Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Erythema Multiforme”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1983

Possible drug-induced pemphigus-like antibodies with the clinical manifestation of erythema multiforme.

A patient with bullae and target lesions on the extremities and mucous membranes was seen with the clinical picture of erythema multiforme following an episode of pneumonia and a course of penicillin G potassium and tobramycin sulfate therapy. An unusually high titer of intercellular circulating (IC) antibodies was identified in the serum by indirect immunofluorescence (IF) microscopy, but direct lesional IF microscopy study results were negative. These IC antibodies were not true pemphigus antibodies and can best be termed pemphigus-like antibodies. These antibodies were characterized by their ability to fix complement, in contrast to pemphigus antibodies, which apparently fail to do so.

Antibodies↗
PubMed1993

Infectious mononucleosis presenting as erythema multiforme.

Infectious mononucleosis is rarely associated with skin lesions. A 23-year-old woman with acute infectious mononucleosis who presented with moderately severe erythema multiforme is reported. The role of steroids in the management of this condition is briefly discussed.

Adult↗
PubMed1996

Reversal of erythema multiforme major with cyclophosphamide and prednisone.

OBJECTIVE: To report a case of erythema multiforme (EM) major treated with cyclophosphamide and prednisone. SETTING: General medicine and dermatology consult services, Department of Veterans Affairs Medical Center. CASE SUMMARY: A 44-year-old man with C4-C5 quadriplegia developed a skin reaction characterized by a painful, generalized maculopapular rash, bullae, ulceronecrotic lesions, and mucosal and epidermal sloughing after taking trimethoprim/sulfamethoxazole. The patient was treated with intravenous cyclophosphamide 150 mg infused over 1 hour every 24 hours and oral prednisone 15 mg every 6 hours. After two doses of cyclophosphamide, formation of bullae and epidermal sloughing had ceased, and the erythema was markedly diminished. Cyclophosphamide was discontinued before the third dose because of evolving leukopenia. Prednisone therapy was continued until the patient was discharged on hospital day 5, at which time the dosage was tapered. DISCUSSION: Cyclophosphamide has been used extensively for other dermatologic reactions. Relief of pain and regression of the lesions in our patient occurred more quickly than anticipated. CONCLUSIONS: Treatment of EM major with cyclophosphamide combined with prednisone appeared to be highly successful in this patient. Cyclophosphamide may be an effective, empiric initial treatment in reversing EM major.

Adult↗
PubMedDate not supplied

Recurrent herpes simplex virus infections and erythema multiforme: a report of three patients.

The widespread preoccupation of the media and patients with herpes prompts this report of two patients who developed erythema multiforme, an allergic response to the herpes simplex virus. While this complication is not new, physicians and nurses working in clinics for sexually transmitted diseases should be aware of this allergic response to infection with herpes simplex virus.

Adult↗
PubMed1997

Epidermal apoptotic cell death in erythema multiforme and Stevens-Johnson syndrome. Contribution of perforin-positive cell infiltration.

OBJECTIVE: To clarify the mechanism of epidermal cell death in erythema multiforme. DESIGN: Retrospective study. SETTING: Academic referral center. PARTICIPANTS: Nine patients with Stevens-Johnson syndrome (SJS), 9 patients with Hebra disease (EMH), and 5 healthy volunteers. INTERVENTIONS: Biopsy specimens were obtained from the border of the fresh lesions before treatment. Control specimens were obtained from normal skin. MAIN OUTCOME MEASURES: Histopathological epidermal apoptosis detected with nuclear DNA fragmentation and counts of dermal immunoreactive perforin-positive infiltrates were compared between SJS and EMH. RESULTS: Eight patients (89%) with SJS showed clear apoptosis with keratinocyte DNA fragmentation. All SJS samples had intensive perforin-positive dermal infiltrates. Only 3 patients (33%) with EMH showed apoptotic change, and it was to a far less extent with far less dermal perforin-positive infiltrates. Control specimens showed no apoptotic cells in the epidermis or expression of perforin in the dermis. CONCLUSIONS: Perforin mediates apoptosis in the pathogenesis of the epidermal cell changes in SJS but not in EMH. In addition to the differences in clinical severity and histopathological conditions, our findings indicate a pathogenic difference between SJS and EMH.

