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Features Departments Information |
 Rowena Therese C. Romero, MD Amy S. Paller, MD
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Dermatology quiz ROWENA THERESE C. ROMERO, MD aFall 1997 A NINE-YEAR-OLD Caucasian boy presented to the dermatology clinic with a hyperpigmented, non-pruritic blistering eruption of five days duration. Because the child was known to have a heart condition and the cause of the eruption was unclear, his pediatrician had started him on systemic antibiotics.  FIGURE 1. Multiple erythematous to hyperpigmented linear streaks running down the chest and abdomen. On examination, we noted several erythematous to hyperpigmented linear streaky patches running down the axillae, the chest and abdomen, and the upper back (Figure 1). There were two intact erythematous bullae with clear yellow fluid on the left abdomen (Figure 2).  FIGURE 2. Intact erythematous bullae on the left abdomen. The most likely diagnosis is:
A. Allergic contact dermatitis Answer: B, Phytophotodermatitis. On further investigation, we learned that the patient had just returned from an eight-day vacation in Mexico City. While in Mexico, his mother had been squeezing limes into his hair, and he subsequently was exposed to the sun. Based on this history and the characteristic cutaneous findings, a diagnosis of phytophotodermatitis was made. Phytophotodermatitis is a toxic dermal eruption caused by the interaction of certain plants and sunlight on human skin. The combination typically produces an erythematous, "sunburn-like" response accompanied by blisters and later followed by hyperpigmentation. Furocoumarins (psoralens), which are very potent photosensitizers, have been identified as the offending agents. The substances occur naturally in four major plant families: Rutacea (i.e., limes, bergamot, the gas plant), Umbelliferae (i.e., celery, parsley, wild carrot, dill), Moraceae (i.e., figs, Ficus sp.), and Leguminosae (i.e., Psoralea sp.).1 Interestingly, Barachee seeds (Psoralea corylifolia) have been used for thousands of years in India to treat vitiligo because of the residual hyperpigmentation that results.2 The radiation responsible for causing phytophotodermatitis is long-wavelength ultraviolet light (i.e., UVA). Studies have shown that the phototoxic effect of psoralens occurs in two stages.3 First, UVA activates the psoralen and induces the formation of DNA psoralen adducts. These provoke nuclear and RNA damage. An indirect oxygen-dependent type II peroxidation reaction then follows and is targeted to damage lipid-rich cell membranes and the heme-protein P-450. Histologically, this results in edema of the skin. Clinically, this phototoxic reaction may range from mild erythema to a severe blistering eruption. Consider phytophotodermatitis whenever you see bizarre and linear erythema, vesicles or bullae, and spots or streaks of hyperpigmentation.4 Because it is a photodermatitis, lesions are usually located on the sun-exposed areas of the body, namely the dorsa of the hands, the wrists, forearms and lower legs. This pattern can likewise suggest an allergic contact dermatitis, so to make a correct diagnosis it's important to take a detailed history. In this case, we found a history of exposure to both a contactant (i.e., the plant) and to sunlight. At present, it is believed that phytophotodermatitis is not an allergic process but rather a toxic phenomenon requiring sufficient quantities of photosensitizers and ultraviolet light. Another condition that follows a photodistribution pattern and at times presents with vesiculobullous lesions is lupus erythematosus. The histopathology, however, of lupus is characteristic, and patients present with other systemic manifestations. Polymorphous light eruption (PMLE) is likewise a photodermatosis; this eruption, though—as its name implies—is more polymorphic, with lesions ranging from papules and vesicles to larger eczematous or urticarial plaques. Furthermore, the lesions of PMLE appear in the spring and subside in the winter. Other causes of acute blistering eruptions can be ruled out with a good history and physical examination. Infections such as bullous impetigo may present acutely but do not manifest solely on sun-exposed areas. Moreover, they do not present with the linear, streaky configuration characteristic of phytophotodermatitis but rather as grouped erythematous macules and papulovesicles that later evolve into bullae with honey-colored crusts. Bullous pemphigoid is a primary blistering disorder; it presents with tense bullae on normal-appearing or erythematous skin and has a predilection for the lower abdomen, anogenital region and posterior thighs. Blisters may also appear on mucocutaneous surfaces. The typical course of phytophotodermatitis includes erythema and blister formation occurring 12 to 48 hours after exposure to both the plant and intense sunlight. Some degree of pain may be present, as well as pruritus. The linear streaky markings occur in the areas that come into contact with the plant and are later exposed to sunlight. In the case of our patient who had limes squeezed into his hair, his distinctive cutaneous lesions were found in the same areas where the juice trickled down—on his chest, abdomen and upper back. Typically the "sunburn-like" reaction resolves spontaneously in three to ten days, depending on its severity, and is followed by hyperpigmentation of variable duration. In very mild cases, the initial erythema may go unnoticed, and the hyperpigmentation that follows may be the only visible cutaneous clue to the diagnosis. Scarring is a rare sequela. The histopathological findings in phytophotodermatitis are non-specific, and a skin biopsy is warranted only if the history and physicial examination fail to give a clear diagnosis. Mild disease shows single-cell epidermal necrosis with its characteristic eosinophilia and pyknotic nucleus. More severe cases demonstrate intraepidermal and subepidermal vesiculation and spongiosis. Pigmentary incontinence occurs early and is the only feature of the hyperpigmented sequela, since scarring is uncommon. As demonstrated in this case, limes are a frequent culprit in this phototoxic eruption. Although most limes processed in the United States are coated with an inert wax, whenever the peel is disrupted, contact with the psoralen is possible. Several published reports cite limes as the cause for phytophotodermatitis and usually involve people on vacation who happened to be drinking or preparing margaritas.5 Gross et al reported an interesting case of phytophotodermatitis in a day camp.6 This occurred in a number of children who made pomander balls in an arts and crafts class. In making these balls, the children punctured the skin of limes with scissors and were thus exposed to the psoralen. Sunlight exposure followed during the camp's outdoor activities. Management of phytophotodermatitis is mainly symptomatic. Cool compresses and analgesics may be helpful during the acute erythematous stage. Antibiotic ointments may be applied over open blisters. Topical steroids may be used to decrease the inflammation but are of no benefit for the hyperpigmentation. Because the eruption is likely to reccur with another similar incident, avoiding the combination of contact with the offending plant and sunlight exposure is recommended. REFERENCES 1. Stoner J, Rasmussen J: Plant dermatitis. J Am Acad Dermatol 1983;9:1–15. 2. Juckett G: Plant dermatitis. Postgraduate Medicine. 1996;100:159–171. 3. Finkelstein E, Afek U, et al: An outbreak of phytophotodermatitis due to celery. Int J Dermatol 1994;33:116–118. 4. Webb JM, Brooke P: Blistering of the hands and forearms. Arch Dermatol 1995;131:834–5, 837–8. 5. Egan C, Sterling G: Phytophotodermatitis: A visit to margaritaville. Cutis 1993;51:41–42. 6. Gross T. Ratner et al: An outbreak of phototoxic dermatitis due to limes. Am J Epidemiology 987;125:509–514. |