Hypersensitivity syndromes; erythema multiforme, erythema nodosum, urticaria.
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Erythema Multiforme↗
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Erythema multiforme.
Erythema multiforme is a cutaneous reaction pattern manifested by well-demarcated plaques on the trunk and extremities. Target, or "iris," lesions, with central clearing, are characteristic of this disorder. Erythema multiforme may be a mild condition (erythema multiforme minor), or it may be a severe, possibly life-threatening condition (erythema multiforme major or Stevens-Johnson syndrome). Toxic epidermal necrolysis, manifested by widespread epidermal desquamation, is the most severe form of this disorder. The three most common triggers for erythema multiforme are herpes simplex infection, mycoplasma infection and drug reactions. Drugs that can precipitate erythema multiforme include sulfonamides, penicillins, phenylbutazone and phenytoin. The appearance of the characteristic lesion is usually diagnostic. However, conditions such as tinea corporis, lupus erythematosus, herpetic gingivostomatitis, Behçet's disease and erosive lichen planus, among others, may mimic erythema multiforme. For mild cases, treatment is supportive, with antibiotics used for secondary skin infections. For severe causes, many physicians use systemic corticosteroids, although this treatment is not universally endorsed.
Adrenal Cortex Hormones↗
A suspected case of codeine-induced erythema multiforme.
Erythema multiforme usually presents as an acute inflammatory reaction involving the skin and mucous membranes. Systemic symptoms and organ involvement also can occur. The disease is associated with many illnesses and drugs. A two-year-old child presented to the Family Practice Center with a probable codeine-induced episode of erythema multiforme. The patient had been treated with Actifed-C Expectorant for a suspected viral upper respiratory tract infection. The rash was characteristic of erythema multiforme, but there was no involvement of mucous membranes. The rash quickly abated after the discontinuation of the drug and the administration of hydroxyzine. A viral cause for the rash could not be ruled out. When erythema multiforme is precipitated by a particular drug, discontinuation of the offending agent is necessary. The rash should disappear quickly. Adjunctive use of antihistamines may offer some benefit for the patient. Systemic corticosteroids may be necessary for more severe cases.
Child, Preschool↗
Characteristics of the oral lesions in patients with cutaneous recurrent erythema multiforme.
Erythema multiforme may be recurrent and the oral cavity is often affected. A series of 82 patients with unequivocal recurrent cutaneous erythema multiforme were examined to determine the incidence and nature of oral lesions. Seventy per cent of patients had oral lesions, comprising multiple, large, shallow, extremely painful and debilitating ulcers, which affected the entire oral mucosa in over 20%. The buccal mucosa and tongue were the most frequently affected sites in the remainder and the lips were affected in 13% of patients. Lesions generally lasted for 1-3 weeks. In over 60% of cases these attacks followed an episode of herpes simplex virus infection during the preceding fortnight. Recurrent attacks showed a different site distribution from the initial attacks, with a greater proportion having genital as well as skin and oral mucosal involvement. Detailed case histories of five patients are presented to illustrate the role of azathioprine in treating oral lesions and to document a familial case of recurrent erythema multiforme, with severe mucosal involvement.
Adolescent↗
Parvovirus infection of keratinocytes as a cause of canine erythema multiforme.
Erythema multiforme major was diagnosed in a dog with necrotizing parvoviral enteritis. Skin lesions consisted of ulceration of the footpads, pressure points, mouth, and vaginal mucosa; vesicles in the oral cavity; and erythematous patches on the abdomen and perivulvar skin. Microscopic examination of mucosal and haired skin specimens revealed lymphocyte-associated keratinocyte apoptosis at various levels of the epidermis. Basophilic cytoplasmic inclusions were seen in basal and suprabasal keratinocytes. Immunohistochemical staining, performed with canine parvovirus-2-specific monoclonal antibodies, confirmed the parvovirus nature of the inclusions in the nucleus and cytoplasm of oral and skin epithelial cells. This is the first case of canine erythema multiforme reported to be caused by a viral infection of keratinocytes. This case study indicates that the search for epitheliotropic viruses should be attempted in cases of erythema multiforme in which a drug cause cannot be identified.
Animals↗
5-fluorouracil-induced erythema multiforme.
