[Pulmonary changes in erythema nodosum and exudative multiform erythema].
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Erythema↗
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Erythema-multiforme-like eruption on the application site of a nitroglycerin patch, followed by widespread erythema multiforme.
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Dermatitis, Allergic Contact↗
Controversy: are systemic steroids indicated in the treatment of erythema multiforme?
The treatment of erythema multiforme major with systemic steroids became established during the 1950s. Recently, two retrospective case reviews comparing steroid-treated and nonsteroid-treated groups of patients with erythema multiforme found that these agents may be associated with complications. As a result, many clinicians have become uncertain as to the appropriate therapy of this disease entity. We successfully treated the condition with steroids in two children and one adolescent. The controversy over the potential efficacy of such therapy for erythema multiforme persists, however.
Adrenal Cortex Hormones↗
Lamotrigine-induced erythema multiforme mimicking contact dermatitis.
Erythema multiforme is an acute, hypersensitivity reaction of the skin often secondary to medications. Lamotrigine is a relatively new anticonvulsant medication approved for seizure and psychiatric disorders. Although the overall incidence of cutaneous reactions to lamotrigine is high, the incidence of serious eruptions such as erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis is low. Vigilant surveillance for any cutaneous eruption in patients on lamotrigine is important, particularly in the first 8 weeks, as prompt discontinuation of the medication can prevent progression. We report a case of erythema multiforme secondary to lamotrigine, which clinically resembled a contact dermatitis, and review the management of lamotrigine associated cutaneous eruptions.
Adult↗
Acyclovir for recurrent erythema multiforme caused by herpes simplex.
Herpes-associated erythema multiforme can be controlled by continuous suppressive treatment with oral acyclovir. Erythema multiforme is not prevented if oral acyclovir is administered after a herpes simplex recurrence is evident and it is of no value after erythema multiforme has occurred. There is some question whether continuous topical treatment with acyclovir to sites of recurrent herpes will sometimes prevent erythema multiforme. Erythema multiforme may be precipitated by orolabial and genital recurrences and by recurrences on skin of the buttocks and other sites. Some herpetic recurrences are associated with erythema multiforme and some are not and episodes of erythema multiforme are not always associated with clinical herpetic recurrences.
Acyclovir↗
Histoplasmosis presenting as erythema multiforme and polyarthritis.
Erythema multiforme and polyarthritis occurred in association with serologic evidence of primary histoplasmosis. Although such occurrences have been noted in epidemics, recognition of this triad outside of the epidemic setting has been described only once before.
Acute Disease↗
Clinical observations of erythema multiforme in children.
Erythema multiforme (EM), a cutaneous or mucocutaneous disorder, occurs primarily in young adults. To evaluate the precipitating factors, clinical courses, and treatment of this disease in children, 30 cases aged from 1 month old to 15 years of age were studied retrospectively from Jan 1988 to Aug 1998. Twenty-three cases were diagnosed as minor type; the other 7 were of major type (Stevens-Johnson syndrome). Mycoplasma infection was identified in 4 patients, and adenovirus in one patient with EM minor. Cytomegalovirus was found in one EM major patient. Anticonvulsant administration before the skin lesions were recorded in 5 EM major patients and 2 EM minor patients. All cases received supportive treatment during admission. Besides, 6 of 7 patients with EM major, and 11 of 23 EM minor (Group A) received systemic corticosteroid at a dose equal to prednisolone 1-2 mg/kg/day for 3-14 days. One EM major patient and 11 patients with EM minor (Group B) received supportive care only. One EM minor patient with acute idiopathic thrombocytopenia purpura was treated with intravenous immunoglobulin. The mean duration of course of EM minor was 11.8 +/- 2.9 days, and it was 25.1 +/- 9.8 days for EM major. No mortality and no sequelae were noted. The average disease course and hospitalization time were not significantly different between Group A and B: (11.4 +/- 3.1 days vs 12.4 +/- 2.9 days, p = 0.45); (5.4 +/- 2.0 days vs 6.3 +/- 3.1 days, p = 0.47). This study demonstrated that infections, especially mycoplasma, and anticonvulsants play important roles in childhood EM. The skin lesions of EM minor subsided within 2 weeks, and EM major recovered completely within 6 weeks. Systemic corticosteroid may be beneficial to EM major, but probably is unnecessary for patients with EM minor.
