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PubMed2006

Expression of cytokines and chemokine receptors in the cutaneous lesions of erythema multiforme and Stevens-Johnson syndrome/toxic epidermal necrolysis.

BACKGROUND: Erythema multiforme (EM) and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) are caused by a dysregulation of cellular immunity. OBJECTIVES: To evaluate further the potential role of certain cytokines and chemokine receptors in cutaneous lesions of patients affected by EM and SJS/TEN and to establish whether such diseases are polarized preferentially towards a T-helper (Th) 1 or Th2 pattern. METHODS: Biopsy specimens from eight patients with EM, six with SJS/TEN and three healthy controls were stained for immunohistochemical examination using the alkaline phosphatase-antialkaline phosphatase method. The monoclonal antibodies used included those to tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-2, IL-5, IL-13, receptor 3 for C-C chemokines (CCR3), receptor 3 for C-x-C chemokines (CXCR3) and CXCR4. RESULTS: The SJS/TEN specimens showed significantly higher expression of all the cytokines and chemokine receptors (except CXCR3) tested than the EM specimens. Both lesional series showed significantly higher expression of all the receptors tested than the healthy control specimens, with the sole exception of a lower expression of CCR3 in EM specimens. Comparison between molecules associated with a Th1 or Th2 response revealed a predominance of Th1 response in EM and no significant imbalance between Th1 and Th2 in SJS/TEN. CONCLUSIONS: We have provided further evidence that TNF-alpha is strongly expressed in SJS/TEN lesions and therefore it may be involved in the epidermal necrosis featured in such diseases. IFN-gamma may play an important role both in EM and SJS/TEN. IL-2, IL-5 and IL-13 may contribute to the cutaneous immunoinflammation in these diseases. Chemokine receptors may be involved strongly in the recruitment of inflammatory cells in lesional skin. In our cases we found a sharp polarization towards a Th1 pattern in EM, while the SJS/TEN lesions showed a mixed Th1/Th2 pattern.

Adult↗
PubMed1985

Erythema multiforme associated with trazodone therapy: case report.

A 63-year-old woman with treatment-resistant depression was started on trazodone and subsequently developed erythema multiforme (EM), with lesions predominant on the distal parts of the limbs and involvement of the hands and feet, as well as her palms and soles. The patient's treatment course and subsequent remission are described. It is suggested that trazodone therapy be discontinued immediately upon notice of EM. This patient was also taking lithium, which has not been implicated in erythema multiforme.

Depressive Disorder↗
PubMed1997

Corticosteroid treatment of erythema multiforme major (Stevens-Johnson syndrome) in children.

UNLABELLED: The effectiveness of systemic corticosteroids in erythema multiforme major (EMM) is controversial. We therefore evaluated the efficacy of corticosteroids in the treatment of EMM in a prospective study of 16 children with EMM admitted to our department within 3 days from the onset of rash. Ten patients (group A) received bolus infusions of methylprednisolone (4 mg/kg/day) while six had only supportive treatment (group B). The early use of corticosteroids compared to supportive treatment resulted in: (1) significant reduction of the period of fever (4.0 +/- 1.9 vs 9.5 +/- 4.2 days P = 0.01); (2) reduction of the period of acute eruption (7.0 +/- 3.3 versus 9.8 +/- 3.0 days P = 0.08); and (3) milder signs of prostration. Complications were minimal in both groups. CONCLUSION: The early and short course of corticosteroids favourably influences the course of erythema multiforme major in children.

Adolescent↗
PubMed1989

Erythema multiforme minor associated with Mycoplasma pneumoniae infection.

A young Bedouin woman with serologically proven Mycoplasma pneumoniae infection is presented. Along with pulmonary involvement, fever and bullous myringitis, she presented with erythema multiforme minor, a rare complication of mycoplasma infection of which many physicians may not be aware. The skin participation in mycoplasma infections is discussed. Mycoplasma infection should be considered in the differential diagnosis of erythema multiforme.

Adult↗
PubMed1964

HISTOPLASMOSIS IN MONTREAL DURING THE FALL OF 1963, WITH OBSERVATIONS ON ERYTHEMA MULTIFORME.

Although Montreal is in an endemic area, significant clinical histoplasmosis with systemic manifestations has been, until recently, infrequently diagnosed. However, since the autumn of 1963, 31 cases of clinically significant histoplasmosis have been seen by the authors. These were divided into two groups: (1) patients in whom the diagnosis was established on the basis of histological and/or cultural demonstration of the fungus; (2) patients in whom the diagnosis was based on a positive histoplasmin skin test, a complement fixation antibody titre of 1:32 or greater and compatible clinical and radiological findings. An additional group of 11 patients who presented with erythema multiforme was investigated and a heretofore unrecognized relationship between histoplasmosis and erythema multiforme was established.