Erythema multiforme is an immunologically mediated skin reaction to a foreign antigen and can occur with many drugs. We report the first two cases of erythema multiforme induced by 5-fluorouracil (5-FU). The first case was in a man with inoperable gastric carcinoma being treated by continual infusion who developed the classic rash involving the neck and upper chest, along with mouth ulceration and plantar-palmar erythrodysaesthesia. Histological confirmation was made by skin biopsy and the lesions resolved spontaneously. They recurred on restarting 5-FU. The second case was in a woman being given adjuvant bolus 5-FU and folinic acid for Duke's C colon cancer who developed the rash during the first cycle. Again, the lesions settled spontaneously but recurred more severely on the second cycle. When treatment was changed to the specific thymidylate synthase inhibitor, raltitrexed, the course was completed uneventfully.
Aged↗
HLA-B15 association with erythema multiforme.
Erythema multiforme (EM) is a cutaneous reaction pattern which follows numerous infections, drugs, neoplastic and inflammatory disorders in some individuals. We undertook a prospective study of thirty-eight HLA specificities of the -A, -B, and -C series in 16 Caucasian patients with EM and in 140 local Caucasian controls. Seven of 16 patients (44%) with EM and 5 of 9 patients (55%) with EM following herpes simplex infections possessed the HLA-B15 antigen, compared to 7% of local controls and 11.6% of the 1980 WHO Workshop Caucasian controls. Both associations were highly significant (p = 0.0125 and p = 0.02) when corrected for 38 HLA antigens. This is the first reported HLA association for erythema multiforme, a disease which may be a host-specific immune response to various antigens, determined in part by genes linked to HLA-B15.
Erythema Multiforme↗
Photosensitive erythema multiforme and erythema multiforme-like polymorphous light eruption.
BACKGROUND: Photosensitive erythema multiforme (EM) is a rare disorder. It usually occurs only if a herpes virus infection or ingestion of drugs precedes exposure to sunlight in selected patients. METHODS: We report a 37-year-old man who had recurrent EM eruptions following sun exposures over a period of 20 years. Lesions were prevalently located on exposed skin, but unexposed skin and mucosa of the oropharynx were also affected. The patient had poor tolerance to sunlight and denied having herpes simplex infection or using drugs. RESULTS: Provocative phototest induced clinically and histologically similar lesions at low dose thresholds of UVA (10 J/cm2) and UVB (100 mJ/cm2). CONCLUSION: On the basis of clinical and histological findings and results of phototesting, a diagnosis of photosensitive EM was made. The EM-like variant of polymorphous light eruption is discussed in the differential diagnosis.
Adult↗
Erythema multiforme.
Erythema multiforme (EM) is an episodic, variable, self-limited, and often recurrent inflammatory disorder of the skin and mucous membranes. In this article a definition of EM is proposed, its known clinical and histopathologic spectrum is reviewed, an approach to diagnosis and treatment is suggested, and documented evidence regarding its etiology and pathogenesis is presented. EM would appear to be a hypersensitivity reaction to a variety of precipitating agents. It has been directly linked to Mycoplasma pneumoniae and herpes simplex virus infections and possibly is triggered by a number of other infectious agents and by certain drugs. Accumulating observations of diverse immunologic phenomena suggest an underlying immune mechanism of as yet unclear type. Future investigation should be directed toward defining diagnostic criteria, evaluating reported etiologic associations, and clarifying the immunologic basis of this complex and enigmatic disorder.
Diagnosis, Differential↗
Understanding the pathogenesis of HSV-associated erythema multiforme.
Erythema multiforme (EM) is a polymorphic, often recurring eruption caused by exposure to medication or various infections, notably herpes simplex virus (HSV). Understanding the pathogenesis of HSV-associated EM (HAEM) is essential for patient management. We suggest that HAEM results from the combination of viropathic effects mediated by HSV proteins, notably DNA polymerase (Pol), and an immunological reaction to viral antigens. Presumably, viral DNA and proteins ingested by macrophages at HSV lesion sites undergo fragmentation and processing for presentation to T cells with HSV memory. HSV DNA is deposited on the skin, where it is expressed. Activated T cells are recruited to the skin site of Pol expression, directly or indirectly resulting in the generation of an inflammatory cascade. Factors potentially involved in the incidence of recurrences, lesion severity and anatomical localization include the identity of the deposited HSV genes, cutaneous capillary size, degree of vasoconstriction and ambient temperature. Evidence in support of this interpretation is reviewed.
Cytokines↗
HLA DQB1*0301 allele is involved in the susceptibility to erythema multiforme.