Adolescent↗
Erythema multiforme.
In summary, the diagnosis of erythema multiforme is appropriate for a self-limiting or episodic cutaneous or mucocutaneous illness with skin lesions morphologically and histologically compatible. With typical erythema multiforme minor, characterized by classic skin lesions with or without oral erosions, most patients' disease is associated with recurrent herpes simplex infections. This is particularly true with recurrent erythema multiforme. Symptomatic conservative care, antibiotic treatment for purulent secondarily infected oral lesions, and avoidance of systemic steroids are appropriate therapeutic guidelines. The more serious syndrome, erythema multiforme major, or Stevens-Johnson syndrome, is characterized by skin lesions that are somewhat atypical and different from those of erythema multiforme minor in association with erosions on multiple mucosal surfaces. Drugs and mycoplasmal infections are important precipitating factors for erythema multiforme major. Hospitalization and laboratory tests are often required because of the severity of the illness and the occasional damage to other organ systems. Conservative, symptomatic care, withdrawal of any drug that may have caused the illness, treatment of any mycoplasmal infection, and antibiotic therapy for purulent secondarily infected lesions are worthwhile therapeutic measures. Early treatment with systemic steroids may be helpful in preventing further damage, and the risks and potential benefits of such therapy must be evaluated on an individual basis.
Adrenal Cortex Hormones↗
Apoptosis in oral erythema multiforme.
OBJECTIVE: Cell death was evaluated in oral erythema multiforme to test the hypothesis that apoptosis may be a mechanism by which keratinocytes die in this condition. STUDY DESIGN: Ten erythema multiforme and five control oral mucosa biopsy specimens were evaluated in immunohistochemically stained sections for apoptosis-regulating proteins Bcl-2, Bcl-x, Bax, p53, Fas, and Fas-ligand. Apoptotic keratinocytes, determined by a detection method for DNA fragmentation (TUNEL) and by conventional morphologic criteria were counted per high power field. RESULTS: Keratinocyte staining for Bcl-2 protein was comparable in erythema multiforme and controls. Bcl-x expression was reduced in five erythema multiforme cases. Staining for Bax protein differed in six erythema multiforme cases and showed variable intensity in layers under the parakeratin. Only slight differences in staining patterns of Fas and Fas-ligand proteins were noted between erythema multiforme and controls. The number of apoptotic keratinocytes evaluated by morphologic examination was significantly higher in erythema multiforme (mean per high power field, 0.90 +/- 0.2; controls, 0.06 +/- 0.04; p < 0.05, Mann-Whitney test) and was limited in significance by the TUNEL method (erythema multiforme, 0.43 +/- 0.1; controls, 0.02 +/- 0.02). Overexpression of p53 protein was seen in basal keratinocytes in five erythema multiforme specimens (mean, 17.5 +/- 4.03 per high power field; controls 1.2 +/- 0.3). CONCLUSIONS: There is evidence that cell death in erythema multiforme is at least in part due to apoptosis. The apoptotic mechanism may be related to an altered expression of apoptosis-regulating proteins. Although measurable alterations in the phenotypic expression of Fas and Fas-ligand proteins were not apparent, activation of Fas/Fas-ligand system could still be involved in the induction of apoptosis in erythema multiforme.
Adult↗
Oral acyclovir for the prevention of herpes-associated erythema multiforme.
Herpes simplex virus is the single most common precipitator of erythema multiforme. Typically, erythema multiforme lesions appear 10 to 14 days after a recurrent herpes simplex virus infection and attacks can be disabling when they occur at frequent intervals. Prior to the introduction of acyclovir (Zovirax), there was no effective therapy to prevent herpes-associated erythema multiforme. Four patients were treated with a maintenance dose of acyclovir for periods ranging from 10 to 26 months; there were no significant side effects from the drug and only one recurrence of erythema multiforme. Oral acyclovir may become the treatment of choice for herpes-associated erythema multiforme.