Adolescent↗
PubMed2000

Taking aim at erythema multiforme. How to spot target lesions and less typical presentations.

Erythema multiforme is a distinct cutaneous condition characterized by target lesions. Most cases are associated with HSV infection, which may be subclinical. When the classic target lesions are absent, skin biopsy may be necessary to confirm the diagnosis. Treatment is directed at suppressing outbreaks of HSV infection and controlling symptoms during acute episodes.

Erythema Multiforme↗
PubMed2003

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.

Adult↗
PubMed1983

Erythema multiforme: a critical review of characteristics, diagnostic criteria, and causes.

Erythema multiforme (EM), in its modern definition, is an acute, self-limited syndrome with distinctive skin lesions with or without mucosal lesions. Use of the terminology "EM minor" and "EM major" is a reasonable approach to separating the classical mild cutaneous syndrome, as described by Hebra (EM minor), from the usually more severe syndrome, with marked mucosal damage, as described by Stevens and Johnson (EM major). Until objective markers for EM are available, we propose preliminary diagnostic criteria for EM, based primarily on clinical features. Although hundreds of factors have been reported to cause EM, only a limited number are reasonably well documented as possible precipitating agents. Recurrent herpes simplex is an important etiologic factor in EM minor, while mycoplasmal infections and drugs may be associated with EM major. Progress in the understanding of EM will require careful attention to definition and diagnostic criteria and identification of distinct clinical and etiologic subsets within the spectrum of EM.

Erythema Multiforme↗
PubMed1990

An electron microscopic study of oral lesions in erythema multiforme.

The ultrastructure of oral lesions in 6 patients with erythema multiforme (EM) and of one apparently clinically healthy oral mucosa in one patient with recurrent EM during remission is described. Alterations were observed in epithelium, basal lamina and lamina propria. Both intercellular and intracellular oedema, intracellular vacuolization, decreased numbers of desmosomes, and also loss of cytoplasmic organelles and occasional nuclei were noted in the epithelium. Inflammatory cells--mainly lymphocytes--were found intra-epithelially. Several discontinuities together with some evidence of duplication of the basal lamina were seen in five of the six lesional mucosa specimens. The inflammatory infiltrate in the lamina propria consisted mainly of lymphocytes, although plasma cells, neutrophilic and eosinophilic leukocytes, macrophages and mast cells were also found. Some of the mast cells were partly degranulated. The apparently clinically healthy oral mucosa in the patient with EM in remission showed mild inflammatory changes. The changes observed in the lesional mucosa in EM are thus according to our study mostly non-specific inflammatory alterations and are not pathognomonic for EM.

Adolescent↗
PubMedDate not supplied

Erythema multiforme: As a complication of allergen-specific immunotherapy.

Here we present a 25-year-old female patient admitted with a complaint of blistering lesions on her face, neck, chest and extremities appearing after the first dosis of specific immunotherapy and diagnosed as erythema multiforme. To our knowledge, there are no papers in the literature reporting erythema multiforme due to specific immunotherapy.

Adult↗
PubMed2006

The CD40/CD40 ligand system is expressed in the cutaneous lesions of erythema multiforme and Stevens-Johnson syndrome/toxic epidermal necrolysis spectrum.

BACKGROUND: Erythema multiforme (EM) and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) are determined by a dysregulation of cellular immunity. OBJECTIVES: To evaluate the effector role of cellular immunity and the involvement of the CD40/CD40 ligand (CD40L) system in the pathogenesis of EM and SJS/TEN. METHODS: Biopsy specimens from eight patients with EM and six with SJS/TEN were stained for immunohistochemical examination using the alkaline phosphatase/antialkaline phosphatase method. The monoclonal antibodies used included those to CD1a, CD4, CD8, CD40, CD40L, CD68, Fas, Fas ligand (FasL) and myeloperoxidase. RESULTS: The cellular infiltrate in both EM and SJS/TEN lesions was composed mainly of T lymphocytes and CD68+ macrophages. We also detected large amounts of neutrophils. Fas and FasL were very highly expressed in SJS and TEN, but weakly in EM. CD40 staining was strong in all tissue sections; there were numerous CD40L+ cells in SJS/TEN but much fewer in EM. CONCLUSIONS: Activated T lymphocytes and macrophages, but also neutrophils, are presumably the main triggers of mucocutaneous damage in the SJS/TEN disease spectrum. The Fas/FasL system is significantly expressed in SJS/TEN lesions, but not in EM, where this apoptotic pathway presumably does not play a pivotal role in the epidermal damage. We suggest that the CD40/CD40L system may represent an important pathway of induction of SJS/TEN lesions, while in EM it would contribute to the immunoinflammation only as a second-line mechanism.

Adult↗
PubMed1999

Longitudinal study of a patient with herpes-simplex-virus-associated erythema multiforme: viral gene expression and T cell repertoire usage.

