Cases reported "Erythema Multiforme"

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1/14. Persistent erythema multiforme: a report of three cases.

    Three cases of persistent erythema multiforme, two of unknown aetiology and one precipitated by influenza are reported. Lesions were widespread, mostly atypical in appearance and regressed in response to immunosuppressants (systemic steroids and/or azathioprine) or, in one case, to dapsone. One patient developed erythroderma responding eventually to etretinate. histology in all patients was consistent with the mixed, epidermodermal pattern of erythema multiforme. There were no significant laboratory abnormalities nor marked symptomatology apart from itching. The persistent form appears to belong to the spectrum of erythema multiforme being heterogeneous with respect to inducing stimuli, including viral antigens, neoplastic or inflammatory disease or unknown causes. Whenever it is possible, treatment should be adjusted depending on the causative agent.
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2/14. Atypical bullous disease showing features of both erythema multiforme and bullous pemhigoid.

    A 78-year-old man presented with multiple, centrifugal erythema, which tended to coalesce, producing polycyclic configurations. The patient developed an annular, narrow blister that was always visible along the margin of the erythema. histology of a biopsy specimen revealed hydropic degeneration of basal cells, exocytosis of lymphoid cells, and subepidermal blister with necrosis of individual keratinocytes in the blister roof. Direct immunofluorescence studies showed a weak IgG deposition at the basement membrane zone, in a linear fashion, which was confined to the outer side of the blister. immunoblotting of the patient's serum with human epidermal extract demonstrated circulating antibodies, which reacted to 230 kDa BP antigen 1. These findings suggest that this case is characteristic of both erythema multiforme and bullous pemphigoid and it seems likely that this condition could be a manifestation of epitope spreading, although the exact process in the development of immunological disturbances could not be elucidated.
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3/14. Epstein-Barr virus-related persistent erythema multiforme in chronic fatigue syndrome.

    BACKGROUND--erythema multiforme (EM) has been rarely reported in Epstein-Barr virus (EBV)-associated diseases; this includes patients with chronic fatigue syndrome who have chronic or recurrent and disabling illness and an abnormal antibody reactivity to EBV. We describe a patient fulfilling the chronic fatigue syndrome diagnostic criteria who had developed an unusually persistent EM resistant to corticosteroids therapy. The EBV dna was studied in skin EM lesions, throat washings, peripheral mononuclear cells, and plasma. The EBV antigens were studied in skin EM lesions and in mononuclear cells. The patient was followed up to 2 years. OBSERVATIONS--The patient had abnormal titers of antibodies against various EBV antigens and by immunofluorescence she disclosed the EBV nuclear antigen and the viral capsid antigen in the blood vessels of the affected skin. The dot blot hybridization assay detected viral dna in throat washings and mononuclear cells, but not in plasma. The presence of the viral genomic content in lesional skin is suggested by the autoradiographic signal and by the difference from appropriate control specimens. skin lesions and constitutional symptoms cleared after acyclovir sodium therapy and recurred after discontinuation of this therapy. CONCLUSIONS--This is the first EM case in which evidence of the EBV causal role has been provided. The association with chronic fatigue syndrome suggests the EBV role in selected cases of this syndrome.
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4/14. erythema multiforme ID reaction in atypical dermatophytosis: a case report.

    BACKGROUND: erythema multiforme (EM) is an uncommon mucocutaneous disorder, characterized by widespread erythematous-oedematous targetoid lesions, considered as a reaction pattern to many different stimuli. observation: Presentation is made of a classical EM eruption concomitant to an inflammatory, atypical dermatophytosis of the ala nasi, observed in a 37-year-old male at the dermatology Department of Cagliari, italy. methods: Laboratory investigations revealed normal complete blood count and biochemistry profile. A direct microscopic examination with 20% potassium hydroxide of the nasal skin scales and of the vibrissae indicated the presence of dermatophyte hyphae and spores invading the rhinothrix. culture confirmed a Trycophyton mentagrophytes infection. Specific determination of antiviral immunity in the blood (TORCH) was negative for recent infections, while the cell-mediated response, investigated with a delayed skin multitest, showed a marked positivity for the tricophyton antigen. Systemic therapy with terbinafine (250 mg/day) led to complete clinical and mycological recovery of the atypical ringworm in 30 days. Multiforme lesions rapidly improved and completely disappeared in 7 days. CONCLUSIONS: ID reaction to a distant focus of dermatophyte infection very rarely presents as EM. The presented case fits all the essential criteria required for the diagnosis of an ID reaction. The atypical clinical presentation of the ringworm infection, with marked involvement of the intranasal hairs, seems to have induced an inflammatory allergic response, similar to that evoked by sycosis.
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5/14. vancomycin-induced linear IgA disease manifesting as bullous erythema multiforme.

