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Results for “Erythema Multiforme”

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PubMedDate not supplied

Erythema multiforme from betalactams with positive cutaneous tests.

We report the case of a woman who after taking ampicillin and amoxicillin developed two severe cutaneous reactions with generalized erythema and maculopapular rash, which later turned into blisters with subsequent desquamation. She was clinically diagnosed with erythema multiforme syndrome after positive delayed cutaneous tests with benzylpenicillin, amoxicillin and ampicillin allowed for a more specific diagnosis. There are very few references to patients with drug reactions to betalactams who have positive skin prick or intradermal test but show delayed hypersensitivity, as was the case in our patient.

Amoxicillin↗
PubMed1985

Erythema multiforme after use of topical sulfacetamide.

An 8-year-old boy developed erythema multiforme major after topical administration of sodium sulfacetamide for conjunctivitis. He had received systemic treatment with trimethoprim-sulfamethoxazole four months previously without evidence of drug allergy. There was no history of recent exposure to other drugs or evidence of herpes simplex or Mycoplasma infection. After 12 days of treatment with erythromycin ointment, 1% prednisolone eyedrops, systemic prednisone, and intravenous nafcillin, the patient's condition improved dramatically. A slit-lamp examination showed only superficial punctate keratitis. Two months later his visual acuity had improved from 20/200 bilaterally to R.E.: 20/40 and L.E.: 20/30.

Child↗
PubMed1976

A case of unusual SLE related syndrome characterized by erythema multiforme, angioneurotic edema, marked hypocomplementemia, and Clq precipitins of the low molecular weight type.

Our patient and those of Agnello et al. had identical clinical symptoms such as erythema multiforme, arthralgias and angioneurotic edema and both differed from systemic lupus erthematosus in several important points, i.e., in spite of marked hypocomplementemia the nephropathy is not prominent and it needs high-dose steroids to eliminate the clinical and serological abnormalities. In addition to the features reported by Agnello et al. we found increased viral antibody titers in our patient's sera.

Adult↗
PubMed1976

Erythema nodosum and erythema multiforme associated with milker's nodules.

An epidemic of 44 cases of milker's nodules was recorded in the Tampere Central Hospital catchment area in Finland during the autumn of 1974. Exanthema or erythema multiforme-like secondary eruptions were seen in 10 cases. One female patient is reported in detail because of the simultaneous occurrence of erythema nodosum and erythema multiforme. The virological diagnosis was confirmed by electron microscopy.

Adult↗
PubMed1998

Recurrent herpes simplex virus-induced erythema multiforme: different HLA-DQB1 alleles associate with severe mucous membrane versus skin attacks.

In some individuals a local herpetic lesion precipitates a generalized inflammation of the skin, designated as erythema multiforme (EM). We determined the frequencies of the immune response genes of the HLA system by molecular HLA class II typing in 46 patients with EM and in many of their family members. Allele frequencies were correlated with disease form and disease-inducing factors. We found that specific complications of HSV infection occur preferentially in patients with certain HLA-DQB1 alleles. In 21 of the 46 patients EM was induced by recurrent HSV infection. Thirteen of these patients showing only minor or no involvement of mucous membranes had the HLA allele DQB1*0302 (phenotype frequency 61.9% versus 18.8% in controls, p corr = 0.0008) and all three patients with major involvement of mucous membranes had the rare HLA allele DQB1*0402 (phenotype frequency in controls 6,4%, p corr = 0.017).

Alleles↗
PubMed2002

Erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis in children: a review of 10 years' experience.

