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Results for “Erythema Multiforme”

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PubMed1992

Herpes simplex virus in childhood erythema multiforme.

Although an association between herpes simplex virus (HSV) infection and erythema multiforme (EM) minor has been documented in adults, this has not been reported in the pediatric population. This study assessed the potential role of HSV infection in the pathogenesis of EM minor in children. Erythema multiforme skin lesions from 20 children, aged 1 to 16 years, were examined for the presence of HSV by using the polymerase chain reaction. The children included all fit strict clinical criteria for EM minor. Ten had a clinical history of an antecedent herpes infection ("herpes-associated EM"), and 10 did not ("idiopathic EM"). Herpes simplex virus DNA was detected in skin lesions of 8 of 10 children with herpes-associated EM and in 8 of 10 with idiopathic EM. Control skin biopsies from children with other bullous inflammatory diseases were negative. In addition, no HSV could be detected in a biopsy of normal uninvolved skin of a child in whom HSV was present in lesional skin. In situ hybridization on selected biopsies by means of an HSV-specific riboprobe confirmed the presence of HSV and localized it to the epidermis. It is concluded that HSV is a significant precipitating factor for EM minor in children, as it is in adults, and that clinicians should maintain a high index of suspicion of HSV even in the absence of a known history of herpes infection.

Adolescent↗
PubMed1995

Erythema multiforme associated with superficial fungal disease.

An extremely rare case of erythema multiforme associated with dermatophytosis by Trichophyton rubrum infection was reported in a 19-year-old woman. She had a reddish plaque resembling annular ringworm on her left arm. Treatment with an antifungal cream (clotrimazole) on the infected site cleared the condition in three weeks. Spontaneous regression of erythema multiforme in different parts of the body was recognized when the ringworm infection resolved. In recent years, only two cases have been reported in the English literature.

Adult↗
PubMed1985

Drug-induced erythema multiforme: a possible immunologic pathogenesis.

A 37-year-old female developed erythema multiforme 17 days after beginning carbamazepine for complex partial seizures. The carbamazepine was discontinued and phenytoin begun. A new rash developed and phenytoin therapy was stopped. In vitro immunologic studies were conducted in an effort to understand the pathogenesis of the rashes. Enhancement of stimulated in vitro lymphocyte proliferation from the patient occurred in the presence of carbamazepine and phenytoin. Neither drug had an enhancing effect on lymphocyte proliferation from a control subject. These data, together with clinical data, strongly suggest an immunologic pathogenesis for drug-induced erythema multiforme.

Adult↗
PubMed1983

HLA antigen frequency in erythema multiforme and in recurrent herpes simplex.

In this study the HLA antigen frequency was determined in a group of patients with erythema multiforme and in a separate group of patients with recurrent herpes simplex to establish whether either disease had any antigens whose frequency deviated from that of a normal population. The frequency of HLA-B15 was significantly increased in both patient groups (P less than 0.5). The increase in the erythema multiforme group does not appear to be due to the fact that some of the erythema multiforme patients have associated herpes simplex and this increase remained significant after further correction for the number of antigens tested.

Adolescent↗
PubMed2004

Erythema multiforme minor following vaccination with paediatric vaccines.

We present 2 cases of erythema multiforme following a combined tetanus and diphtheria revaccination and a combined diphtheria, tetanus, acellular pertussis inactivated polio and Haemophillus influenzae type B vaccine respectively, suggesting vaccines containing diphtheria and tetanus toxoids as a potential precipitating factor to erythema multiforme.

Diphtheria-Tetanus-Pertussis Vaccine↗
PubMed1994

Eosinophils in oral and cutaneous lesions of erythema multiforme.

The purpose of this retrospective clinicopathologic study was to investigate the presence of eosinophils in oral and skin lesions of erythema multiforme. Seventeen cases were selected which fulfilled clinical and histopathologic criteria for the disease. Twelve out of 13 sections taken from skin biopsies and 4 out of 5 sections taken from oral lesions contained eosinophils in varying densities. The occurrence of eosinophils in the lesions of erythema multiforme is parallelized and discussed with the existence of certain clinical and histopathologic aspects. Therefore, we suggest that eosinophils occur in cutaneous and oral lesions of erythema multiforme and are occasionally numerous.

Adult↗
PubMed2005

Erythema multiforme following polymorphic light eruption: a report of two cases.

