. In contrast to photoallergic reactions, which are immunologically mediated and occur only after prior in susceptible individuals, phytophotodermatitis represents a phototoxic response that is dose-dependent and can develop in anyone upon sufficient exposure to the sensitizer and UVA light.

Mechanism of Action

Phytophotodermatitis arises from a phototoxic reaction where , commonly known as s, penetrate the skin following contact with photosensitizing . These lipophilic compounds are readily absorbed into epidermal cells, where they intercalate between DNA base pairs without initial harm. Upon exposure to A (UVA) radiation in the 320-400 nm range, psoralens absorb photons and undergo a photochemical excitation, leading to the generation of (ROS) through oxygen-dependent Type II reactions and direct covalent bonding in oxygen-independent Type I reactions. The excited psoralens primarily form monofunctional adducts with pyrimidine bases, particularly thymine, in DNA, and upon further UVA exposure, these progress to interstrand cross-links that distort the DNA helix. This crosslinking inhibits DNA replication and transcription, triggering cell cycle arrest, epidermal cell apoptosis, and subsequent release of inflammatory mediators. The resulting cellular damage induces keratinocyte death and stimulates an acute inflammatory cascade, characterized by vasodilation and edema formation in the dermis. The photochemical initiation occurs rapidly, within minutes of combined and UVA exposure, but clinical manifestations emerge delayed due to the time required for failure and inflammatory amplification. Symptoms typically onset around 24 hours post-exposure, peak at 48-72 hours, and involve release—such as and —that promotes , leukocyte recruitment, and prolonged . Environmental factors like heat and moisture enhance the severity by facilitating deeper penetration of psoralens into the , particularly through sweating or wet conditions that increase and absorption. High and elevated temperatures during exposure can thus intensify the phototoxic response and accelerate development.

Etiology

Phototoxic Compounds

Phytophotodermatitis is primarily induced by phototoxic compounds known as linear , a class of secondary metabolites that include psoralens such as 5-methoxypsoralen () and 8-methoxypsoralen (xanthotoxin), as well as the angular furanocoumarin angelicin. These compounds feature a structure consisting of a ring fused to a moiety, which confers their photoreactive properties. The chemical properties of these enable their role in : they are highly lipophilic due to their non-polar aromatic rings, facilitating penetration through the skin barrier upon contact. Additionally, they absorb A (UVA) in the 320–400 nm range, which excites their molecules and leads to the formation of reactive or direct interactions with biological targets, such as generating cyclobutane in DNA. Concentrations of these compounds in plants vary significantly depending on , developmental stage, and environmental factors; for instance, levels can increase up to tenfold under stress conditions like UV exposure, drought, or pathogen attack, as serve as defense metabolites. They are also present in higher amounts in processed plant materials, such as essential oils and perfumes; , for example, can constitute 0.1–1% of bergamot oil. Non-plant sources of these phototoxic compounds are rare but notable in pharmaceutical contexts, where synthetic or extracted forms like (a form of 8-methoxypsoralen) are used in psoralen-UVA ( for dermatological treatments.