Acyclovir↗
Target lesions on the lips: childhood herpes simplex associated with erythema multiforme mimics Stevens-Johnson syndrome.
Erythema multiforme and Stevens-Johnson syndrome are both characterized by areas of epithelial necrosis. An important clinical feature that distinguishes the two is the extensive mucosal necrosis in Stevens-Johnson syndrome but not in erythema multiforme. Because significant and serious complications may develop with Stevens-Johnson syndrome and not with erythema multiforme, it is important to differentiate between the conditions. We describe three boys with herpes simplex virus-associated erythema multiforme who had severe necrosis of the lips develop and were initially diagnosed with Stevens-Johnson syndrome. The lip lesions were large target lesions of erythema multiforme rather than the extensive necrosis seen in Stevens-Johnson syndrome and all three had a benign course.
Child↗
Unusual leukoderma after erythema multiforme: a case report.
Erythema multiforme is an inflammatory disorder of the skin that usually fades without sequelae. It is well known that after inflammatory events, hyper- or hypochromic spots can remain, especially in skin types III-VI, but achromia is very rare. We report a case of residual leukoderma after erythema multiforme.
Child↗
Erythema multiforme minor in children.
Erythema multiforme minor is an acute, self-limited cutaneous or mucocutaneous disorder. Although it most commonly afflicts young adults, it is also frequently seen in children. An antecedent infection with herpes simplex virus is often the precipitating factor. Recent studies detailing the usual clinical course and histologic features of erythema multiforme minor, together with investigative studies examining potential pathomechanisms, have begun to provide a clearer picture of this disease process such that a more rational approach to therapy is now possible.
Acyclovir↗
Detection of a herpes simplex viral antigen in skin lesions of erythema multiforme.
The commonest variety of erythema multiforme follows a lesion caused by a recurrent herpes simplex virus infection. In studying the immunopathogenesis of herpes-associated erythema multiforme, we examined skin lesions for the presence of a herpes simplex viral antigen by an indirect immunofluorescence test using a monoclonal antibody to a major type-common glycoprotein antigen, gB. Focal staining showed this antigen to be present in epidermal cells in 12 of 16 skin biopsy specimens. The staining was similar to, but less intense than, that seen in biopsy samples of lesions of recurrent herpes simplex virus infections. Similar findings were not seen in control skin biopsy specimens from lesions of other skin diseases; a control monoclonal stain also was negative in biopsy specimens. These findings suggest that the immune reaction and subsequent tissue damage of herpes-associated erythema multiforme are due to the presence of herpes antigens in the skin.
Antibodies, Monoclonal↗
Identification of herpes simplex virus DNA in lesions of erythema multiforme by the polymerase chain reaction.
An association between erythema multiforme and herpes simplex virus infection has been supported by clinical studies and by the detection by immunofluorescence of herpes viral antigen in sera and skin biopsy specimens of patients with erythema multiforme. In rare cases, the virus has also been isolated in cultures of skin biopsy specimens of erythema multiforme. To investigate further the association between erythema multiforme and herpes simplex virus, we used the polymerase chain reaction for herpes simplex virus to examine skin lesions from patients with erythema multiforme. In this study herpes simplex virus DNA was detected in 11 of 31 biopsy specimens of erythema multiforme; six additional cases showed equivocal amplification results, which is suggestive of low amounts of viral DNA. Seven skin and mucosal biopsy specimens with the histologic changes of herpes virus infection served as positive controls: all were positive for herpes simplex virus DNA. Viral DNA was not detected in control biopsy specimens from skin excised for unrelated conditions. These studies support the association of herpes simplex virus in the pathogenesis of some cases of erythema multiforme. The polymerase chain reaction provides a quick and effective method of detecting herpes simplex virus in lesions of herpes-associated erythema multiforme. Furthermore, the polymerase chain reaction may delineate those cases of erythema multiforme that are etiologically related to herpes virus infection and therefore might be treated with acyclovir to prevent recurrence.
