[Intense erythema multiforme and erythema nodosum of primary tuberculous infection].
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Erythema multiforme follows administration of several drugs or infection with various agents, including herpes simplex virus, a syndrome designated herpes simplex virus associated erythema multiforme. Lesional skin from 21 of 26 (81%) herpes simplex virus associated erythema multiforme patients was positive for herpes simplex virus gene expression as evidenced by reverse transcriptase-polymerase chain reaction with primers for DNA polymerase and/or immunohistochemistry with DNA polymerase antibody. Reverse transcriptase-polymerase chain reaction and immunohistochemistry studies indicated that herpes simplex virus associated erythema multiforme lesional skin from 16 of 21 (76%) DNA polymerase positive herpes simplex virus associated erythema multiforme patients was also positive for interferon-gamma, a product of T cells involved in delayed-type hypersensitivity (p < 0. 0001 by Pearson correlation coefficient). Interferon-gamma signals were in infiltrating mononuclear cells and in intercellular spaces within inflammatory sites in the epidermis and at the epidermis/dermis junction. Herpes simplex virus lesional skin was also positive for DNA polymerase [five of five (100%)] and interferon-gamma [four of five (80%)], but lesional skin from drug-induced erythema multiforme patients was negative. Lesional herpes simplex virus associated erythema multiforme keratinocytes also stained with antibody to transforming growth factor-beta [14 of 23 (61%)] and cyclin-dependent kinase inhibitor waf [12 of 18 (67%)]. Staining was also seen in keratinocytes from herpes simplex virus lesions [five of five (100%)], but not in normal skin. By contrast, staining with antibody to tumor necrosis factor-alpha, another pro-inflammatory cytokine, was seen in seven of 11 (64%) drug-induced erythema multiforme patients, but not in herpes simplex virus or herpes simplex virus associated erythema multiforme patients, and lesional keratinocytes from drug-induced erythema multiforme patients were negative for transforming growth factor-beta and cyclin-dependent kinase inhibitor waf. We interpret the data to indicate that herpes simplex virus associated erythema multiforme pathology includes a delayed-type hypersensitivity component and is mechanistically distinct from drug-induced erythema multiforme.
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INTRODUCTION: The objective of this study was to evaluate the efficacy of thalidomide in the treatment of chronic erythema multiforme unresponsive to usual treatments. PATIENTS AND METHODS: Twenty-six patients with chronic erythema multiforme were given thalidomide 100 mg/day after other treatments had failed, particularly acyclovir and prednisone. RESULTS: Twenty patients had recurrent erythema multiforme and were given thalidomide at the beginning of an episode. The duration of the episodes was reduced by 11 days on the average. Six of the patients had subintrant erythema multiforme and were given continuous treatment. Lesions disappeared within 5 to 8 days and remission was maintained with low dose-treatment. DISCUSSION: The spectacular results obtained here should be verified in a controlled study.
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We report two cases of borreliosis (Lyme disease) with unusual cutaneous manifestations, erythema multiforme, and persistent erythema. The lesions in both of our patients had distinctive histopathologic features. To our knowledge, this is the first report of erythema multiforme and persistent erythema as early cutaneous manifestations of Lyme disease.
Recurrent erythema multiforme is one of three distinct clinical subtypes of erythema multiforme. We present a 42-year-old man with a 10-year history of recurrent herpes simplex virus-induced erythema multiforme. Our patient was debilitated by the frequency of his attacks and the associated pain, for which he often required leave from work. The frequency, duration and morbidity of the attacks were poorly controlled using oral prednisone and oral aciclovir. Three episodes of his recurrent herpes simplex virus-induced erythema multiforme were treated with intermittent oral cyclosporin. Oral cyclosporin rapidly reduced his symptoms and led to rapid resolution of his erythema multiforme, provided the cyclosporin was commenced on day 1 or 2 of the erythema multiforme episode. Consequently, his quality of life has dramatically improved. We recommend the use of intermittent oral cyclosporin for recurrent, debilitating episodes of erythema multiforme.
