Phytophotodermatitis: Case Report and Review of the Literature Paul H
Total Page：16
File Type：pdf, Size：1020Kb
REVIEW Phytophotodermatitis: Case Report and Review of the Literature Paul H. Janda, DO; Sanjay Bhambri, DO; James Q. Del Rosso, DO; Narciss Mobini, MD Phytophotodermatitis is a common phototoxic dermal reaction caused by the interaction between certain plants, sunlight, and human skin. The causal agents in plants have been identified as furocouma- rins, which are photoactive compounds. Although the plants causing phytophotodermatitis vary, in the United States phytophotodermatitis most commonly occurs following exposure to plants belonging to the Rutaceae and Umbelliferae families. COS DERM 3 hytophotodermatitis is a common phototoxic and then followed by hyperpigmentation. Phytophoto- dermal reaction caused by the interaction dermatitis is associated with minimal symptomatology between certain plants, sunlight, and human and morbidity, although persistent hyperpigmentation skin. Klaber1 was the first to coin the term in may be bothersome or worrisome to some patients, espe- 1942. The causalDo agents in plantsNot have been cially Copy when it occurs at commonly exposed locations (ie, identifiedP as furocoumarins, which are photoactive com- face and hands).4 Accurately recognizing the symptoms of pounds.2 Although the plants causing phytophotoderma- phytophotodermatitis is important in avoiding misdiag- titis vary, in the United States phytophotodermatitis most nosis and preventing repeated episodes of exposure; phy- commonly occurs following exposure to plants belonging tophotodermatitis has been misdiagnosed as a cutaneous to the Rutaceae and Umbelliferae families.3 Phytopho- sign of child abuse.6-8 todermatitis is a phototoxic reaction, occurring in skin exposed to UV radiation after contact with plants con- CASE REPORT taining furocoumarins.4,5 The clinical changes most com- A 9-year-old white female, accompanied by her mother, monly include erythema, followed by vesiculation with presented with a 4-week history of perioral hyperpig- development of bullae in the skin 24 to 72 hours later mentation. Macular hyperpigmentation, characterized by a homogenous light brown color, was noted without Dr. Janda is an intern and Dr. Bhambri is Chief Resident, perivermilion sparing. The eruption was asymptomatic. Dermatology, Valley Hospital Medical Center, Las Vegas, Nevada. Both the patient and her mother did not recall any previ- Dr. Del Rosso is Clinical Associate Professor, Dermatology, ous eruption or irritation such as redness or a rash around University of Nevada School of Medicine, Las Vegas; Clinical the mouth area. The remainder of the cutaneous exami- Associate Professor, Dermatology, Touro University College of nation, including oral and ocular mucosae, was negative Osteopathic Medicine, Henderson, Nevada; and Dermatology for any significant findings. Residency Director, Valley Hospital Medical Center, Las Vegas. Past medical and family histories were unremarkable, Dr. Mobini is Clinical Assistant Professor, Department of including dermatologic disorders. Medication history Pathology and Internal Medicine (Dermatology), University of was also unremarkable. There was no history of allergies, Nevada School of Medicine, Las Vegas. including any to medications. The authors report no conflicts of interest in relation to this The main diagnostic considerations were postinflam- article. matory hyperpigmentation developing after contact VOL. 21 NO. 2 • february 2008 • Cosmetic Dermatology® 99 Copyright Cosmetic Dermatology 2010. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. PHYTOPHOTODERMATITIS dermatitis. Photodermatitis, including phytophotoder- Later, in 1916, freund described hyperpigmented matitis, was also considered. Initial questioning did not skin lesions resulting from exposure to bergamot oil in uncover any contactant or photocontactant. perfume and the sun, a condition currently known as The attending dermatologist was highly suspicious of berloque dermatitis.10 Oppenheim, in 1934, coined the phytophotodermatitis, despite denial by the patient and term dermatitis bullosa striata pratensis to describe an her mother of repeated exposure to limes or lemons. erythematous, bullous eruption in a bizarre configura- Questioning regarding recent travel revealed a 2-week tion appearing on sunbathers who had been lying in vacation in fort Lauderdale, florida. repeated querying grass.10,11 It was in 1942 that Klaber introduced the led to the patient finally admitting that she loved eating term phytophotodermatitis to elucidate the role of plants limes and lemons, especially lemons; in fact, she admitted (phyto) and light (photo) in the manifestation of derma- to eating slices of both