BACKGROUND: Erythema multiforme is a polymorphous self-limited, often recurrent eruption that can follow herpes simplex virus (HSV) infection, hereby designated HAEM. Studies of relatively large groups of patients during one recurrent episode indicated that HAEM pathogenesis is associated with HSV gene expression, Vbeta2 T cell infiltration of lesional skin and altered T cell receptor (TCR) repertoire usage by HSV-stimulated peripheral blood mononuclear cells (PBMC). However, HAEM recurrences are not always preceded by overt HSV eruptions and virus cannot be isolated from HAEM lesional skin. Therefore, it is unknown whether all HAEM recurrences experienced by a given patient are HSV related. OBJECTIVE: The studies described in this report were designed to examine whether all HAEM recurrences experienced by a given patient are HSV related. METHODS: We describe one patient who was studied longitudinally during 6 HAEM recurrences and in the intervening lesion-free periods. Lesional skin from all HAEM episodes was studied for HSV gene expression and infiltration by Vbeta2 and Vbeta3 T cells. PBMC obtained at these times were assayed for TCR repertoire usage upon HSV stimulation. RESULTS: Lesional skin from all HAEM episodes was positive for HSV gene expression (RNA and protein) as well as Vbeta2 T cell infiltration. HSV-stimulated PBMC obtained at these times had an altered TCR repertoire characterized by a predominance of Vbeta2 cells. The duration of viral gene expression, Vbeta2 cell infiltration and altered TCR repertoire usage correlated with the duration of clinical symptoms. CONCLUSION: The data suggest that HSV and a virus-specific immunopathology component are involved in the causation of all HAEM episodes experienced by the patient.

Adult↗
PubMed1976

Erythema multiforme in children. Response to treatment with systemic corticosteroids.

It is generally accepted that the correct treatment for patients with severe erythema multiforme is systemic corticosteroids. This paper is a review of thirty-two paediatric patients with severe erythema multiforme (Stevens-Johnson syndrome) who were treated with either large doses of systemic corticosteroids or supportive care only. Those patients treated with steroids did not recover sooner than those treated in other fashions and the steroid treated group had a significant incidence of medical complications. This retrospective study proves nothing but it does suggest that treatment of patients with the Stevens-Johnson syndrome with systemic corticosteroids may be associated with significant side effects and prolonged recovery.

Adolescent↗
PubMed1984

Cutaneous immunofluorescence study of erythema multiforme: correlation with light microscopic patterns and etiologic agents.

Direct immunofluorescence microscopy was positive in 88% of forty-one skin biopsy specimens from thirty-four patients with the clinical diagnosis of erythema multiforme. The most common finding, present in 67% of positive specimens, was the cytoid body, or fluorescent keratinocyte, which stained most often with IgM (homogeneously) or with C3 (speckled). Other findings included basement membrane zone (BMZ) fluorescence, primarily with fibrinogen and C3, and vascular fluorescence, most commonly C3 in a granular pattern. Correlation of direct immunofluorescent and light microscopic findings revealed that (1) the fluorescent keratinocyte was prevalent only in epidermal and mixed patterns, correlating with the eosinophilic necrotic keratinocyte by light microscopy, and (2) vascular fluorescence was most prominent in dermal forms. Herpes simplex-associated erythema multiforme showed exclusively a mixed histologic pattern, whereas the drug-related form was primarily epidermal.

Adolescent↗
PubMed1983

Lymphocyte subsets and Langerhans cells/indeterminate cells in erythema multiforme.

A peroxidase-antiperoxidase study using monoclonal antibodies directed against T and B lymphocytes and Langerhans cells/indeterminate cells (LC/IC) was undertaken in order to understand more clearly the changes observed in erythema multiforme. At the various stages of development, from normal skin to target lesions, the quantity of inflammatory cells differed, but in each case the number of T8+ (cytotoxic/suppressor) cells was greater than the number of T4+ (helper/inducer) cells in the epidermis, whereas the latter exceeded the former in the dermis. Concomitant with the initial epidermis changes, there was an increase in the number of T6+ (LC/IC) cells in the upper and lower epidermis. With slight to moderate basal unit destruction, the number of LC/IC in the upper epidermis exceeded those in the lower epidermis. With severe basal unit destruction, there was a loss of LC/IC in the lower epidermis as detected by T6 reactivity. In fully formed blisters, the LC/IC in the upper half of the epidermis were decreased in parallel with the degree of epidermal necrosis. The character of the lymphocytic inflammatory infiltrate and redistribution in LC/IC are similar to those findings described in allergic contact dermatitis. The clinical, histologic, and immunopathologic changes in erythema multiforme appear to be due in part to cellular immune mechanisms with the lymphocyte as the predominant effector cell, and our data suggest a possible role for LC/IC in this disorder.

Erythema Multiforme↗