A 29-year-old left-handed man presented for evaluation of hyperpigmented patches and resolving erythema on the right flexor wrist and dorsal hand; the hand also had residual desquamation at the sites of prior blisters. There were no abnormalities on the left wrist or hand. The appearance of pruritic and erythematous-based bullae had begun 2 weeks earlier when the patient spent several hours outside on a porch drinking margaritas. In addition to pre-made mixes, sliced and squeezed fresh limes were used in the preparation of the drinks. He was not on any medications and had no reported drug allergies nor pertinent past medical history. ____________________________
Phytophotodermatitis is a phototoxic reaction caused by contact with certain plant substances (furanocoumarins) in combination with sunlight. In 1938, Kuske showed that plant furanocoumarins caused photosensitization. Phytophotodermatitis has occurred in patients throughout the world; however, the exact incidence remains unknown and varies according to the population and the risk of exposure to furocoumarin-containing compounds. All individuals — including men and women, young and old — have the potential for exposure to furanocoumarins since they are found in a wide variety of plants.1 The most common family of plants with furocoumarin components are Umbelliferae, Rutaceae and Moraceae. Some of the most common fruits, plants and vegetables that cause this condition are angelica, anise seed, bavachee, buttercup, carrots, celery, dill, fennel, fig, gas plant, hogweed, lemons, limes, mustard, parsley, parsnip and rue (see Table 1). Different names are given for this condition depending on the etiology of the agent, such as berloque dermatitis (also called perfume dermatitis) and lime dermatitis or the other “lime” disease.1-6
Phytophotodermatitis present as erythematous patches, papules, plaques and/or bullae; pruritus is a common accompanying symptom. The lesional morphology can appear as streaks, depending on where the chemicals were in contact with the skin. The perioral area and the hands are the most common sites to develop the condition; however, lesions can occur on other locations.7 Resolution occurs with post-inflammatory hyperpigmentation that develops 1 to 2 weeks after exposure. However, the hyperpigmentation can persist for 2 to 12 months. Berloque dermatitis, a unique type of phytophotodermatitis, occurs when bergapten, a component of bergamot oil used in some perfumes, contacts the skin and is followed by sun exposure. The condition presents around the face or neck and is characterized by erythema and hyperpigmentation. Actual berloque dermatitis has become rare because of the current replacement of the bergamot oil with artificial derivatives in novel perfumes. The clinician also needs to consider the possibility of phytophotodermatitis, because the initial presentation of lime-associated dermatosis can mimic other conditions such as cellulitis or child abuse, as the following cases demonstrate.5,8,9 In one case, a 9-year-old Caucasian girl presented with painful blistering eruptions on the upper extremities. Erythematous streaks were noted on her left arm and unusual hyperpigmented macules were discovered on the neck and left thigh. Cellulitis was initially suspected. However, the family provided additional history of squeezing limes while at the beach to the consulting pediatric dermatologist, resulting in the correct diagnosis of lime-associated phytophotodermatitis.5 Another patient, a 2-year-old Hispanic boy, was examined for management of burns thought to have been caused by child abuse. Well-demarcated, erythematous plaques with bizarre streaked patterns were observed on the upper extremities and lower abdomen. Subsequently, it was discovered that both the patient and his mother had contact with lime trees while swimming at a relative’s house. The diagnosis of lime-associated phytophotodermatitis was made and the suspicion of child abuse was dropped.5 Proper diagnosis of phytophotodermatitis requires a thorough patient history and physical examination. Yet, the patient may not volunteer the essential information and a high index of suspicion by the healthcare provider is necessary. Phytophotodermatitis is suggested by contact with furanocoumarin-containing plants. The hallmark hyperpigmentation subsequently appears as strange patterns on the affected areas. Additionally, skin biopsy during the acute presentation can help to confirm the diagnosis.
Microscopic examination of phytophotodermatitis during the acute phase shows epidermal necrosis, the presence of migrating neutrophils, and inflammation. Spongiosis is present as well as apoptotic cells, characterized by small size and pyknotic nuclei. Examination of older lesions shows hyperkeratosis, acanthosis, and pigment incontinence.4,10
Several conditions can present in a similar appearance to phytophotodermatitis (see Table 2).1,5,6,7,8,9,11 Cellulitis is characterized by redness, swelling, warmth and pain, which can appear similar to phytophotodermatitis due to its red streaking. However, cellulititis may also present with additional symptoms such as fever, headache and chills. Contact dermatitis can result from either an immunologic reaction to an allergen or cutaneous reaction to a skin irritant. Allergic contact dermatitis is frequently caused by plants such as poison ivy, poison oak and poison sumac. Common causes of irritant contact dermatitis are detergents and cleaning products. A patient with contact dermatitis can present with pruritic erythematous patches or plaques and/or bullae; less commonly, the condition can present with urticarial lesions. Atopic dermatitis is a chronic inflammatory pruritic disease in which the skin reacts abnormally to irritants, particular foods and environmental allergens. Patients can present with widespread erythema, scaling, lichenification and pruritus. In the younger individuals, the antecubital and popliteal fossae, the face and the hands are usually affected.
Furanocoumarins readily undergo photo-excitation and subsequently will transfer the energy to other molecules. Ultraviolet A radiation causes furanocoumarins to absorb energy, leading to a high-energy state, which is reactive. This high-energy state can cause damage by two different mechanisms. The first mechanism involves direct covalent linkage between the furanocoumarins and epidermal cell’s DNA, resulting in cross-linking between pyrimidine bases. The second mechanism involves the formation of reactive oxygen species from the high-energy state furanocoumarins. The reactive oxygen species can lead to damaged lipids, proteins and nucleic acids, which subsequently can result in cell death and necrosis. Stimulation of melanocytes occur secondary to interaction with the furanocoumarins molecules, resulting in hyperpigmentation.2,3
Treatment involves identifying and eliminating the cause of the condition. Conservative treatment for the lesions is often all that is required for the management of phytophotodermatitis. Acutely, soaking or draining the blisters can help relieve swelling and discomfort. Topical corticosteroids, oral corticosteroids, or both can be used in more severe cases. When desired, postinflammatory hyperpigmentation can be treated with bleaching creams that contain hydroquinones.7,8 Education of the patient and family is also important for future prevention. Therefore, avoiding exposure to the culprit plant chemicals and sun as well as wearing sunscreen to decrease phototoxicity are recommended. Our patient was given an emollient cream and advised to avoid further exposure to sunlight on the affected areas.
The key to establishing the diagnosis is considering the possibility of phytophotodermatitis and asking the appropriate detailed questions regarding earlier exposure to photosensitizing compounds. In addition, when lime-associated phytophotodermatitis occurs in the setting of margarita preparation, we respectfully suggest that the condition be referred to as “margarita dermatitis.”
Mr. Riahi is a medical student at the Medical School, The University of Texas Medical Branch, Galveston, TX. Dr. Cohen is with the University of Houston Health Center, University of Houston, Houston, TX; the Department of Dermatology, The University of Texas; M.D. Anderson Cancer Center, Houston, TX; and the Department of Dermatology, University of Texas-Houston Medical School, Houston, TX. Mr. Robinson is director of the University of Houston Health Center, University of Houston, Houston, TX. Dr. Gray is with the University of Houston Health Center, University of Houston, Houston, TX. Dr. Khachemoune, the Section Editor of Derm Dx, is with Department of Dermatology, State University of New York, Brooklyn, NY. Disclosure: The authors have no conflict of interest with any material presented in this column.
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