Aged↗
Virus induced erythema multiforme and Stevens-Johnson syndrome.
Erythema Multiforme is an acute, self-limited inflammatory cutaneous disorder characterized by distinctive target lesions. Stevens-Johnson syndrome (SJS) is defined as severe erythema multiforme with mucosal involvement, visceral involvement, or both. Both diseases are part of a continuum of immunologically mediated mucocutaneous diseases at various grades of severity. Viral infections are known triggers of these skin disorders. We report the success of a management strategy of acyclovir and prednisone for herpes simplex virus-associated erythema multiforme. In addition we describe the apparent first case of primary varicella infection as a direct cause of SJS. The two cases are presented and a single-case statistical analysis has been employed to evaluate the significance of the management protocol. The method of analysis is presented in the appendix. When a patient with primary varicella infection develops bullous lesions, SJS should be considered in the differential diagnosis, as early and intense corticosteroid therapy may be lifesaving. A regimen of prophylactic acyclovir and therapy for an exacerbation of herpetic lesions with acyclovir and prednisone was effective in inducing significant control of recurrent erythema multiforme secondary to herpes simplex in our patient.
Acyclovir↗
[Erythema multiforme majus and Chlamydia pneumoniae infection].
BACKGROUND: Erythema multiforme majus of infectious origin is an acute eruptive syndrome seen more commonly in young subjects and characterised by an appearance of round target lesions. In most cases, it is associated with infection involving Herpes simplex virus or Mycoplasma pneumoniae. We report an original case of erythema multiforme majus subsequent to infection with Chlamydia pneumoniae. CASE REPORT: An 18 year-old man was hospitalised for management of generalised skin rash comprising lesions in rings, associated with bullous and post-bullous lesions, chiefly in the oral (preventing eating) and genital areas in a setting of febrile cough. Various bacterial agents (Mycoplasma pneumoniae, Chlamydia pneumoniae) and viral agents were suspected, but serological testing for Chlamydia pneumoniae alone was positive with IgM of 128 IU and IgG of 64 IU. The outcome was favourable within several days following administration of symptomatic treatment (rehydration, mouthwashes, etc.) and aetiological treatment (acyclovir: 30 mg/kg/d, ofloxacine: 400 mg/d). At D15, serologic tests for Mycoplasma pneumoniae continued to be negative. Anti-Chlamydia pneumoniae IgM and IgG were 256 IU. At D30, IgM was 128 IU while IgG remained at 256 IU. DISCUSSION: The existence of a systematic skin rash comprising typical target lesions and mucosal lesions in the oral and genital areas suggested to us a diagnosis of erythema multiforme majus. Screening for the agents generally responsible was negative and drug-induced rash was ruled out. Serological tests for Chlamydia pneumoniae were positive at various times, resulting in diagnosis of erythema multiforme majus secondary to infection with Chlamydia pneumoniae. Following demonstration of the presence of Chlamydia pneumoniae using reliable methods and the elimination of other causes of erythema multiforme majus, dermatologists should opt for this aetiology in order to optimise treatment.
Acyclovir↗
Erythema multiforme due to pyrazinamide.
Drug-induced erythema multiforme is reported with many antimicrobial and antipyretic medications. We present one patient who experienced erythema multiforme and urticaria after administration of pyrazinamide for treatment of cutaneous tuberculosis. The side-effects of pyrazinamide include hepatic or dermatologic disorders, but erythema multiforme has not yet, to our knowledge, been described. Clinical features and discontinuation and reintroduction of the drug led us to consider pyrazinamide the cause of the erythema multiforme, but allergologic studies remained negative, except for the presence of circulating immune complexes. The mechanism of this eruption remains obscure, and definite withdrawal of pyrazinamide seems to be the best therapeutic choice.
Aged↗