    BACKGROUND: vancomycin-induced linear immunoglobulin a (IgA) disease, an autoimmune, blistering disease in response to vancomycin administration, is characterized by a subepidermal, vesiculobullous eruption and linear IgA deposition along the basement membrane zone on direct immunofluorescence. CASE REPORT: We report the case of an 81-year-old man treated with vancomycin who developed diffuse erythema multiforme and tense bullae involving the palmoplantar surfaces. Discontinuation of vancomycin therapy resulted in complete resolution of this patient's cutaneous eruption. RESULTS: biopsy of a representative skin lesion demonstrated lichenoid interface dermatitis with focal subepidermal clefting, dyskeratosis, and prominent eosinophils. Direct immunofluorescence showed linear basement membrane staining with immunoreactants to IgA; indirect immunofluorescence demonstrated the presence of circulating IgG antibodies binding in an intercellular pattern. immunoprecipitation studies using the patient's serum revealed 210, 130, and 83 kDa target antigens. CONCLUSIONS: Presenting with an initial clinical picture suggestive of bullous erythema multiforme, this patient's subsequent clinical course and direct immunofluorescence confirm the diagnosis of linear IgA bullous disease (LABD). His indirect immunofluorescence findings and immunoprecipitation results suggest that circulating non-IgA antibodies may represent a newly recognized immunopathologic feature of vancomycin-induced linear IgA disease, underscoring the variable and unpredictable manifestations of this drug-induced cutaneous disease.
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6/14. 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.
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7/14. 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.
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8/14. erythema multiforme associated with autoreactivity to 17 alpha-hydroxyprogesterone.

    We report a case of a 23-year-old woman who was afflicted with disseminated skin erythema multiforme-like eruptions that started at the menarche, relapsed at the premenstrual periods, dramatically spread during two pregnancies and cleared after abortion; the skin lesions responded dramatically to thalidomide treatment. A high-affinity binding factor to 17 alpha-hydroxyprogesterone (17-OHP) was found in the serum of this patient. Her lymphocytes did not proliferate in vitro after exposure to exogenous 17-OHP but showed significant chromatin activation. There was a decreased expression of hla antigens at the surface of the patient's blood lymphocytes. This is a unique well-documented case of erythema multiforme most possibly due to autoreactivity to 17-OHP; the precise mechanism(s) of this autoreactivity has not been established.
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9/14. Epidermal autoantibodies in erythema multiforme.

    We report a case of refractory erythema multiforme associated with atypical epidermal autoantibodies. The patient was a 63-year-old woman with clinical and histologic features of erythema multiforme and a large mediastinal T cell lymphoma. Immunofluorescence studies disclosed high serum titers of cell surface antibodies against epidermal keratinocytes in a pattern typical of pemphigus vulgaris. The epidermal antigen reacting with these circulating antibodies was characterized by incubating 14C-labeled keratinocytes with serum. The patient's serum pattern precipitated multiple proteins keratinocytes antigens), but not the 130,000- and 85,000-dalton polypeptides characteristic of pemphigus vulgaris. Thus autoantibodies reacting selectively with non-pemphigus vulgaris epidermal keratinocyte antigens may be the cause of a false-positive immunofluorescence test for pemphigus vulgaris.
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10/14. Bacterial endotoxin (lipopolysaccharide) as a cause of erythema multiforme.

    The classic iris lesions in a patient with erythema multiforme bullosum were reproduced grossly as well as microscopically by the intradermal injection of a variety of heat-killed, gram-negative bacteria, as well as their common endotoxin, lipopolysaccharide W. in vitro exposure of the patient's blood to these antigens induced specific fibrin microclots characteristic of a hypersensitivity state. It is possible that some cases of erythema multiforme associated with a variety of respiratory, gastrointestinal, or urinary tract infections may represent a single specific delayed sensitivity reaction to the bacterial endotoxin, lipopolysaccharide.
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