OBJECTIVE: To review 10 years' experience in a tertiary care paediatric hospital of erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). In addition, to apply a recently described classification system for EM, SJS and TEN in children. DESIGN: Retrospective study of all children with a discharge diagnosis of EM, SJS or TEN over a 10-year period. SETTING: A university tertiary care paediatric hospital. PATIENTS: Sixty-one paediatric patients with a discharge diagnosis of EM, SJS or TEN. MAIN OUTCOME MEASURES: Epidemiology, laboratory features, causative factors, treatment methods, complications and mortality of EM, SJS and TEN in this group of patients. Comparison of correlation with aetiology of old and new classification systems in a paediatric population. RESULTS: Mucous membrane involvement was documented in 61% of patients. Ocular involvement was seen in 39%. Complications occurred in 21% cases, all of whom had SJS or TEN. Only one patient died as a result of their skin condition. Corticosteroids were used in 18% of cases; 95% of whom had a discharge diagnosis of SJS or TEN. The drugs most commonly identified as aetiological agents were sulphonamides and penicillins (26% each). The most frequently implicated infectious agent was herpes simplex virus (19.7%). Classification of study cases according to Bastuji-Garin et al. indicates a strong trend toward bullous EM cases being attributable to infection and SJS/TEN cases to drugs. There was no such clear trend with respect to aetiology when diagnosis was done without the classification system. CONCLUSION: EM, SJS and TEN rarely cause mortality but significant morbidity is seen. Infectious agents, particularly herpes simplex virus, and drugs, especially the sulphonamides and penicillins, are the most common aetiological agents. The classification system proposed by Bastuji-Garin et al. correlates better with aetiology than the practice that preceded it.

Child↗
PubMed1990

Herpes simplex virus antigens and inflammatory cells in oral lesions in recurrent erythema multiforme. Immunoperoxidase and autoradiographic studies.

Herpes simplex virus (HSV) antigens were sought in 15 biopsy specimens from both lesional mucosa and clinically healthy looking oral mucosa between attacks in patients with erythema multiforme (EM). Four of the eight biopsy specimens obtained from lesional EM mucosa stained positively with HSV-1-and/or HSV-2-specific antisera applied in direct immunoperoxidase staining. Of the 16 tissue specimens used as controls, two displayed positive staining with HSV-1 and/or HSV-2. Five of the seven biopsy specimens from macroscopically healthy oral mucosa obtained between attacks from patients with recurrent EM stained positively with HSV-1 and/or HSV-2. Of the six tissue specimens used as controls, three stained positively. Most of the local inflammatory mononuclear cells belonged to the T cell series, mainly to the CD-4 subset. A small proportion of the local T cells were blast transformed as assessed by CD-25 expression and [3H]thymidine incorporation. This, together with the findings showing a lower degree of activation in the biopsy from macroscopically healthy looking mucosa between attacks suggest an active role of the cell-mediated immune response in the genesis of oral lesions in EM. The persistence of HSV antigens, and the well-established role of HSV as a precipitating factor in recurrent EM, suggest that HSV may be involved, but since HSV seems to be present in other mucosal lesions as well as in clinically healthy mucosa, quite frequently an additional, hitherto unknown factor must be present in order that EM may occur.

Antigens, Viral↗
PubMed1984

Bullous mastocytosis: diffuse cutaneous mastocytosis with extensive blisters mimicking scalded skin syndrome or erythema multiforme.

Bullous mastocytosis (diffuse cutaneous mastocytosis) is a rare form of mast cell disease that begins during the first month of life and causes extensive blisters that mimic scalded skin syndrome or bullous erythema multiforme. Discrete pigmented macules, papules, and nodules are absent and the characteristic leathery induration of skin may not develop until 6 months of age. Skin biopsy shows a subepidermal blister with mast cells at the base. The most serious complications are gastrointestinal hemorrhage and shock. The symptoms of bullous mastocytosis may be modified by a number of new therapeutic agents.

Burns↗
PubMed1989

Cutaneous relapse of nasal T-cell lymphoma clinically mimicking erythema multiforme.

Lymphomatous involvement of skin usually manifests as plaques, maculopapules, papulonodules, tumorous masses or ulcerated eruptions. We report an unusual case in which the cutaneous relapse of nasal T-cell lymphoma clinically mimicked erythema multiforme by the abrupt onset of lesions and the presence of targetoid and vesicular lesions. Histologically, the lymphomatous involvement was predominantly periadnexal, with destructive infiltration of blood vessels, nerves and sweat glands. Early biopsy of all unexplained cutaneous eruptions in patients with malignant lymphoma is therefore recommended.

Adult↗
PubMed2004

[Erythema multiforme caused by carbamazepine].

The antiepileptic carbamazepine can reduce aggressive behaviour and can be used as a mood stabilizer. We present a case report of a patient suffering from borderline personality disorder who was treated with carbamazepine and developed erythema multiforme.

Anticonvulsants↗
PubMed1988

Association of herpes simplex virus-induced erythema multiforme with the human leukocyte antigen DQw3.