Involved Plant Families

Phytophotodermatitis is most frequently associated with plants from the (formerly Umbelliferae), , and families, which contain high concentrations of furocoumarins such as psoralens that act as photosensitizers upon skin contact followed by ultraviolet A exposure. These families are widespread in temperate and subtropical regions, contributing to cases through everyday activities like and handling. The family includes numerous species implicated in phytophotodermatitis, particularly in occupational and recreational outdoor settings. Key examples are Apium graveolens (), Pastinaca sativa (wild parsnip), and (giant hogweed), which are common in , , and along riverbanks in temperate zones. Exposure often occurs during farming, , or weeding, where from bruised stems or leaves contacts the skin. , an , has been linked to severe reactions in forestry workers due to its high furocoumarin content. Rutaceae family plants are prevalent in culinary and cosmetic applications, leading to widespread cases globally, especially in tropical and subtropical areas. Prominent species include Citrus aurantifolia (lime), Citrus limon (lemon), and Citrus bergamia (bergamot), often encountered during food preparation like squeezing limes for drinks or applying bergamot oil in perfumes. These citrus fruits, cultivated worldwide, frequently cause linear blistering patterns from juice splashes on exposed skin during outdoor activities such as barbecues or beach outings. The Moraceae family is represented chiefly by Ficus carica (common fig), whose milky sap is rich in psoralens and poses risks in Mediterranean climates and global cultivation areas like the Himalayas. Contact typically happens in gardening or harvesting, with cases reported among hobbyists handling leaves or unripe fruit. Other families contribute less commonly but are notable in specific contexts. The Fabaceae family includes Psoralea corylifolia (babchi or scurf pea), used in traditional herbal remedies in Asia, leading to exposures via topical applications. Asteraceae (Compositae) species, such as Tagetes patula (French marigold) and Parthenium hysterophorus (parthenium weed), have emerged in recent reports, particularly post-2020 studies on herbal and wild plant interactions in Europe, North America, and India. Overall, over 40 plant families exhibit phototoxic potential, but exposures remain tied to gardening, food preparation (e.g., lime juice on skin during sunny activities), and herbal uses.

Clinical Features

Symptoms and Signs

Phytophotodermatitis manifests in an acute phase typically 24 to 72 hours following exposure to phototoxic plant compounds and subsequent ultraviolet A radiation, presenting as an exaggerated sunburn-like erythema accompanied by edema, tenderness, and a burning sensation. In severe cases, this evolves into the formation of vesicles and bullae, reflecting intense phototoxic damage to keratinocytes and epidermal cells. The reaction progresses over the following days, with resolution of the acute leading to within 1 to 2 weeks, often without the development of systemic symptoms such as fever, unless secondary bacterial occurs. This self-limited course underscores the localized nature of the phototoxic insult. Manifestations vary by type, with individuals of fair experiencing more pronounced blistering due to lower protection, whereas those with darker tones may exhibit less visible but similar underlying epidermal injury. The delayed onset is attributed to an required for absorption and UVA-induced DNA cross-linking, and symptoms can be exacerbated by factors such as occlusion or sweating, which enhance penetration of the phototoxic agents.

Patterns and Complications

Lesions in phytophotodermatitis characteristically follow the pattern of contact with photosensitizing plant sap or prior to ultraviolet A (UVA) exposure, resulting in sharply demarcated, irregular distributions on sun-exposed skin. Linear streaks commonly arise from brushing against plants containing furocoumarins, such as wild parsnip or , creating elongated erythematous or hyperpigmented bands along the path of contact. Drip marks manifest as splash-like or elongated lesions when from fruits like limes contacts the skin, often appearing on the hands, forearms, or ; a notable example is the "lime necklace" pattern, where juice dripping from squeezed limes forms pendant-like streaks around the during beverage preparation. These configurations can produce bizarre, non-uniform shapes, including handprint-like impressions from direct handling or intersecting lines from multiple exposures, sometimes simulating patterns of external trauma. The primary complication is postinflammatory , which emerges after resolution of acute and typically persists for weeks to months, with resolution often taking 2-6 months in many cases. In individuals with darker phototypes, this hyperpigmentation may become permanent in a subset of patients, lasting beyond a year or indefinitely without intervention. Scarring is rare but can occur in severe cases involving extensive blistering or full-thickness epidermal damage, potentially necessitating surgical management. Secondary bacterial may develop if blisters rupture, leading to in susceptible areas, though this is uncommon with prompt recognition. Ocular involvement is possible if photosensitizing sap contacts the eyes followed by UVA exposure, potentially causing with symptoms of , tearing, and temporary vision impairment; however, evidence linking phytophotodermatitis to permanent blindness is limited and primarily based on outdated reports from high-dose exposures. In pediatric patients, the linear or splash-like lesion patterns frequently lead to misdiagnosis as non-accidental injury, prompting unwarranted investigations, as seen in cases where juice from wild or lime contact mimics inflicted burns or bruises on the arms, legs, or torso.