Erythema multiforme (EM) is an acute, episodic inflammatory disorder of the skin and mucous membranes of various etiology that could be related to immunologic hypersensitivity response. EM has been previously reported to be associated with serologically defined HLA-DRw53 and DQw3 antigens. In this report, we reevaluate the role of HLA class II alleles in EM manifestations. With use of the polymerase chain reaction, followed by sequence-specific oligonucleotide hybridization, 35 unrelated Caucasian EM patients and 80 randomly selected healthy subjects were studied, and the DRB3, DRB4, DQA1, and DQB1 alleles were analyzed. The comparison of frequencies of these alleles indicates that (i) susceptibility to EM disease is more associated with the HLA-DQ than the HLA-DR subregions and (ii) that the DQB1*0301 is the most frequent allele among EM patients. Sixty-six percent of the patients had the DQB1*0301 allele compared to 31% of the controls (RR = 4.1; p less than 0.001). An even stronger DQB1*0301 association was found in the patient group with herpes-associated EM (76%; RR = 6.5; p less than 0.001). Our data demonstrate a clear association between an HLA-DQB1 allele and susceptibility to EM.
Adolescent↗
Autoantibodies to desmoplakin I and II in patients with erythema multiforme.
Erythema multiforme (EM) represents a syndrome of chronic recurrent inflammatory skin disease. Depending on the severity and extent of skin and mucosal involvement, it is defined either as EM minor or EM major. In this study we demonstrate the presence of autoantibodies (aAbs) against desmoplakin I and II, two major proteins of the desmosomal plaque, in six of six patients with the severe variant of EM, EM major. Light microscopic studies of lesional skin and mucous membranes localized in vivo bound immunoglobulin G (IgG) in a dotted desmosomal pattern along the cytoplasmic membranes of keratinocytes. By immunoelectronmicroscopy, in vivo bound IgG was confined to the desmosomal plaques. These findings were confirmed by indirect immunolocalization studies that demonstrated the presence of IgG aAbs in the serum of patients during active disease. These aAbs did not only bind to desmosomal plaques of epithelial cells where they colocalized with defined murine monoclonal antibodies directed against desmoplakin I and II, but also labeled the intercalated discs of myocardial cells. Biochemical characterization of circulating IgG aAbs revealed desmoplakin I and II as actual target autoantigens. By passive transfer of serum into newborn mice, in vivo binding of serum aAbs to keratinocytes was shown. The findings presented in this study imply a humoral immune response in certain patients with EM major and indicate a potential pathogenetic role of aAbs against desmoplakin I and II in this disease.
Animals↗
High-molecular-weight kininogen is cleaved in active erythema multiforme.
Erythema multiforme (EM) is an inflammatory disorder of the skin, which may include mucous membrane involvement, that features target (iris) lesions. Mediators specifically involved in EM are not well characterized; its pathogenesis remains enigmatic. In this study, evidence for participation of kinins in the pathophysiology of inflammation in EM was investigated by assessing cleavage of high-molecular-weight kininogen (HMWK) in plasma. These data were compared with analyses of plasmas from patients with serum sickness, chronic idiopathic urticaria/angioedema, and from normal control subjects. Patients with EM demonstrated significant levels of circulating cleaved HMWK in plasma during active disease (p less than 0.01), which declined during remission/recovery. Plasmas from patients with EM obtained during active disease also demonstrated significant levels of 94 kd C1 inhibitor (p less than 0.01) and C1 inhibitor-kallikrein complexes. Patients with serum sickness and chronic idiopathic urticaria/angioedema did not demonstrate these findings and did not differ from normal control subjects (p = not significant). Although the kininogenase responsible for HMWK cleavage in EM has not been conclusively demonstrated, these findings suggest that HMWK cleavage resulted from activation of the contact system and that some of the manifestations of EM in selected patients may in part be accounted for by inflammatory and proinflammatory actions of kinins. Based on these preliminary findings, it will be important to establish whether or not HMWK cleavage in EM is a general finding in patients with this disorder. Further investigation is needed to characterize more clearly kininogenase activity and elucidate the possible role of kinin generation in EM.
Adult↗
Oral manifestations of erythema multiforme.