We report two patients in whom episodes of polymorphic light eruption were followed by recurrent erythema multiforme on exposed and nonexposed sites. Treating the polymorphic light eruption with prophylactic PUVA and/or oral prednisolone or cyclosporin prevented the development of erythema multiforme, suggesting that the two events are related. It is possible that erythema multiforme develops as a response to the same causative antigen as polymorphic light eruption.

Adult↗
PubMed1994

Examination of non-involved skin, previously involved skin, and peripheral blood for herpes simplex virus DNA in patients with recurrent herpes-associated erythema multiforme.

The association between infection with HSV and the subsequent development of erythema multiforme is well established, although the role that the virus plays in the pathogenesis of this disorder is not known. HSV DNA has been detected in cutaneous lesions of herpes-associated erythema multiforme (HAEM), and it has been suggested that the tissue damage seen in these lesions is virus-specific. In the current, prospective study, we examined biopsies of lesional, non-involved, and previously involved but healed skin, in addition to specimens of peripheral blood, from patients with HAEM, for HSV DNA by using the polymerase chain reaction. HSV DNA was detected in lesional skin of 10 of 11 patients compared to 2 of 11 non-involved skin biopsies obtained at the same time. HSV was present in 4 of 6 blood specimens obtained during the acute episode. Five patients returned 3 months after the acute episode resolved for biopsies of previously involved skin. HSV was detected in 4 of these 5 biopsies. Thus, the presence of HSV DNA in the skin of patients with HAEM appears to be predominantly in areas of clinical involvement; the virus remains in those cutaneous sites for up to 3 months without evidence of clinical disease; and HSV DNA may be detected in the peripheral blood cells during acute HAEM. Based on these findings, we suggest that the virus plays a role in lesion development, that the skin may function as a site of viral persistence, and that hematogenous spread of viral DNA may be an important factor in the development of HAEM.

Blood↗
PubMed1991

Erythema multiforme after contact dermatitis in response to an epoxy sealant.

A case of erythema multiforme associated with an allergic contact dermatitis in response to an epoxy-based compound is presented. Patch tests revealed a positive reaction to both the epoxy resin and the hardener. Chemicals applied directly to the skin should be considered as a potential cause of erythema multiforme.

Arm↗
PubMed1980

Histopathologic spectrum of oral erythema multiforme.

The histopathologic tissue patterns found in twenty-five patients with oral erythema multiforme were as variable as the clinical appearances. The biopsies served an important role in ruling out malignancy, dysplasia, and other classified diseases. While all of the specimens were designated as showing nonspecific inflammatory reactions, in many biopsy specimens there were sufficient characteristic connective tissue and epithelial changes to suggest a tissue diagnosis consistent with the clinical diagnosis of erythema multiforme.

Adult↗
PubMed1978

Erythema multiforme and the Stevens-Johnson syndrome.

Erythema multiforme (EM) is clinically characterized by a "minor" form and a "major" form. The latter is known as the Stevens-Johnson syndrome. Infections (particularly herpes simplex and Mycoplasma pneumoniae) and drugs seem to predispose toward the development of EM. The pathogenesis is poorly understood. The treatment is supportive. Prognosis varies with the severity of the eruption. Recurrences are commonly seen.

Diagnosis, Differential↗
PubMed2006

Polyhexamethylenebiguanide hydrochloride exposure and erythema multiforme in a physician.

A 52-year-old woman physician developed recurrent erythema multiforme. Occupational and environmental exposure assessment suggested a disinfectant containing polyhexamethylenebiguanide hydrochloride (PHMB), Phagosept. Elimination of the product was followed by disappearance of symptomatology. Literature search revealed cases of sensitization and anaphylaxis due to contact with PHMB, but to our knowledge, this is the first report on PHMB-induced erythema multiforme.

Biguanides↗
PubMedDate not supplied

Erythema multiforme, potential complicating factor in dental therapy.

Erythema Multiforme, (E.M.) is an interesting dermatologic disease which has oral manifestations. It presents a diagnostic dilemma because the oral cavity has the ability to produce varied manifestations. The range of possible etiologies fo oral disease is immense. Therefore, the dentist must have a differential diagnosis for all oral lesions. The following case report represents a differential diagnosis problem which hampered routine dental therapy. The oral soft tissue lesions needed to be managed before the endodontic therapy could be completed.

Adult↗
PubMedDate not supplied

Erythema multiforme: a literature review and case report.

