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This is a case report of an Atrophic Juvenile Erythema Multiform that has occurred in a ten year old white girl. She has been having symptoms since age three, presenting severe flares of lesions that looked like multiform erythema. When the lesions healed a loose scar was left involving the whole skin. Some of the histological and pathogenic mechanisms of the disease are discussed.
UNLABELLED: A total of 42 children with erythema multiforme (aged 0.1 to 15.8 years, median 6.1 years) were treated between 1978 and 1997 at the Department of Paediatrics, University of Bern, Switzerland. Antecedent infections were noted in 30 cases: Mycoplasma pneumoniae infection (n = 14), acute upper respiratory tract disease (n = 10) and herpes simplex infection (n = 6). Four cases were associated with antecedent medication (n = 3) or immunization (n = 1). In 12 of the 30 patients in whom erythema multiforme followed an infectious disease, drugs described in the literature as inducers of erythema multiforme had been given for symptoms not suggestive of the condition. In the remaining eight children no precipitating agent could be detected. CONCLUSION: In this survey infections were found as a definite or at least presumptive trigger of erythema multiforme in 71% of cases. Drugs (including immunization) implicated as triggers of erythema multiforme played a definite causative role in 10% and a presumptive role in a further 29% of patients. In 19% of patients an associated condition was not diagnosed.
Erythema multiforme of the mouth is an acute vesiculo-ulcerative lesion, which presents a diagnostic and therapeutic challenge to the clinician. Herpes simplex is described as the most frequent cause of this disease. Controversy exists in the literature as to the definition of oral erythema multiforme and the role of systemic corticosteroids in its treatment. Recent treatment protocols advocate the use of systemic acyclovir, especially in cases triggered by the herpes simplex virus. Two cases of successful treatment of oral erythema multiforme with systemic corticosteroids after acyclovir treatment had failed are presented.
Two patients developed classical erythema multiforme while taking oral terbinafine. A case of Stevens-Johnson syndrome occurring after terbinafine therapy has recently been described, but there have been no published reports of an association with erythema multiforme until now.
Recurrent erythema multiforme is a rare disorder, clinically characterized by symmetrically distributed, erythematous, and bullous skin and mucous lesions, mainly precipitated by a preceding herpes simplex infection. In rare cases, EM presents continuous or persistent relapses, and has been related to an Epstein-Barr virus infection. We report 2 cases of severe, persistent erythema multiforme, treated with thalidomide, with complete disease suppression in both cases. Thalidomide induces immunomodulator, anti-inflammatory, and anti-angiogenic effects, and may be considered as the elective treatment of this rare variety of erythema multiforme. However, in order to avoid neuropathic side effects, patients under thalidomide therapy should be monitored every 6 months with nerve conduction studies while taking the drug.
Erythema multiforme is a skin condition frequently associated with herpes simplex virus and has a tendency to recur. Oral acyclovir has been successful in suppression of the disease. Here we report a patient who had recurrent erythema multiforme associated with recurrent polyarthritis that responded to oral acyclovir suppression therapy.
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Erythema multiforme is a chronic, inflammatory mucocutaneous disease that can occur in both genders at any age. Although the cause remains obscure, a wide range of antigens and factors, including herpesvirus and other infections, has been suggested as triggering the disease. In the present study of 95 patients, we found that patients with oral involvement alone tend to predominate over those who have oral and lip, or oral, lip, and skin disease. There were also more women than men. Our study further confirmed that erythema multiforme cannot be characterized solely as a disease that is cyclical and self-limiting. The dramatic response to corticosteroids and to the immunoregulating agent levamisole, as well as the fact that patients with erythema multiforme are otherwise essentially healthy, suggests that erythema multiforme may be caused by a transient autoimmune defect, possibly triggered by multiple factors. Because 19 patients with oral candidiasis responded to antifungal therapy, a possible antigenic role for these organisms is suggested.
A patient with erythema multiforme developed many nevocytic nevi, including a large cluster of such lesions at the sites of healed blisters. The development of eruptive nevocytic nevi in this pattern suggests that cutaneous injury plays a role in their pathogenesis.
The diagnosis of erythema multiforme was established on the basis of physical examination, biopsy specimen evaluation, and the patient's medication history. Use of a triamcinolone mouthrinse and discontinuation of Triphasil-28 contraceptive led to resolution of the lesions.
Erythema multiforme is reported for the first time in 2 South African horses. Both horses displayed a sudden, fulminant outbreak of raised, non-alopecic and non-pruritic plaques over the dorsolateral aspects of the neck and trunk. In both cases the distribution of the lesions was bilaterally symmetrical. Histopathological findings included hydropic degeneration of basal epidermal cells, eosinophilic necrosis of individual or groups of keratinocytes, intra-epidermal and sub-epidermal cleft formation and mixed, dermal, perivascular infiltrates. An initiating cause could not be identified in either case. Both horses underwent gradual spontaneous remission within 3 months.
BACKGROUND: Erythema multiforme (EM) is a vesiculobullous disorder with variable manifestations which predominantly affects the skin. It is regarded as a hypersensitivity disorder which is triggered by multiple factors such as infection, drugs and food. Varicella zoster virus (VZV) has rarely been reported as an etiological agent, despite its high incidence as a pathogen in childhood. PATIENTS: We describe two children in whom EM preceded VZV infection. In the first, a 5-year-old boy, EM was followed 3 days later by a classical disseminated varicella eruption. The diagnosis was reached by clinical, epidemiological and serological means. The second patient was a 13-year-old boy with EM which was followed 2 weeks later by Ramsay-Hunt syndrome. The diagnosis was confirmed by skin biopsy, positive serology and viral culture. CONCLUSION: The association of EM and VZV infection is probably more common than reported. In clinical cases of EM, VZV should be included in the list of possible causative agents.