limes and lemons every day while titis.10 The work of Kuske established the relationship on vacation. The patient also admitted being concerned between the chemical components of certain plant tis- that she would need to stop. The attending dermatologist sues and the development of phytophotodermatitis.1 discussed phytophotodermatitis with the patient and her furthermore, Kuske and associates presented evidence mother, mentioning that limes and lemons combined that the photosensitizing substances responsible for with UV (sunlight) exposure are common causes of this phytophotodermatitis were of the furocoumarin group. type of skin discoloration. Jensen and Hansen12 determined the wavelengths that produce the typical lesions of phytophotodermatitis: DISCUSSION 320 to 400 nm.11,13,14 Historical Aspects Phytophotodermatitis has a long, interesting history Photochemistry that dates back to 1000 to 1500 BC. Patients with vitiligo Phytophotodermatitis is classified as a phototoxic reac- in China, egypt, and India had certain plant extracts tion.1,3,15,16 The skin contains a compound that absorbs UV applied to the affected areas and were then instructed radiation and is excited to a reactive state to yield direct to lie in the sun.9 In 1834, Kalbrunner isolated ber- toxic effects.15,17 furocoumarins are the chemical com- COS 10DERM 1,3,4,10,11,18-20 gapten (5-methoxypsoralen) from Citrus bergamia. pounds implicated in phytophotodermatitis. Plants Commonly Associated DoWith Not Phytophotodermatitis Copy Family Botanical Name Common Name Rutaceae Citrus acida Lime Citrus aurantifolia Persian lime Citrus bergamia Bergamot Citrus limon Lemon Citrus paradisi Grapefruit Citrus sinensis Sweet orange Pelea anisata Mokihana Umbelliferae Anethum graveolens Dill Apium graveolens Celery Daucus carota Wild carrot Daucus sativus Garden carrot Foeniculum vulgare Sweet fennel Pastinaca sativa Parsnip Petroselinum crispum Parsley Moraceae Ficus carica Fig 100 Cosmetic Dermatology® • february 2008 • VOL. 21 NO. 2 Copyright Cosmetic Dermatology 2010. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. PHYTOPHOTODERMATITIS They are tricyclic hydrocarbons composed of a furan Important Contributory Factors ring condensed on benzopyrone. Linear furocoumarins Despite the common pathogenesis of phytophotoderma- (psoralens) are more phototoxic than angular furocou- titis, reports exhibit marked variation in the severity of marins (angelicin).18 These substances are found in a reaction.4,16,25 for instance, there are reports of decreased number of plant families, including Rutaceae (com- severity of reaction on areas of skin that have a thicker mon lime and bergamot) and Umbelliferae (celery, stratum corneum. Pigmentation from previous sun garden and wild carrots, parsley, sweet fennel, dill, and exposure also plays a protective role.4,26 Hispanics and parsnip).13 The Table provides a more comprehen- African Americans, who have naturally higher amounts sive list. of melanin in their skin, are less affected.4,27 Intactness The UV spectrum is traditionally divided into 3 sub- of the stratum corneum, number of hair follicles, and divisions: UVC (200–290 nm), UVB (290–320 nm), and degree of skin hydration all contribute to the absorption 4,19 UVA (320–400 nm). UVA is further divided into UVA2 of the phototoxic compounds. The ability of a pho- (320–340 nm) and UVA1 (340–400 nm). UVA is associ- tosensitizer to be absorbed through the skin is another ated with aging effects, whereas UVB causes sunburn. important variable and depends on the vehicle by which furocoumarins cause phytophotodermatitis by the photosensitizer is applied.20,28 Other contributory forming phototoxic compounds on exposure to UVA factors have been demonstrated, such as sweating, heat, radiation.4,10,11,13,15,16,18 On exposure to UVA radiation, friction, and longer duration of sun exposure, all of which furocoumarins absorb photons to form highly reactive, exacerbate phototoxic effects.4,29 Lastly, furocoumarin energy-rich triplets. Two distinct reactions occur. The concentration has been shown to vary in certain plants, direct photochemical (type I) reaction occurs indepen- and differing reactions may indicate this variability.1,2 dently of oxygen and involves furocoumarins and DNA. Covalent bonding of the activated furocoumarins to Clinical Features the pyrimidine bases on opposite strands of epidermal- Phytophotodermatitis is the manifestation of a photo- cell DNA occurs, causing interstrand cross-linking, sensitizing compound combined with exposure to UV cell injury, and inhibition COSof DNA synthesis.14 It is thisDERM radiation. Cutaneous signs of inflammation appear after collective phenomenon that plays a major role in the a latent period of approximately