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A new case of erythema multiforme is described, characterized by multiforme eruption of erythematous papules, plaques and occasional bullous lesions. The acute stage lasts several seeks, then atrophy is noted. The face appears senile. Histopathologically, the lesions show erythema multiforme in the acute phase; in the atrophic stage, a disappearance of the elastic fibers was observed.
Previous reports have shown an increased frequency of certain HLA antigens in association with erythema multiforme, including HLA-B15(B62), HLA-B35, HLA-A33, HLA-DR53 and, more recently, HLA-DQB1*0301. A strong association with HLA-DQ3 has been documented in patients with recurrent erythema multiforme. We have performed HLA typing in 39 patients with recurrent erythema multiforme, of whom 33 were associated with herpes simplex virus infection. The results were compared with 309 controls. In the recurrent erythema multiforme patients there was a statistically significant increase in HLA-B62 and HLA-B35. An increase in HLA-DR53 was also found, although this did not reach statistical significance. There was no increase in HLA-A33. The presence of HLA-DQ3 in the study population approached that in the controls. Finally, the study population demonstrated a trend towards a reduction in the HLA antigens A1, B8 and DR3. The study confirms the previously reported associations with HLA-B62 (B15), HLA-B35 and HLA-DR53. We have been unable to confirm an association of HLA-A33 or HLA-DQ3 with erythema multiforme. The HLA antigens A1, B8, and DR3 are associated with autoimmune disease, reflecting an increased host response to tissue self antigens. Their absence in patients with recurrent erythema multiforme (REM) may be an indicator of a poor host response to an antigen, which in the case of REM is the herpes simplex virus.
A patient with systemic scleroderma is described who developed a cutaneous eruption of papules and vesicobullae. Over time, the latter turned into papules. The histopathological and immunofluorescence features of the papular lesions were unequivocally those of lichen planus, while those of the bullous lesions reminded of erythema multiforme. Histologically, erythema multiforme shares common features with lichenoid reactions, such as necrotic keratinocytes. Our case suggests that erythema multiforme and lichen planus may coexist or succeed each other as different stereotype immune reactions against the same antigen(s) within the epidermis.
Lesions of erythema multiforeme from seventy-five patients have been studied histologically. In addition to peculiar intercellular epidermal oedema, subepidermal separation and a lymphohistiocytic inflammatory infiltrate in the papillary dermis, epidermal cell necrosis was observed in a variable percentage of the lesions. While dermal disturbance was a predominant finding in the macular lesions, focal or generalized keratinocytic necrosis was seen in the macular, papular, bullous and iris lesions in that order of frequency. Significant numbers of eosinophils were present in the inflammatory infiltrate in 60% of the bullous and 28% of the macular lesions. Our findings suggest that erythema nultiforme represents a tissue reaction with spectral expression, one end presenting as a predominantly dermal disturbance and the other merging into the adult type of toxic epidermal necrolysis. Yet, the histological features remain sufficiently characteristic for differentiation from other erythematous and vesiculobullous eruptions.
Early cutaneous lesions of erythema multiforme or mucosal lesions of the Stevens-Johnson syndrome contain delicate granular deposits of immune reactants and/or complement components lodged in the walls of vessels of the papillary dermis. Such deposits are not present in normal, unaffected skin although they can be caused to occur there by injection of substances which increase vascular permeability. Factors which cause accumulation of mononuclear cells in the papillary dermis have not been elucidated but we suggest that receptors for the C3d fragment of the third component of complement could be responsible. Factors which cause intercellular edema in the epidermis, epidermal-dermal separation, or necrotic keratinocytes are unknown. We, and others, may now measured immune complexes in the serum of patients experiencing these reaction patterns by means of Raji cell radioimmunoassay, C1q precipitation, 125I-C1q binding, cryoprecipitation and with monoclonal rheumatoid factor. Cryoimmunoglobulins have also been described and antigens of Herpesvirus hominus have been measured in the cryoprecipitate of 2 patients who experienced erythema multiforme following recurrent herpesvirus infection. Erythema multiforme commonly accompanied serum sickness reactions which occurred following injection of immune horse serum in the 1980s (von Pirquet and Schick). Such reactions are now well established as due to circulating immune complexes in antigen excess.
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.