Diagnosis

Clinical Diagnosis

The clinical diagnosis of phytophotodermatitis relies primarily on a detailed history and , as the condition presents with characteristic features following exposure to photosensitizing plants or fruits and subsequent A (UVA) . During history-taking, clinicians should elicit reports of contact with psoralen-containing substances, such as fruits (e.g., limes or lemons), figs, or , combined with exposure within the preceding 24 to 48 hours. Relevant contexts often include occupational exposures, such as agricultural work or bartending, or recreational activities like handling lime in cocktails during outdoor events. Patients may describe an initial burning or stinging sensation rather than itching, with symptoms developing delayed after exposure. On , the is supported by identifying a phototoxic , such as linear streaks, drips, or bizarre shapes corresponding to the site of contact and sun exposure, often sparing covered or photo-protected areas like the eyelids or clothing-covered . Typical lesions appear as erythematous patches that may progress to blisters in the acute phase, followed by postinflammatory in a streaky or splash-like distribution. No routine tests or are required, as the is clinical; phototesting or patch testing is rarely indicated and reserved for presentations where the history is unclear. Phytophotodermatitis has been reported in recreational contexts, such as "margarita dermatitis" from lime juice in cocktails during sun-exposed vacations, including beach trips to .

Differential Diagnosis

Phytophotodermatitis must be differentiated from other photodermatoses, contact dermatitides, and mimic conditions that present with similar erythematous, vesicular, or hyperpigmented patterns on sun-exposed skin. Accurate identification relies on a detailed history of plant or exposure combined with UVA light, typically followed by a characteristic 24- to 72-hour delay in onset, which distinguishes it from more immediate reactions. Among photodermatoses, (PMLE) is a common mimic, featuring pruritic papules, vesicles, or plaques on sun-exposed areas such as the arms and legs, often with symmetrical distribution and sparing of the face; it typically erupts within hours to days of initial summer sun exposure and recurs seasonally without requiring exogenous photosensitizers. In contrast, phytophotodermatitis exhibits asymmetrical, linear or drip-like patterns corresponding to plant contact sites, lacks intense pruritus, and depends on prior contact with psoralen-containing plants. presents with immediate (within minutes) formation of itchy wheals and upon light exposure, resolving within hours, unlike the delayed, non-urticarial blistering and burning in phytophotodermatitis. Contact dermatitis, both allergic and irritant types, can resemble phytophotodermatitis through localized and vesicles but lacks photodependence. requires prior to an (e.g., ), produces pruritic lesions independent of light exposure, and can be confirmed via patch testing, whereas phytophotodermatitis is a nonimmunologic phototoxic reaction without . or chemical burns cause immediate onset of and upon direct contact, without the characteristic delay or need for UVA activation seen in phytophotodermatitis. Other differentials include berloque dermatitis, a phototoxic reaction from bergamot oil or psoralens in perfumes applied to areas like the neck or hands, producing streak-like similar to phytophotodermatitis but linked to cosmetic use rather than handling. Drug-induced , often from systemic agents such as tetracyclines (e.g., ), NSAIDs, or diuretics, results in widespread or symmetrical eruptions on photoexposed skin and is identified by recent medication , differing from the localized, exposure-patterned lesions of phytophotodermatitis. Non-accidental injury or may mimic the linear streaks of phytophotodermatitis, particularly in pediatric cases, but is excluded by corroborating of accidental plant contact and absence of other abuse indicators. Key differentiators include the patient's history of exposure to psoralen-rich plants (e.g., , ) followed by sun exposure and the delayed onset, which are unique to phytophotodermatitis. , if performed, reveals non-specific findings such as necrotic , sunburn cells, mild , and minimal lymphocytic infiltrate without , helping to rule out (prominent and ) or infectious causes (e.g., with multinucleated giant cells). These phototoxic patterns, such as linear vesiculation, further support differentiation when aligned with exposure history.

