Drugs and Wells' syndrome: a possible causal relationship?

In April 1997, a as-year-old woman presented with a 3-day history of multip le papules and vesicles on the fingers and wrist of her right hand. She rep orted that she had been taking nonsteroidal anti-inflammatory drugs contain ing tenoxicam and diclofenac sodium, and had no history of an insect bite. The medical history also included pruritic erythema on her trunk 1 month be fore her initial visit, and oral tenoxicam and diclofenac sodium treatment for ankle arthralgia 2 days before the skin lesions appeared. At that time, her dermatologist had told her that the skin lesions might be due to an in sect bite and were secondarily infected. She took amoxicillin for the lesio ns, and during the following days developed bullous lesions on her hands an d feet. The patient was diagnosed with "drug reaction" at another hospital based on a histopathologic examination of the affected skin. Treatment with topical corticosteroids and oral antihistamines was ineffective. Physical examination revealed a few crusted, erythematous, papular lesions on the dorsal aspects of the patient's feet, bullous lesions on her right w rist, and vesiculopapules on her fingers. She had no fever or other abnorma l clinical findings. Laboratory studies showed a white blood cell count of 6000/mL with 16.5% eo sinophils, A bacterial culture of the content of one of the bullous lesions was negative. The results of stool tests for parasites and ova were negati ve. Clinical and laboratory findings were in line with the diagnosis of dru g reaction. The patient was advised not to take nonsteroidal antiinflammato ry drugs. The skin lesions resolved rapidly on treatment with wet compresse s of Burow's solution and oral prednisolone (40 mg/day). The dose of predni solone was gradually reduced, and was discontinued after 3 weeks. The patie nt was readmitted in July 1997 for an indurated, erythematous plaque on her left foot, a lesion that resembled cellulitis. Her history at that time in cluded the initiation of amoxicillin treatment for a gingival abscess 2 day s before the skin lesion appeared. The lesion regressed after amoxicillin w as discontinued and the patient received an intramuscular injection of tria mcinolone acetonide. Several months later, in October 1997, she developed a similar cellulitis-l ike lesion on her right ankle. This time there was no history of drug intak e. We obtained a skin biopsy from the lesion, and histopathology revealed a n intense eosinophilic infiltrate in the dermis and extending into the subc utaneous tissue. Flame figures were abundant (Fig. 1). We also observed ede ma and erythrocyte extravasation in the dermis. Based on these features and her history, a diagnosis of Wells' syndrome was made. The skin lesion reso lved spontaneously, and she has experienced no lesion recurrence since.