[Etiological and clinical data on diseases of the erythema multiforme group].
Explore the source record for details and available documents.
Erythema Multiforme↗
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.
Erythema multiforme associated with contact dermatitis to poison ivy: three cases and a review of the literature.
Erythema multiforme (EM) is a hypersensitivity reaction that occurs mainly after exposure to certain medications or in the setting of infection, most commonly that due to herpes simplex virus. Rare cases of EM have been reported after allergic contact dermatitis due to various substances. There has been one case in the literature of EM following Rhus contact dermatitis. We report three patients who developed EM after allergic contact dermatitis due to poison ivy. In all three patients, targetoid lesions developed primarily on the palms and soles, either after a brief course of prednisone or during its taper. Two of the patients have had more than one episode of EM after poison ivy dermatitis. Although EM has been described after allergic contact dermatitis due to a variety of antigens (nickel being the most common), there is only one report in the literature of EM following Rhus contact dermatitis. Given the prevalence of allergic contact dermatitis due to poison ivy, this may be an under-reported complication.
Adolescent↗
Detection of HSV-specific DNA in biopsy tissue of patients with erythema multiforme by polymerase chain reaction.
Formalin-fixed paraffin-embedded skin biopsies of lesions of erythema multiforme (EM) from 32 patients and 13 controls were examined for the presence of herpes simplex virus (HSV) by polymerase chain reaction (PCR) and for histological findings by direct immunofluorescence and staining with haematoxylin and eosin. HSV-specific DNA was detected in 23 (72%) patients. A history of recurrent skin rash was present in 59% of the PCR-positive cases, while 55% had had suspected HSV infections. Only two PCR-positive specimens were found in patients without a history of recurrent rash and/or previous oral lesions. One biopsy was positive for HSV by conventional cell cultures. There was no significant difference in histology between HSV-related and HSV-negative cases of EM. In the 13 control specimens [bullous pemphigoid (3), dermatitis herpetiformis (2), lichen planus (1), aphthous ulcer (1), fixed-drug eruption (1), varicella-zoster (1), hypereosinophilic syndrome (1), photocontact dermatitis (1), contact dermatitis (1), and cellulitis (1)], no HSV-DNA was detected.
Adult↗
Expression of herpes simplex virus DNA fragments located in epidermal keratinocytes and germinative cells is associated with the development of erythema multiforme lesions.
Skin from acute and healed herpes simplex virus or herpes simplex virus-associated erythema multiforme (HAEM) lesions was examined by polymerase chain reaction with primers for DNA polymerase, ICP8, thymidine kinase (5' end of herpes simplex virus genome), and ICP27 (3' end of herpes simplex virus genome). The primers were herpes simplex virus specific and equally sensitive. The four herpes simplex virus genes were seen in acute herpes simplex virus lesions, but except for one patient, only polymerase (or polymerase and ICP8) were seen in 7-d healed lesional skin. Herpes simplex virus DNA was not seen 1-1.5 mo after healing. HAEM skins from 18 of 24 patients (75%) were positive for polymerase DNA and four of 24 (17%) were also positive for ICP8 or thymidine kinase DNA. Only one tissue (4%) was positive for polymerase, ICP8, and ICP27 DNA. Skin from healed HAEM lesions was still polymerase DNA positive 1-3 mo after lesion resolution. The polymerase DNA signal was in the basal and spinous cell layers of the epidermis and in the outer root sheath of the hair follicle. Polymerase RNA was identified by reverse transcriptase polymerase chain reaction in skin from acute, but not healed polymerase DNA positive HAEM lesions, suggesting that polymerase expression is associated with HAEM lesion development.
DNA Fragmentation↗
Dimorphic exanthema manifested as reticular maculopapular exanthema and erythema multiforme major associated with pyrazolon derivatives.
The non-steroidal anti-inflammatory drugs, especially various pyrazole or pyrazolon derivatives, were one of the classes of drugs commonly implicated in erythema multiforme or Stevens-Johnson syndrome/toxic epidermal necrolysis. Reticular exanthem was a rare morphological pattern of maculopapular drug eruptions. Here we report a case of dimorphic exanthema presenting with partly reticular maculopapular exanthema and erythema multiforme-like lesions, associated with pyrazolon derivatives. Patch testing showed negative reaction to the suspected drugs. The possible mechanism underlying the association of dimorphic exanthema with NSAIDs is discussed.
Aged↗
Lichen planus, erythema nodosum, and erythema multiforme in a patient with chronic hepatitis C.
