Erythema multiforme is a self-limiting skin condition characterized by the abrupt appearance of red papules of various sizes, some of which evolve into target lesions. It has been determined that erythema multiforme is often precipitated by herpes simplex virus (HSV) infection. Weston and Morelli conducted a retrospective case series evaluation of 12 children with erythema multiforme to examine its clinical associations, frequency and evolution, and the response to antiviral treatment with acyclovir.
Twelve children (7 boys and 5 girls) in whom HSV-associated erythema multiforme developed were evaluated. Mean age at disease-onset was 8.1 years. Eight of the children had a history of preceding herpes labialis and two children had a history of herpes facialis. Two children had no history of an obvious HSV lesion. The children were seen initially in consultation and were followed for a minimum of three years.
During the initial clinic visit, cultures for HSV were obtained from preceding herpes lesions; biopsies were obtained from early papules, and frozen sections were analyzed for HSV DNA sequences after polymerase chain amplification. HSV was detected in the biopsies of all 12 children, including two children with negative viral cultures and the two children with no history of an HSV lesion. All the children were examined during subsequent attacks of erythema multiforme, and the duration of lesions was determined by follow-up visits. Response to therapy with acyclovir was evaluated by a decrease in the mean duration or number of new episodes, or the absence of any recurrences over a three-year period.
The average time from preceding HSV infection to the onset of skin lesions of erythema multiforme was 3.9 days (range: zero to 11 days). Overall, the time from infection with HSV to outbreak of erythema multiforme varied from episode to episode in all the children. The episodes lasted an average of 10.6 days with a mean occurrence of 2.6 episodes annually.
Most lesions associated with erythema multiforme were on the hands and arms, with fewer on the face and legs. There was always complete resolution of symptoms between episodes, and none of the children developed complications of the disease or progressed to erythema multiforme major (also called Stevens-Johnson syndrome).
Four children were initially treated with topical acyclovir without obvious benefit. Six children were treated with oral acyclovir, 25 mg per kg per day for 10 days, at the onset of one or more episodes of erythema multiforme. No alteration in the frequency or duration of their illness was observed. Three children were treated prophylactically with oral acyclovir at a dosage of 20 mg per kg per day for six months and had no episodes of HSV infection or erythema multiforme during this time. For the six months prior to receiving prophylactic acyclovir treatment, these patients averaged 3.5 episodes. During a three-year period after receiving prophylaxis, only one of the children had a recurrence. This recurrence lasted just three days.
The authors conclude that their findings further support the role of HSV in the development of erythema multiforme. In addition, it would appear that topical acyclovir or the treatment of single episodes of erythema multiforme with oral acyclovir has no effect on the clinical course of the skin condition. Consideration should be given to a six-month course of prophylactic acyclovir for children with frequent recurrences of erythema multiforme.