Erythema multiforme is a florid mucocutaneous disease characterized by oral, cutaneous, and ocular manifestations. The cutaneous lesions are pathognomonic because of their unique "target-like" appearance. A severe form of EM has been termed "Stevens-Johnson Syndrome". Although the etiology of EM is unknown, much of the research suggests an immunological association with HSV. The diagnosis of EM is based on signs and symptoms, and a differential diagnosis should include other ulcerative, mucocutaneous diseases, such as erosive lichen planus, pemphigus, varicella zoster, ANUG, TEN, aphthous stomatitis, and primary HSV. Therapeutic measures are palliative, including a soft bland diet, topical anesthetics, and corticosteroids. A case of EM is described which underscores the appearance of the disease and its clinical course.

Adult↗
PubMed1992

Clinical response to levamisole in thirty-nine patients with erythema multiforme. An open prospective study.

Patients with erythema multiforme (EM) often have chronic or recurring oral lesions that cause intense pain and interfere with a variety of functions including eating and speech. Previous studies suggest that levamisole restores to normal the function of phagocytes and T lymphocytes, and activates the inflammatory response. In our previous double-blind study 8 of 13 patients with EM had a decrease in severity and frequency of attacks. The purpose of this open prospective study was to evaluate short-term and long-term clinical efficacy of levamisole in patients with mucocutaneous EM. Thirty-nine patients with mucocutaneous EM seen in the Oral Medicine Clinic, School of Dentistry, University of California-San Francisco, comprised our study group. Levamisole was used alone in 17 patients or in combination with prednisone in 22 patients and was given as a single dose of 150 mg/day for 3 consecutive days. Thirty-one patients showed a complete response from levamisole (alone in 13 and in combination with prednisone in 18). Four showed a partial response of signs and symptoms, and four others had no benefits from levamisole whether alone or in combination. The most common side effects from levamisole were skin rash, tiredness, weakness, myalgia, taste change, and insomnia.

Adolescent↗
PubMed1999

[Erythema multiforme. A heterogeneous pathologic phenotype].

The term Erythema Multiforme (EM) include actually a wide range of clinical expressions, from exclusive oral erosions (Oral EM) to mucocutaneous lesions (EM Minor), sometimes with severe involvement of multiple mucosal membrane (EM major, Stevens-Johnson syndrome [SJS]) or with involvement of a large area of the total body surface (toxic epidermal necrolysis [TEN]). However, this terminology is not worldwide accepted and often the various clinical categories show some overlapping features. Among the great number of suspected etiological factors, herpes simplex virus is involved in many cases of EM minor whereas SJS and TEN are caused in 80% of cases by systemic drugs, mainly by anticonvulsivants, sulfonamides, nonsteroidal anti-inflammatory drugs and antibiotics. Several oral EM seem idiopathic, but data on this topic are very few. There is no specific or consistent microscopic and immunopathologic pattern of EM and the diagnosis should be done by excluding other similar diseases. The treatment include the use of antivirals for EM minor, mainly if recurrent, and of immunosuppressants (especially systemic corticosteroids) for SJS. TEN patients require adequate supportive care and often they have to be treated in emergency departments. Finally, patients with exclusive oral lesions may be treated with both topical and systemical corticosteroids.

Adolescent↗
PubMed2005

CD34+ cells in the peripheral blood transport herpes simplex virus DNA fragments to the skin of patients with erythema multiforme (HAEM).

Herpes simplex virus (HSV)-associated erythema multiforme (HAEM) is a recurrent disease characterized by the presence and expression of HSV DNA fragments in lesional skin. Our studies examined the mechanism of viral DNA transport to the skin of HAEM patients. CD34+ cells were isolated from the blood of normal subjects and HSV and HAEM patients during acute lesions and at quiescence. They were cultured with cytokines that favor their differentiation into Langerhans cells (LC) precursors (CD1a+/CD14-) and examined for HSV replication, HSV-induced cellular alterations, viral DNA fragmentation, and clearance. CD34+ cells from all study groups were non-permissive for HSV replication but infection favored their differentiation into CD1a+/CD14- LC precursors and upregulated E-cadherin expression, thereby assisting LC targeting to the skin. Only HAEM patients had CD34+ cells that retained viral DNA fragments, notably polymerase DNA, for at least 7 d of in vitro culture. The percentages of circulating CD34+ (and CD34+/CLA+) cells were significantly higher in HAEM patients at the time of acute lesions. A similar increase was not seen for HSV patients. The data are the first report implicating CD34+ cells in HAEM pathogenesis, likely by transporting HSV DNA fragments to lesional skin.

Adult↗