Antibodies, Monoclonal↗
PubMed1996

Autoantibodies against desmoplakin I and II define a subset of patients with erythema multiforme major.

In a previous report, we described autoantibodies against the desmosomal plaque proteins desmoplakin I and II (dp I and II) in patients with erythema multiforme (EM) major. In the present study we investigated ten EM major and eight EM minor patients for circulating autoantibodies and performed clinical and immunomorphological evaluations. Seven out of ten EM major patients revealed anti-dp I and II autoantibodies. Antigens were biochemically characterized by Western blotting and immunoprecipitation of epithelial-cell-derived protein extracts. These autoantibodies bind in vivo to lesional skin/mucosa in a pemphigus-type dotted pattern along the cytoplasmic membranes of keratinocytes. Ultrastructural immunolocalization studies confine in vivo bound autoantibodies to the cytoplasmic desmosomal plaque. Autoantibody binding studies with the sera of such patients demonstrate that the target antigens are not restricted to squamous epithelia but are also expressed in simple and transitional epithelia, on hepatocytes, and on cells of mesenchymal origin, e.g., myocardial cells. Comparing the clinicopathological features of ten patients with EM major, we could not define any discriminating clinical symptoms among patients with or without autoantibodies. Histopathological examination, however, revealed that only patients with EM major and autoantibodies against dp I and II show suprabasal acantholysis in lesional skin and mucous membranes, suggesting a potential role of the humoral immune response in the pathogenesis of this disease. These findings suggest that these autoantibodies define a subset of patients within the clinical spectrum of EM.

Adult↗
PubMed1998

Erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis in northeastern Malaysia.

BACKGROUND: Previous studies have reported that drugs and infections are common causes of erythema multiforme (EM) and Stevens-Johnson syndrome (SJS). Toxic epidermal necrolysis (TEN) is mainly related to drugs. No study has been conducted in Kelantan, the northeastern state of Malaysia, to assess these cutaneous reactions. METHODS: A retrospective study of all hospitalized cases of EM, SJS, and TEN was conducted covering an 8-year period from 1987 to 1994. RESULTS: There were four cases (13.8%) of EM, 22 cases (75.9%) of SJS, and three cases (10.3%) of TEN. Drugs as a definitive cause was observed in one case (25%) of EM, 12 cases (54.5%) of SJS, and two cases (66.7%) of TEN. Drugs as a probable cause was observed in seven cases (31.8%) of SJS and one case (33.3%) of TEN. The male to female ratio was equal in EM and SJS. Antiepileptics were the commonest culprits, followed by antibiotics. One patient died of SJS and one patient died of TEN, giving mortality rates of 4.5% and 33.5% respectively. Fever was noted in 18 patients (62.1%). Leukocytosis was noted in 10 patients (34.5%), and nine patients (31.0%) had elevated liver transaminase enzymes. No significant correlation was noted between these biochemical changes and cutaneous eruption. Secondary infections were observed in 11 patients (37.9%): Staphylococcus aureus was the commonest isolated organism. CONCLUSIONS: This study shows that drugs remain the commonest culprit in SJS and TEN. Despite adequate treatment, the mortality rate remains high, especially in TEN. These findings are similar to those of other reported studies.

Adolescent↗
PubMed1995

Erythema multiforme with mucous membrane involvement and Stevens-Johnson syndrome are clinically different disorders with distinct causes.