Management

Prevention

Preventing phytophotodermatitis involves minimizing contact with phototoxic plant compounds, particularly , and subsequent exposure to ultraviolet A (UVA) radiation. Individuals handling such as those in the or families during , cooking, or should wear protective gloves, long-sleeved clothing, and long pants to create a physical barrier against sap or juice. Immediately after potential exposure, thoroughly washing the affected skin with soap and water as soon as possible, ideally within 30 minutes to 2 hours, can remove residual photosensitizing agents and reduce the risk of reaction. To further mitigate risk, avoiding direct for at least 48 hours following contact with suspect plants is recommended, as the phototoxic reaction typically develops within this window upon UVA exposure. Applying broad-spectrum with an SPF of 30 or higher and high UVA protection before outdoor activities provides an additional layer of defense, especially for those in high-risk professions like . Awareness of psoralen-containing products is essential; consumers should avoid cosmetics, fragrances, or essential oils derived from like bergamot or that may contain these compounds, opting instead for phototoxicity-tested formulations. High-risk activities, such as preparing lime-based drinks like s outdoors, can lead to "margarita burns," so washing hands promptly after handling fruits and applying is advised to prevent inadvertent exposure. In environmental settings, removing like from gardens and public spaces through manual cutting of the or targeted application helps eliminate local hazards. campaigns targeting agricultural workers emphasize education on recognition of phototoxic , use of protective gear, and prompt decontamination to reduce incidence in farming communities.

Treatment

Treatment of phytophotodermatitis primarily involves symptomatic relief and supportive measures, as the condition is self-limiting and resolves without specific antidotes. Initial management focuses on avoiding further exposure to ultraviolet A (UVA) light to prevent exacerbation, alongside gentle cleansing of the affected area with soap and water to remove residual photosensitizing compounds. Cool wet compresses are recommended to soothe acute inflammation and edema, while emollients such as petrolatum or ceramide-based moisturizers help maintain skin barrier function and reduce discomfort. Oral analgesics, including nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, or acetaminophen, are used for pain control, with more potent options like opioids reserved for severe cases. For mild to moderate , , or pruritus, topical therapies form the cornerstone of intervention. Moderate-potency corticosteroids, such as 1% or triamcinolone 0.1% cream, applied twice daily for up to two weeks, effectively reduce and itching. Calamine lotion provides additional symptomatic relief for pruritus, and topical antihistamines may be employed if histamine-mediated is prominent. In cases of persistent , topical inhibitors like offer an alternative to steroids, particularly for involvement. Indomethacin, administered orally at 50-75 mg daily for adults, has been noted to mitigate phototoxic responses in some protocols. Severe phytophotodermatitis, characterized by extensive involvement exceeding 30% of , bullae formation, or , requires escalation to systemic therapies and potential hospitalization. Oral corticosteroids, such as at 0.5-1 mg/kg/day for 5-10 days with a taper, are indicated to control widespread inflammation. Admission to a burn unit may be necessary for wound care, including of necrotic tissue and monitoring for secondary bacterial infections, though prophylactic antibiotics are not routinely recommended unless clinical signs of infection (e.g., purulence, fever) are present. In such instances, topical agents like or oral antibiotics (e.g., cephalexin) are used judiciously. Post-inflammatory hyperpigmentation, a common appearing 1-2 weeks after the acute phase, typically resolves spontaneously within 2-6 months but can persist longer in darker types. Management after resolution of active includes topical depigmenting agents like 4% cream applied twice daily, or retinoids such as tretinoin 0.05%, to accelerate fading. Adjunctive therapies, including 20% or chemical peels, may be considered for refractory cases, always under dermatologic supervision to avoid irritation. Strict photoprotection with broad-spectrum sunscreens (SPF 30+ with UVA blockers) is essential during this phase. Recent updates in dermatologic practice as of 2025 emphasize non-pharmacologic interventions, such as cooling compresses and emollients, as first-line for most cases, with antibiotics reserved strictly for confirmed infections to minimize resistance risks. This approach aligns with broader guidelines prioritizing conservative, symptom-directed care over aggressive .