After identification of the hepatitis C virus (HCV) in 1989, evidence was established supporting its role in the pathogenesis of a number of cutaneous diseases. This evidence ranges from mere epidemiologic associations, such as lichen planus, to molecular biological investigations that have identified the virus in the pathologic tissues of cutaneous vasculitis, vasculitis with mixed cryoglobulinemia, and porphyria cutanea tarda. We describe a 52-year-old man who was diagnosed with chronic hepatitis C, preceding the appearance of lichen planus, erythema nodosum, and erythema multiforme that coincided with the reactivation of viral replication.
Erythema Multiforme↗
Drug eruption (erythema multiforme type) due to a digestive enzyme drug.
An 84-year-old Japanese male had pruritic indurated erythema on his upper limb and left lower abdomen, which had developed abruptly two months before visiting our hospital. Hematological examination showed eosinophilia, 550/mm3. Histopathological findings were suggestive of erythema multiforme in response to a drug. By means of patch tests and a p.o. challenge test, Aczym, a digestive enzyme drug, was shown to be the cause of his condition. Further study revealed that the specific ingredients involved were pancreatin and Taka-diastase. An eruption resulting from ingestion of a digestive enzyme drug has not previously been reported.
Aged↗
Bullous erythema multiforme following herpes zoster and varicella-zoster virus infection.
Four cases of herpes zoster-induced bullous erythema multiforme (EM) are reported. Three patients presented with widespread skin lesions 10 to 14 days after an episode of thoracic herpes zoster. In these patients a high increase in varicella-zoster virus (VZV) antibody titer was detected, indicating secondary VZV infection. Histologic examinations of skin biopsy from a patient with widespread lesions (case 4) revealed a mixture of EM, toxic epidermal necrolysis and herpetic virus infection. VZV should be included in the list of infectious agents able to trigger EM and Stevens-Johnson syndrome.
Acyclovir↗
Erythema multiforme (Stevens-Johnson syndrome)--chart review of 123 hospitalized patients.
The charts of 123 patients hospitalized with erythema multiforme were reviewed. Antecedent infections and the administration of drugs were associated with 15 and 32% of the cases, respectively. Pyrexia arthralgia, photosensitivity, abnormal liver function tests and abnormal urine sediment were common findings. The length of stay in hospital was 12.6 +/- 0.7 days (mean +/- SE), time to initial improvement after onset was 10.3 +/- 0.6 days and time to complete resolution was 23.0 +/- 2.4 days. The presence of bullous skin lesions and greater overall severity were associated with longer hospitalization. Antecedent respiratory tract symptoms were related to shorter hospitalization. Steroid therapy was not associated with a shorter time for initial improvement to occur, while the average length of stay in hospital was 4.2 days longer than that for the patients not treated with corticosteroid.
Age Factors↗
Herpes simplex virus-associated erythema multiforme in prepubertal children.
OBJECTIVE: To examine clinical associations, evolution of the condition, and response to treatment of erythema multiforme (EM) in prepubertal children. DESIGN: A retrospective case series evaluation of children younger than 13 years with EM. SETTING: Ambulatory care university hospital. PATIENTS: Referral patients from pediatricians serving a population of 3.2 million. INTERVENTIONS: Results of treatment of each EM episode with topical acyclovir or oral acyclovir at a dose of 25 mg/kg per day and 6-month prophylaxis with oral acyclovir at a dose of 20 mg/kg per day were evaluated. OUTCOMES: Age at EM onset, preceding illness, and number and duration of episodes during a 3-year period were recorded. RESULTS: Twelve children (7 boys and 5 girls) in whom herpes simplex virus (HSV)-associated EM developed were evaluated. Preceding lesions were herpes labialis in 8 children and herpes facialis in 2 children. Two children had no obvious HSV lesion. The mean age at onset of disease was 8.1 years, and the mean time from the preceding HSV to the onset of skin lesions was 3.9 days (range, 0-11 days). Episodes of EM lasted a mean of 10.6 days. In 9 children, the EM was recurrent, with a mean of 2.6 episodes per year. All 12 children, including those with negative viral cultures for HSV or no HSV history had HSV detected in their target lesions by polymerase chain reaction amplification of DNA obtained from skin biopsy specimens. Six of 12 children were treated with oral acyclovir at a dose of 25 mg/kg per day for 1 or more individual episodes, without reduction in the episode. Three children underwent 6-month prophylaxis with oral acyclovir at a dose of 20 mg/kg per day and remained disease free during treatment. After discontinuation of the prophylactic treatment with acyclovir, 1 child relapsed at 4 months. The other 2 children had no further episodes during a 3-year period. CONCLUSIONS: The HSV-associated EM is a recurrent disease that can be precipitated by sun exposure and does not progress to Stevens-Johnson syndrome. Childhood HSV-associated EM may be unresponsive to treatment with oral steroids or oral or topical acyclovir. Frequent recurrences of EM may be abrogated by prophylactic treatment with acyclovir.