We studied the genetic markers in human leukocyte antigen (HLA) region HLA-A, -B, -C, -DR, -DQ, C2, Bf, C4A, and C4B of 31 patients with erythema multiforme (EM) and their families. In contrast to the complement allotypes, which showed no deviation from the distribution in the normal population, two HLA class II antigens occurred in much higher frequency in patients with EM. The frequency of HLA-DQw3 (77.4%) increased with high significance compared with normal Caucasian control individuals (41.2%). An even stronger DQw3 association was found in the patient group with postherpetic EM (88.8%; relative risk, 9.41). Interestingly, all patients suffering from frequently recurrent EM were found to have the DQw3 allele (relative risk 44.2). The previously reported association to HLA-B15 was also seen and may be due to a linkage disequilibrium with the HLA-DR4 allele (66.6% in recurrent EM). Our data provide further evidence that classic recurrent EM is related to herpes simplex virus infection and should be regarded as a distinct entity within the enigmatic EM syndrome. DQw3 may serve as a helpful marker for distinguishing this entity from other diseases with EM-like lesions.

Adolescent↗
PubMed1990

The incidence of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis. A population-based study with particular reference to reactions caused by drugs among outpatients.

We carried out a study to estimate the incidence of erythema multiforme (EM), Stevens Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN) requiring hospitalization and to determine which drug therapies were associated with these reactions. We reviewed the clinical records of all patients who were hospitalized with these discharge diagnoses at Group Health Cooperative (GHC) of Puget Sound, Seattle, Wash, from 1972 through 1986. During this 14-year period, an average of about 260,000 persons, with demographic characteristics similar to those of the general population, received their care from GHC, and there were about 25,000 admissions to hospitals per year at the GHC hospitals. Based on International Classification of Diseases-Adapted coding, a total of 61 suspect cases of EM, SJS, or TEN were identified from the computerized hospital discharge file. Based on record review and the application of a uniform set of diagnostic criteria, a total of 37 patients (61%) were classified as having EM, SJS, or TEN. Of these, 16 cases (43%) were attributed to drugs administered to these patients prior to hospitalization. The overall incidence of hospitalization for EM, SJS, or TEN due to all causes was 4.2 per 10(6) person-years. The incidence of TEN alone due to all causes was 0.5 per 10(6) person-years. The incidence of EM, SJS, or TEN associated with drug use were 7.0, 1.8, and 9.0 per 10(6) person-years, respectively, for persons younger than 20 years of age, 20 to 64 years of age, and 65 years of age and older. Drug therapies with reaction rates in excess of 1 per 100,000 exposed individuals include phenobarbital (20 per 100,000), nitrofurantoin (7 per 100,000), sulfamethoxazole and trimethoprim, and ampicillin (both 3 per 100,000), and amoxicillin (2 per 100,000). Overall, our data suggest that cases of EM, SJS, and TEN sufficiently severe to require hospitalization are infrequent among outpatients using well-established drug therapies. A continuing challenge is the evaluation of these severe cutaneous reactions that are associated with newly marketed or less frequently prescribed drug therapies.

Adolescent↗
PubMed1975

The staphylococcal scalded-skin syndrome versus erythema multiforme.

This article reports a case of scalded-skin syndrome in a young child. Characterized by a generalized exfoliative dermatitis resembling scalded skin, the disease may involve the oral mucosa and must be differentiated from Stevens-Johnson syndrome (erythema multiforme). Since the etiology is specific, the disease can be treated with antibiotics with dramatic results.

Administration, Oral↗
PubMed1998

Photo Koebner phenomenon in erythema-multiforme-like eruption induced by contact dermatitis due to bufexamac.

A photo Koebner phenomenon following contact dermatitis due to bufexamac is described. A 52-year-old man presented with dermatitis on his buttocks and an erythema-multiforme (EM)-like eruption near the original lesion and on sun-exposed areas. He had been using bufexamac ointment (Anderm(R)) around and inside the anus for a few weeks before he noticed exacerbation. On patch testing, he exhibited severe contact sensitivity to bufexamac. Phototesting performed on his first visit showed that he had an abnormal reaction to UVB. An EM-like eruption similar to the original lesions developed around the irradiated sites. In this case, photosensitivity does not seem to be a drug-induced photoallergy due to systemic or topical use, but rather a photo Koebner phenomenon.

Administration, Topical↗