BACKGROUND: Serum sickness-like reactions (SSLR) and erythema multiforme are common adverse effects of cefaclor therapy and can be associated with significant morbidity. No standardized evidence-based protocol for the optimal treatment of drug-induced SSLR exists. OBJECTIVES: To define the standard of care used by physicians treating adverse reactions associated with cefaclor. METHODS: A retrospective review of the medical records of children discharged from a pediatric emergency room with a diagnosis of adverse events to cefaclor was conducted. Charts of patients were reviewed to determine which therapy was prescribed. RESULTS: During the study period, 74 cases of adverse events attributed to cefaclor presented to the emergency department. SSLR were the most common pattern of adverse events seen (31 cases, 42%), followed by urticarial reactions (26 cases, 35%) and erythema multiforme (17 cases, 23%). An antihistamine was the treatment most often prescribed (88%) for erythema multiforme. Significantly more children with SSLR than with erythema multiforme or urticaria were treated with prednisone, either alone or in combination (P<0.05). CONCLUSIONS: The treatment most often prescribed for serious cefaclor-associated erythema multiforme was an antihistamine. In the case of SSLR, an antihistamine and prednisone were most commonly used. Prospective randomized, controlled trials are needed to define the role of various therapeutic agents and to determine the optimal therapy for SSLR and other serious adverse drug reactions.
Thirteen patients with oral erythema multiforme were assessed immunologically by skin testing and in vitro tests (lymphocyte transformation and rosettes). The results suggested a possible defect in cell-mediated immunity for most patients in this group.
OBJECTIVE: The objective was to report a severe skin reaction, erythema multiforme major, following administration of docetaxel. CASE SUMMARY: A female patient receiving weekly docetaxel for metastatic breast cancer developed a severe skin reaction characterized by blistering target lesions on her upper and lower extremities as well as painful ulcers of her oropharynx. The diagnosis of erythema multiforme major was made and high-dose hydrocortisone began, with gradual resolution of her symptoms. DISCUSSION: The semi-synthetic taxoid docetaxel, which is increasingly being used in the treatment of breast cancer, has been associated with several adverse skin reactions, including hypersensitivity, nail pigmentation, nail onycholysis, erythrodysethesia, and scleroderma. We report the first case of erythema multiforme major (Stevens-Johnson syndrome) following docetaxel. Erythema multiforme major is a rare inflammatory skin disease associated with certain drugs (i.e., sulfonamides, non-steroidal anti-inflammatory agents, anticonvulsants). It is characterized by a distinguishing target skin lesion and ulceration of mucosal surfaces. In severe cases, systemic manifestations such as pneumonitis can also occur. Treatment involves use of moderate to high-dose corticosteroids. SUMMARY: Clinicians using docetaxel should be aware of the variety of skin reactions that can occur, how they can be avoided and their severity reduced. Severe skin reactions such as occurred with our patient should be recognized and treated promptly in consultation with a dermatologist.
Recurrent oral erythema multiforme is a distinct, but less-well-recognized variant of the erythema multiforme group of diseases. It is characterized by recurrent blistering of the mouth, periodic recurrences, prolonged duration, and considerable morbidity. The cause is unknown; however, a number of precipitating factors have been suggested. Patients with severe involvement usually require orally administered corticosteroids for adequate control.
Erythema multiforme (EM) is a targetoid eruption with interface pathology often triggered by a hypersensitivity response to a variety of infections, most commonly herpes simplex virus. Hepatitis C virus is rarely associated with EM. We present a 37-year-old man with an 8-year history of severe EM unresponsive to valacyclovir, acitretin, and cyclosporin, and marginally responsive to high-dose prednisone. The eruption had cleared 6 years previously during treatment with interferon for his concurrent hepatitis C virus. Although his viral titer was undetectable, we initiated therapy with interferon and ribavirin. The patient responded dramatically within 2 months and remained clear of EM after 1 year of continued interferon therapy. This is the third case reported in the world literature documenting a response of EM to interferon, and the first case in which hepatitis C virus was undetectable in serum prior to interferon therapy.
Cicatricial pemphigoid (CP) and erythema multiforme (EM) are bullous diseases that involve the skin and mucous membranes including the conjunctiva. Of all the bullous diseases, CP and EM not only involve the conjunctiva most frequently but also cause the most severe conjunctival disease. A chronic, progressive disease, CP is characterized by shrinkage of the conjunctiva, symblepharon, entropion, trichiasis, dry eye, and finally reduced vision from corneal opacification. It is primarily a disease of the elderly that affects more women than men and is characterized by blisters or bullae in a subepithelial location and immunoglobulins and complement bound to the basement membrane zone of skin and mucous membranes including the conjunctiva. Circulating antibodies to the basement membrane zone can be demonstrated occasionally. Treatment includes artificial tears, topical antibiotics, correction of entropion and trichiasis, therapeutic soft contact lenses, and systemic immunosuppressive therapy including corticosteroids. An acute, generally self-limited, inflammatory disorder of the skin and mucous membranes, EM occurs primarily in young, healthy individuals. The most frequent precipitating factors are (1) drugs and (2) infections caused by Mycoplasma pneumoniae and herpes simplex. Conjunctival involvement ranges from a mild catarrhal conjunctivitis which terminates without sequelae to membranous conjunctivitis which may heal leaving scarring, symblepharon, and even ankyloblepharon. Histopathologic findings include subepithelial bullae and perivascular mononuclear cell infiltrates. Patients with EM have circulating immune complexes and immunoreactant deposition in the blood vessel walls of the dermis. After the acute episode has subsided, they may require artificial tears, topical antibiotics, correction of entropion and trichiasis, therapeutic soft contact lenses, tarsorrhaphy, and mucous membrane grafts.