The association between erythema multiforme (EM) and herpes simplex virus (HSV) infection has long been appreciated, although the exact role which HSV may play in the pathogenesis of this herpes-associated EM (HAEM), is unknown. Previous studies have suggested, but not definitively demonstrated, the presence of HSV in lesions of HAEM. The presence of HSV would support the hypothesis that an immune-mediated response directed against HSV-specific antigens in the skin is central to lesion development in HAEM. The purpose of this study was to examine lesions of EM for the presence of HSV DNA by using the polymerase chain reaction (PCR). In addition, in situ hybridization using an HSV-specific RNA probe was performed to further localize the HSV nucleic acids within the skin. DNA was extracted from formalin-fixed, paraffin-embedded specimens of cutaneous lesions of HAEM and also from EM for which no precipitating factor could be documented, otherwise known as idiopathic EM (IPEM). DNA from lesions of bullous pemphigoid served as a negative control. Using PCR to specifically amplify HSV sequences which might be present, and then performing Southern analysis, we demonstrated HSV DNA in 9/13 HAEM and 6/9 IPEM biopsies. No HSV was detected in six lesions of bullous pemphigoid. In situ hybridization of three cutaneous HAEM lesions using an 35S-labeled HSV-specific RNA probe localized the HSV nucleic acids predominantly to the epidermis. Three biopsies of chronic dermatitis, used as negative controls, did not demonstrate this specific hybridization. These findings confirm the presence of HSV in lesions of HAEM and are consistent with the concept of an HSV-specific immune-mediated pathogenesis for this disease. In addition, most cases of IPEM appear to be herpes associated despite the absence of clinically apparent HSV infection.
In a prospective study of erythema multiforme, forty-two cases were selected with the use of defined criteria. In thirty-three cases (79%), the erythema multiforme occurred following a lesion of recurrent herpes simplex; in four cases (10%), it was related to administration of a sulfonamide drug. Herpes-associated erythema multiforme (HEM) was largely recurrent erythema multiforme minor and was characterized histopathologically by inflammatory changes, such as spongiosis and exocytosis, and by focal liquefaction degeneration of the basal cell zone of the epidermis. Sulfa-associated erythema multiforme (SEM) was a nonrecurrent illness with widespread cutaneous and mucosal damage associated with prominent histologic necrosis of epidermal cells. The deposition of C3 and fibrin along the dermoepidermal junction and the deposition of IgM, C3, and fibrin around dermal blood vessels by immunofluorescence microscopy were similar in both groups. Although HEM and SEM may have somewhat different clinical and histologic features, there is significant overlap in the pattern of tissue damage.
We report a case of bullous erythema multiforme caused by an exotic wood, pao ferro (Machaerium scleroxylon). A 25-year-old female, a luthier (guitar maker) who often handles a variety of woods, developed bullous erythema multiforme. A patch test confirmed a positive reaction to one of the exotic woods, pao ferro. A subsequent accidental short contact with pao ferro 5 months following the first incidence induced a similar exudative erythema. Exotic woods such as pao ferro should be added to the list of contact allergens that can induce bullous erythema multiforme.
INTRODUCTION: Persistant erythema multiforme is a rare form of erythema multiforme with subacute typical and atypical lesions that occur during several months. Some cases are associated with chronic viral infection. CASE REPORT: A 23 year-old man, with a past history of intravenous drug addiction and chronic hepatitis C virus infection, presented persistant erythema multiforme for 18 months. The histopathological picture was those of infectious erythema multiforme and the seric total complement level was low. Two courses of alpha-interferon treatment were quickly efficient on cutaneous lesions, and relapse occurred after discontinuation. DISCUSSION: In previously reported cases of persistant erythema multiforme, etiologic complementary investigations are not always specified. However, viral infections should be considered. In cases of chronic infection, hepatitis C may induce immune disorders through persistent antigenic stimulation.
We report a 6-month-old girl with erythema multiforme minor occurring during the course of a herpetic whitlow. Erythema multiforme minor is unusual in infants, and in this population herpes simplex virus has not been reported as a significant etiologic factor. The clinical coexistence of erythema multiforme minor and the herpetic lesion is also atypical. To our knowledge, this is the first report of erythema multiforme minor associated with a concomitant HSV infection in an infant.
Mycoplasma pneumoniae is an important and highly relevant cause of bullous erythema multiforme, isolated mucositis, and Stevens-Johnson syndrome in children. In this article, we present two children with respiratory Mycoplasma pneumoniae infection and associated cutaneous findings within the spectrum of erythema multiforme. We review the literature associating these three entities with Mycoplasma pneumoniae infection and discuss controversies regarding the classification of erythema multiforme, as well as update reported infectious causes of the bullous form. Many understand the erythema multiforme spectrum to include bullous erythema multiforme, mucositis, and Stevens-Johnson syndrome in the order of increasing severity. We feel that this relationship should be reconsidered to help better understand the prognosis and outcomes. It is our opinion that bullous erythema multiforme is a separate, yet related condition that can occur in the context of Mycoplasma pneumoniae infection. With many similarities to mucositis and Stevens-Johnson syndrome, bullous erythema multiforme can be considered part of a spectrum of disease that includes Stevens-Johnson syndrome. Unlike mucositis and Stevens-Johnson syndrome, bullous erythema multiforme caused by Mycoplasma pneumoniae infection has low morbidity for the child. Mycoplasma pneumoniae-associated mucositis and Stevens-Johnson syndrome seem to occur along a spectrum with separate prognosis and potential pathogenesis compared with bullous erythema multiforme. Making the distinction between these conditions is valuable for predicting the child's prognosis. Patients who develop symptoms consistent with these conditions should be appropriately evaluated for Mycoplasma pneumoniae infection and closely monitored.