Hyperpigmentation and vesicles after beach vacation

Journal of Family Practice, Dec, 2006 by Andrea L. Darby-Stewart, Frederick D. Edwards, Karin J. Perry

A 21-year-old woman traveled to Florida for spring break, accompanied by her fiance and friends. While there, she developed a raised, pruritic 10-cm x 30-cm lesion on her right lateral chest wall. A local pharmacist thought she was having an allergic reaction and recommended topical hydrocortisone cream and oral diphenhydramine (Benadryl). In spite of this therapy the rash progressed.

Five days after returning home, she presented to the emergency department, where she was diagnosed with herpes zoster. The rash was described as multiple vesicles in a dermatomal distribution on the right side of her torso. She was started on famciclovir (Famvir) and given a prescription for hydrocodone with acetaminophen (Vicodin).

Four days later she presented to her primary care physician because she continued to develop areas of hyperpigmentation around her mouth, on the chin, upper chest and breasts, thighs, and forearms. The original lesion on the right lateral thorax had dried, crusted, and was beginning to peel. It was no longer pruritic. The rash had never been painful and she had not taken any hydrocodone. She was most concerned about the disfigurement caused by the rash and wondered if she was having a reaction to the famciclovir. She had suffered no injuries or trauma, and did not engage in substance abuse.

While in Florida she did sun on the beach with friends, but she used sunblock regularly. She had used the same skin products and sunblock for many years. Upon questioning, she recalled drinking citrus beverages while out in the sun. Her history was otherwise unremarkable. Her only prescription medication before onset of the rash was montelukast (Singulair) prescribed for allergic rhinitis.

Examination revealed a bizarre pattern of hyperpigmentation with small punctate lesions on the upper chest, linear lesions on the posterior right arm and thighs, and broad areas of darkened skin on the lower face and chin (FIGURE 1). There was a broad patch of dense hyperpigmentation with desquamation on that right lateral chest wall that appeared to be healing (FIGURE 2).

[FIGURES 1-2 OMITTED]

* What is your diagnosis?

* Diagnosis: Phytophotodermatitis

This patient has phytophotodermatitis, a phototoxic dermatologic reaction that occurs with exposure to ultraviolet light after contact with certain plants. Hyperpigmentation and vesicle or bullae formation are hallmarks of the process.

The sun-sensitizing chemicals are furocoumarins, found in many plants (TABLE). (1) Psoralen, the same substance used in PUVA treatments, is one of the furocoumarins. These agents contact the skin when juice is released from the fruit or stem or by direct contact with leaves. (2)

This patient remembered eating flesh limes on the beach and posing for a photograph next to her fiance, when he placed his right hand around her back and on her right thorax (FIGURE 1). Limes have a high concentration of psoralens and are often the culprit in phytophotodermatitis. (1,3) It is therefore incumbent on the clinician to know this and ask about lime and plant exposure when suspecting this diagnosis.

Erythema typically develops within 24 hours of sun exposure and contact with furocoumarin-containing plants. Vesicles or bulla may develop within 72 hours. Hyperpigmentation occurs over 1 to 2 weeks and can persist for 6 to 12 months. Hyperpigmentation can appear in bizarre streaks or patterns depending on where the chemicals contacted sun-exposed skin. Areas that have formed bulla typically exfoliate within 10 to 14 days. (3)

* Differential diagnosis

The differential diagnosis for this process includes herpes zoster, atopic dermatitis, allergic contact dermatitis, porphyria cutanea tarda, chemical or thermal burn, and abuse. (2,4) While chemical or thermal burn and abuse are suspected with the appropriate history, the remainder of the diagnoses have defining characteristics allowing for proper identification.

Herpes zoster is caused by the reactivation of latent varicella zoster virus. Itching or burning precedes cutaneous eruption of red swollen plaques with vesicles of various sizes, which umbilicate or rupture. These lesions occur in a discreet dermatomal distribution. (5)

Atopic dermatitis has poorly understood pathophysiology. It typically starts in infancy and causes pruritus, eczematous lesions, xerosis, and lichenification of the skin. (5)

Allergic contact dermatitis is a delayed hypersensitivity reaction that requires prior sensitization. It is classically described as pruritic papules on an erythematous base. (5)

Porphyria cutanea tarda is a caused by an inborn enzyme deficiency in the heme biosynthetic pathway that results in mechanical fragility, subepidermal bullae, hypertrichosis, and pigmentation. (5)

* Pathophysiology of phytophotodermatitis

In the presence of ultraviolet A (UVA) irradiation, psoralens cause DNA cross-linkage in the skin. This stimulates increased melanin production with resultant hyperpigmentation. It may also cause the development of radicals, which damage cell membranes and intracellular contents, resulting in edema, erythema, and the formation of vesicles or bullae. (3)