The protean manifestations of erythema multiforme range from minor variants through Stevens-Johnson Syndrome, bullous erythema multiforme, and toxic epidermal necrolysis. Herpes simplex virus is a common etiologic agent for minor varieties particularly if they are recurrent. Certain drugs also cause severe varieties of erythema multiforme. Although no form of therapy is recognized as generally effective, many are used in treating this group of diseases. Local wound care is also important.
BACKGROUND: A characteristic feature of erythema multiforme is an acute inflammatory reaction of the skin with an infiltrate largely composed of mononuclear cells around the upper dermal vessels and in the dermal-epidermal interface. OBJECTIVE: To determine the composition and localization of leukocyte subsets and corresponding expression of chemokines with chemoattractant properties for lymphocytes and macrophages. MATERIALS AND METHODS: Immunohistochemical analysis was performed to localize leukocyte subsets (CD1(+), CD3(+), CD4(+), CD8(+), and CD68(+)). Expression of transcripts and proteins of chemokines (macrophage chemoattractant protein [MCP] 1); macrophage inflammatory protein [MIP] 1 alpha and MIP-1 beta; regulated on activation, normal T-cell expressed and secreted [RANTES]; growth-related oncogene alpha; epithelial-derived neutrophil attractant 78; interleukin 8; macrophage interferon-gamma inducible gene [Mig]; and interferon-gamma inducible protein 10) was determined by in situ hybridization and immunohistochemical analysis. SETTING: Department of Dermatology, University of Würzburg Medical School. RESULTS: High levels of messenger RNA expression of MCP-1, RANTES, Mig, and interferon-gamma inducible protein 10 were detected and localized in the interface zone and subepidermal infiltrate. In contrast, other investigated chemokines (growth-related oncogene alpha, interleukin 8, epithelial-derived neutrophil attractant 78, I-309, MIP-1 alpha, and MIP-1 beta) were minimally expressed or absent. Protein expression of MCP-1, RANTES, Mig, and interferon-gamma inducible protein 10 was high in the interface zone and low in the subepidermal infiltrate. The messenger RNA expression and protein immunoreactivity patterns overlapped. According to the expression profiles, Mig, interferon-gamma inducible protein 10, MCP-1, and RANTES were expressed by basal keratinocytes above and mononuclear cells within the inflammatory foci. CONCLUSION: These cytokines are important agents in the cytokine network and contribute to the cell-specific and spatially restricted recruitment of mononuclear cells in the acute inflammation of erythema multiforme lesions.
A 20-year-old college student developed an immunologic hypersensitivity reaction, erythema multiforme minor, 1-2 weeks after receiving a meningococcal conjugate vaccine. He had no history of erythema multiforme, nor had he received any other vaccine or drug therapy. The temporal relationship between the development of erythema multiforme and the vaccination suggests that the meningitis vaccine probably was the causal agent. The occurrence of this distinct cutaneous reaction, with the potential for a serious complication such as erythema multiforme major or Stevens-Johnson syndrome on rechallenge, should serve as a warning against repeated booster vaccinations in patients who develop reactions such as this one.
OBJECTIVE: To report a case of erythema multiforme and hypersensitivity myocarditis caused by ampicillin. CASE SUMMARY: A 13-year-old boy was treated with ampicillin and gentamicin because of suspected septicemia. Medications were discontinued when erythema multiforme and congestive heart failure caused by myocarditis occurred. The patient was treated with methylprednisolone and gradually improved. Macrophage-migration inhibition (MIF) test with ampicillin was positive. DISCUSSION: After most infections causing erythema multiforme and myocarditis were ruled out, a drug-induced allergic reaction was suspected. Positive MIF test for ampicillin showed sensitization of the patient's lymphocytes to ampicillin. CONCLUSIONS: Hypersensitivity myocarditis is a rare and dangerous manifestation of allergy to penicillins.
A case of erythema multiforme and Rhus contact dermatitis is presented herein. Due to the association of nephritis and other complications with Rhus poison oak, we recommend that patients with contact dermatitis due to poison ivy who incur secondary erythema multiforme be hospitalized and closely monitored.
We describe a case of erythema multiforme in a 2-week-old boy. He had no remarkable antecedents, and a polymerase chain reaction-based technique failed to detect herpes simplex virus DNA in the skin biopsy specimen. To our knowledge, only one previous biopsy-proven case of erythema multiforme during the neonatal period has been reported.