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Skin lesions of erythema multiforme show time-dependent changes from early papular erythema to the late target lesion which consists of a peripheral elevated erythematous area and a central depressed area. We investigated the pathomechanism of erythema multiforme, by examining the papular erythema and target lesion separately. In the early papular erythema, a small number of polymorphonuclear leukocytes and nuclear debris were seen intermingled with mononuclear cells around the slightly swollen blood vessels, on which immunoglobulin and complement components were deposited. Circulating immune complex levels were occasionally elevated. Sera from the patients generated high levels of reactive oxygen species and nitroblue tetrazolium test revealed positive reaction on the infiltrating cells around the blood vessels. These findings suggest that the papular erythema develops via incomplete type III allergic reaction, followed by damage through reactive oxygen species. In the target lesion, the activity of histamine-N-methyltransferase, which is the major histamine-degrading enzyme, was markedly decreased in the peripheral elevated erythematous area and it was recovering in the central clearing area. ICAM-1 and HLA-DR antigens were expressed on the surfaces of the keratinocytes. An increased number of epidermal Langerhans cells and CD4 cell infiltration were observed in the peripheral elevated erythematous area, while a decreased number of epidermal Langerhans cells and CD8 cell infiltration in the central depressed area were observed. These findings suggest that impaired histamine metabolism and cellular allergic reactions play important roles in the development of the target lesion.
A subset of erythema multiforme (erythema multiforme) is associated with herpes simplex virus (HSV) infection; viral cultures of erythema multiforme lesions are, however, usually negative and viral antigens difficult to identify. Polymerase chain reaction (PCR) has been used to demonstrate the association, hence, is currently the only available sensitive diagnostic means for HSV-associated erythema multiforme. A nested PCR, which could simultaneously detect and genotype HSV in erythema multiforme lesions and in clinical swab specimen was developed using the DNA polymerase gene of HSV as target gene because it is the only detectable HSV gene in a high proportion of erythema multiforme lesions. The PCR has demonstrated its robust sensitivity on swab samples by being able to detect further 45.3% HSV cases in comparison with virus isolation with 100% specificity in both detection and genotyping confirmed by virus isolation and DNA sequencing. This study represents the first investigation of typing HSV virus in HSV-associated erythema multiforme patients, and the finding that 66.7% of the patients was attributed to HSV1, 27.8% to HSV2, and 5.6% to HSV1 and 2 co-infection may reflect the distribution of HSV1 and 2 in local general population.
Erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis are related disorders of skin and mucous membranes, which are typically associated with antecedent medication use or infection. We review 108 cases of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis from Texas Children's Hospital, Houston, Texas, from 1981 to 1991, and illustrate the characteristic skin and mucosal lesions. In addition, we describe in detail two unusual cases requiring intensive airway management. Head and neck manifestations were present in 4 of 79 patients (5%) with erythema multiforme and 26 of 28 patients (93%) with Stevens-Johnson syndrome. In Stevens-Johnson syndrome, mucosal involvement of the lip (93%), conjunctiva (82%), oral cavity (79%), and nose (36%) were most common. Antecedent medication use was identified in 59% of erythema multiforme patients and 68% of Stevens-Johnson syndrome patients. We note a striking increase in the number of cases in our series caused by cephalosporins. Fifty percent of Stevens-Johnson syndrome patients required supplemental hydration or alimentation because of the severity of the oral cavity involvement. The head and neck mucosal manifestations largely respond to local care, and the routine use of prophylactic antibiotics or systemic steroids is not recommended.
Erythema multiforme is a vesiculobullous condition that may affect skin and/or mucosa. Oral lesions are characterized by hemorrhagic crusting of the lips and ulceration mainly of the non-keratinized mucosa. This paper describes a patient who presented with gingival lesions as well as the more typical oral signs of erythema multiforme.