Epidemiology and

Occurrence and Risk Factors

The incidence of phytophotodermatitis is unknown and likely underreported due to frequent misdiagnosis as other dermatoses such as burns or , particularly in children. Cases peak during summer months when radiation levels are higher and outdoor activities increase, with additional surges during tropical vacations involving exposure. The condition occurs globally but shows higher reporting rates in Mediterranean and tropical regions, where phototoxic like figs and are abundant and environmental conditions favor their growth. Key risk factors include occupational exposure among individuals handling phototoxic plants, such as farmers, gardeners, landscapers, chefs, food processors, and bartenders who frequently contact celery, citrus, or figs. Recreational activities also contribute, including preparing lime-based beach drinks or hiking near wild plants like hogweed, which can lead to inadvertent skin contact followed by sun exposure. Children face elevated risk through play and exploration involving plants, often resulting in linear or handprint-like patterns from juice handling. Demographically, phytophotodermatitis exhibits no predilection and affects , from infants to adults. It manifests across types, though postinflammatory is more persistent and cosmetically distressing in individuals with darker tones. Cases have been linked to international travel and , where vacationers encounter unfamiliar phototoxic during outdoor pursuits in sunny destinations. As of 2025, regional increases have been reported, such as in due to exposure to , prompting calls for greater public awareness.

Historical Background

Phytophotodermatitis has roots tracing back over 3,000 years, with ancient civilizations recognizing the phototoxic effects of certain plants, though often in the context of therapeutic applications rather than adverse reactions. In ancient Egypt around 1550 BCE, texts like the Ebers Papyrus describe the use of plant extracts, including from figs (Ficus carica), combined with sunlight to treat skin conditions such as vitiligo, inadvertently highlighting risks of sap-induced blisters and inflammation. Similar practices appear in ancient Indian records from 1500–1000 BCE, where psoralen-containing plants were applied topically followed by sun exposure for depigmentation disorders, sometimes resulting in unintended phototoxic eruptions; Chinese records date from the Tang Dynasty (618–907 CE) onward. These early observations laid the groundwork for understanding the interaction between plant-derived furocoumarins and ultraviolet light, though the mechanisms were not yet elucidated. By the 19th and early 20th centuries, more systematic reports emerged, shifting focus to accidental exposures. In 1834, (5-methoxypsoralen), a key furocoumarin, was isolated from bergamot ( bergamia), marking an early chemical identification of phototoxic agents. The condition gained attention through cases like "meadow dermatitis" or dermatitis bullosa striata pratensis, first described by in 1934 (with earlier allusions possibly to 1926 reports), linked to (Pastinaca sativa) and other family plants during agricultural work, causing linear blisters after sun exposure. In 1916, Freund documented berloque dermatitis from bergamot oil in perfumes, emphasizing citrus-related risks. The term "phytophotodermatitis" was formally coined in 1942 by Robert Klaber to describe phototoxic reactions from plants like (Apium graveolens), distinguishing it from other dermatitides. These reports underscored occupational hazards in farming and handling, with wavelengths of 320–400 nm identified as triggers by Jensen and Hansen in 1930. Key milestones in the mid-to-late advanced both clinical understanding and therapeutic applications. The saw the development of PUVA (psoralen plus UVA) therapy, pioneered by researchers like Parrish and Wolff in 1974, which harnessed oral or topical s with controlled UVA irradiation to treat and , building directly on phytophotodermatitis mechanisms but minimizing risks through dosing. The brought increased recognition of citrus-induced cases, dubbed "bartender's dermatitis" or "margarita burn," from lime (Citrus aurantifolia) juice in beverages, with reports surging among hospitality workers due to global culture. In the 2020s, invasive species like giant hogweed () have drawn renewed attention, with poison control centers noting severe burns from its high content, prompting campaigns on invasive plant management. Culturally, phytophotodermatitis reflects a dual legacy of benefit and peril in . Plants like rue () have been used for centuries in European folk remedies for digestive issues and as insect repellents, despite known risks of severe blistering upon sun exposure, as documented in historical herbals. Similarly, fig sap's application in ancient Egyptian and Indian healing persisted, even as adverse reactions were anecdotally noted, influencing modern awareness through poison control data that tracks recreational and occupational exposures. These practices highlight how empirical knowledge evolved into scientific caution, with high-impact contributions like PUVA transforming potential harms into targeted therapies.

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