Acyclovir↗
Erythema multiforme: a review.
Explore the source record for details and available documents.
Erythema Multiforme↗
Clinicopathologic correlation in erythema multiforme and Stevens-Johnson syndrome.
BACKGROUND AND DESIGN: To confirm the recent hypothesis that the spectrum of severe erythema multiforme (EM) is actually composed of two different disorders, we retrospectively studied 38 such cases, particularly in regard to their histopathologic features. Based on photographs and a recent proposal, the cases were classified as EM major when the eruption consisted of typical or raised atypical target lesions located on the extremities and/or the face or as Stevens-Johnson syndrome when the eruption consisted of flat atypical target lesions or purpuric macules that were widespread or distributed on the trunk. The cases were also assessed for causal agent. A biopsy specimen was obtained in each case. Several histologic parameters were analyzed (and scored) without clinical data and correlated to the clinical pattern. These parameters were first studied in a global assessment and then in a detailed evaluation. RESULTS: The global assessment showed two different histological patterns: (1) a predominantly inflammatory pattern characterized by a lichenoid infiltrate and epidermal necrosis that mainly affected the basal layer; and (2) a predominantly necrotic pattern in which major epidermal necrosis and minimal inflammatory infiltration were found. The former pattern was associated with EM major, the latter with Stevens-Johnson syndrome (P < .001) and with drug-related cause (P < .001). The detailed evaluation showed also less epidermal necrosis, and more dermal inflammation, and more exocytosis in EM major. Conversely, there was more epidermal necrosis, less dermal inflammation, and less exocytosis in Stevens-Johnson syndrome. The difference was statistically significant for the inflammation and exocytosis. CONCLUSIONS: This study suggests that the two different symptomatologies in the spectrum of severe EM correlate with two different patterns of histopathologic changes. A prospective multicentered study should be conducted to definitively characterize these entities.
Erythema Multiforme↗
Phenothiazine--another possible etiologic agent in erythema multiforme. Report of a case.
A case report is presented which offers evidence that administration of a phenothiazine drug resulted in erythema multiforme of the oral cavity in a psychotic patient. The condition remissed after discontinuation of the medication.
Acute Disease↗
Multifocal fixed drug eruption mimicking erythema multiforme.
A 38-year-old woman presented with a widespread bullous eruption that recurred during menstruation. Skin biopsy suggested erythema multiforme. As she was receiving synthetic progesterones for dysmenorrhoea the diagnosis of an auto-immune progesterone dermatitis was considered. However, subsequent investigations confirmed the diagnosis to be a fixed drug eruption to mefenamic acid taken for dysmenorrhoea.
Adult↗
Erythema multiforme during cytomegalovirus infection and oral therapy with terbinafine: a virus-drug interaction.
The authors report a case of erythema multiforme in a 32-year-old woman who was also taking oral terbinafine for an onychomycosis. The patient data analysis showed serological positivity for cytomegalovirus (IgM and IgG) and hepatitis C virus and serological titre of antinuclear antibody was elevated. After a brief review of the literature the authors propose the possibility of virus-drug interaction as a model of adverse drug reactions.
Adult↗
[Demonstration of herpes simplex virus from efflorescences of a case of exudative erythema multiforme].
Explore the source record for details and available documents.
Erythema Multiforme↗
Erythema multiforme major in a 2-month-old child with human immunodeficiency virus (HIV) infection.
A case is presented of severe erythema multiforme occurring in a 2-month-old boy from Zimbabwe which was probably triggered by phenobarbitone. He later developed the acquired immunodeficiency syndrome and serological tests suggested that it was a congenital HIV-I infection.
Acquired Immunodeficiency Syndrome↗
Persistent B-cell lymphopenia, multiorgan disease, and erythema multiforme caused by Mycoplasma pneumoniae infection.
We report a 6-year-old girl in whom Mycoplasma pneumoniae infection presenting with erythema multiforme, multiorgan, and hematologic dysfunctions induced a long-standing, marked B-cell lymphopenia. An increase of CD8+ lymphocytes was also detected. We suggest that a selective cytotoxic T lymphocyte-dependent B cell lysis and the expansion of super-antigen activated CD8+ T cells may account for the multiorgan and hematologic disturbances triggered by M. pneumoniae.
Acetaminophen↗