BACKGROUND AND DESIGN: It was recently suggested that erythema multiforme (EM) majus and Stevens-Johnson syndrome (SJS) could be separated as two distinct clinical disorders with similar mucosal erosions but different patterns of cutaneous lesions. To test that hypothesis, we made a single-center retrospective study of severe EM with skin and mucosal involvement. Based on a review of clinical photographs, the skin lesions were reclassified as EM when these lesions were made of typical or raised atypical targets that were located on the extremities and/or the face, or as SJS when these lesions were made of flat atypical targets or purpuric maculae that were widespread or distributed on the trunk. Another investigator who was blinded for that clinical classification related each case to its more probable cause (eg, herpes infection or drug-induced reaction), by using scores derived from the medical charts. RESULTS: The majority (80%) of 76 cases could be classified as one of the two disorders: 28 as EM (37%), 33 as SJS (43%), and 15 as "undetermined" (20%). By using causal scores, the 76 cases were classified as herpes-induced (n = 18 [24%]), drug-induced (n = 40 [52%]), and "other" (n = 18 [24%]). There was a strong correlation between the clinical classification and the probable cause (K = 0.87, P < .001). Specifically, EM was mostly related to herpes (17 of 28 cases) or to other causes (eight of 28 cases); however, EM was rarely related to drugs (three of 28 cases), while SJS was nearly always related to drugs (28 of 33 cases) and never to herpes. CONCLUSIONS: The results of this study support the suggestion that EM with mucosal lesions and SJS could be distinguished on the basis of two different clinical patterns. In addition, a strong relationship was observed between each pattern and specific causes. This is one more piece of evidence that suggests that EM with mucosal lesions and SJS are actually two different diseases.

Adolescent↗
PubMed1999

Acarbose-induced generalised erythema multiforme.

A 58-year-old man with diabetes mellitus was treated with acarbose 300 mg daily. 13 days after the start of treatment with acarbose, generalised erythema multiforme developed with blood eosinophilia. Tissue eosinophilia was also found histologically. A challenge test for acarbose confirmed allergic reaction clinically and histologically.

Acarbose↗
PubMed1989

Erythema multiforme following cardizem therapy: report of a case.

A 63-year-old male developed severe, painful ulcerations shortly after beginning therapy for angina with diltiazem (Cardizem). Erythema multiforme is a common adverse reaction to medications. The case report, as well as the role of the dentist in diagnosis and management of these clinical presentations, is discussed.

Diltiazem↗
PubMed2003

Detection of herpes simplex virus genomic DNA in various subsets of Erythema multiforme by polymerase chain reaction.

BACKGROUND: The wide variation in the detection of herpes simplex virus (HSV) DNA (36-75%) by polymerase chain reaction (PCR) in erythema multiforme (EM) may be partly attributed to differences in case selection in terms of subsets of EM studied. OBJECTIVE: To determine the frequencies of detection of HSV DNA in specific subsets of EM. METHODS: Nested PCR was used to detect HSV DNA in skin biopsies with histologically proven EM. RESULTS: PCR was performed on skin biopsies from 63 patients with EM. HSV DNA was detected in 3/11 (27.2%) of single-episode HSV-associated EM (HAEM), 6/10 (60%) of recurrent HAEM, 1/4 (25%) of single-episode idiopathic EM and 6/12 (50%) of recurrent idiopathic EM. HSV DNA was not detected in atypical EM (0/11), suspected drug-induced EM (0/9) or Stevens-Johnson syndrome (0/6). CONCLUSION: The overall PCR positive rates of HAEM (42.9%) and idiopathic EM (43.8%) were comparable suggesting that idiopathic EM is likely to be related to a subclinical HSV infection.

Biopsy↗
PubMed1993

The herpes-specific immune response of individuals with herpes-associated erythema multiforme compared with that of individuals with recurrent herpes labialis.

Infection with herpes simplex virus (HSV) is the most common precipitating factor in the development of erythema multiforme (EM). It is not known why only a few of the many individuals who experience recurrent HSV infection also develop herpes-associated EM (HAEM), although a difference in the HSV-specific immune response has been postulated. The purpose of this study was to compare the HSV-specific immune response of individuals with HSV infection alone with that of individuals with HAEM. There were 21 patients in each of the two groups. Four parameters of the HSV-specific immune response were examined: (1) anti-HSV IgG titers were measured by ELISA; (2) antibody neutralization was assessed using a plaque assay; and (3) antibody-dependent complement-mediated cytotoxicity, and (4) antibody-dependent cellular cytotoxicity were investigated using a previously described in vitro HSV-specific cytotoxicity assay. No statistically significant differences were detected between the two patient groups. Thus, a difference in these HSV-specific immune mechanisms does not explain the development of HAEM in some individuals with recurrent HSV infection.

Antibody Formation↗