Erythema multiforme is a reactive mucocutaneous disorder in a disease spectrum that comprises a self-limited, mild, exanthematic, cutaneous variant with minimal oral involvement (EM minor) to a progressive, fulminating, severe variant with extensive mucocutaneous epithelial necrosis (SJS and TEN). Significant differences exist among EM minor, EM major, SJS, and TEN with regards to severity and clinical expression; however, all variants share two common features: typical or less typical cutaneous target lesions and satellite-cell or more widespread necrosis of the epithelium. These features are considered to be sequelae of a cytotoxic immunologic attack on keratinocytes expressing non-self-antigens. These antigens are primarily microbial (viruses) or drugs and in rare instances histocompatibility antigens [5]. Although the precise pathogenesis is unknown, there is a tendency to consider EM both minor and major as part of one spectrum that is most often triggered by viral infections, and SJS and TEN as a separate one most often elicited by drugs with EM major and SJS representing a bridge in the continuum of EM. The oral manifestations of the spectrum of EM range from tender superficial erythematous and hyperkeratotic plaques to painful deep hemorrhagic bullae and erosions. Other mucosal surfaces including ocular, nasal, pharyngeal, laryngeal, upper respiratory, and anogenital may be involved. Scarring sequelae from ocular and pharyngeal involvement cause morbidity. The oral EM variant is an underrecognized form of EM. Most patients have chronic or recurrent oral lesions only, but one third have oral and lip lesions and one quarter have oral, lip, and skin lesions. This variant is a reaction pattern similar to EM minor, EM major, SJS, and TEN. The diagnosis of oral EM is one of exclusion. Careful clinical evaluation for other chronic mucocutaneous diseases, such as pemphigus, paraneoplastic pemphigus, mucous membrane pemphigoid, and lichen planus, is a necessary component of the diagnosis. The value of a biopsy specimen studied by both routine histopathologic and immunopathologic methods is fundamental to excluding the other causes for this variant of EM.
Diagnosis, Differential↗
AN EPIDEMIC OF ERYTHEMA MULTIFORME AND ERYTHEMA NODOSUM CAUSED BY HISTOPLASMOSIS.
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Adolescent↗
[Intense erythema multiforme and erythema nodosum of primary tuberculous infection].
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Erythema Multiforme↗
Herpes simplex virus associated erythema multiforme (HAEM) is mechanistically distinct from drug-induced erythema multiforme: interferon-gamma is expressed in HAEM lesions and tumor necrosis factor-alpha in drug-induced erythema multiforme lesions.
Erythema multiforme follows administration of several drugs or infection with various agents, including herpes simplex virus, a syndrome designated herpes simplex virus associated erythema multiforme. Lesional skin from 21 of 26 (81%) herpes simplex virus associated erythema multiforme patients was positive for herpes simplex virus gene expression as evidenced by reverse transcriptase-polymerase chain reaction with primers for DNA polymerase and/or immunohistochemistry with DNA polymerase antibody. Reverse transcriptase-polymerase chain reaction and immunohistochemistry studies indicated that herpes simplex virus associated erythema multiforme lesional skin from 16 of 21 (76%) DNA polymerase positive herpes simplex virus associated erythema multiforme patients was also positive for interferon-gamma, a product of T cells involved in delayed-type hypersensitivity (p < 0. 0001 by Pearson correlation coefficient). Interferon-gamma signals were in infiltrating mononuclear cells and in intercellular spaces within inflammatory sites in the epidermis and at the epidermis/dermis junction. Herpes simplex virus lesional skin was also positive for DNA polymerase [five of five (100%)] and interferon-gamma [four of five (80%)], but lesional skin from drug-induced erythema multiforme patients was negative. Lesional herpes simplex virus associated erythema multiforme keratinocytes also stained with antibody to transforming growth factor-beta [14 of 23 (61%)] and cyclin-dependent kinase inhibitor waf [12 of 18 (67%)]. Staining was also seen in keratinocytes from herpes simplex virus lesions [five of five (100%)], but not in normal skin. By contrast, staining with antibody to tumor necrosis factor-alpha, another pro-inflammatory cytokine, was seen in seven of 11 (64%) drug-induced erythema multiforme patients, but not in herpes simplex virus or herpes simplex virus associated erythema multiforme patients, and lesional keratinocytes from drug-induced erythema multiforme patients were negative for transforming growth factor-beta and cyclin-dependent kinase inhibitor waf. We interpret the data to indicate that herpes simplex virus associated erythema multiforme pathology includes a delayed-type hypersensitivity component and is mechanistically distinct from drug-induced erythema multiforme.
Cyclin-Dependent Kinase Inhibitor p21↗
Erythema multiforme and erythema nodosum.
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Dermatologic Agents↗