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A bipolar patient is described in whom erythema multiforme major, or Stevens-Johnson syndrome, developed after treatment with carbamazepine. The systemic and dermatological manifestations and some of the known causes of the syndrome are discussed.
Rowell's syndrome (RS) is a rare presentation of lupus erythematosus (LE) with erythema multiforme-like lesions associated with antinuclear, anti-La (SS-B)/anti-Ro (SS-A) antibodies and rheumatoid factor (RF) positivity. This syndrome is suggested to be a different variant of cutaneous lupus erythematosus by some authors in literature. Here we present a 64-year-old woman with LE and a 51-year-old woman with LE and Sjögren syndrome (SS) who had erythema multiforme-like eruptions and discuss the coexistence of lupus erythematosus and erythema multiforme.
We describe a case of cow-transmitted parapoxvirus infection--also known as milkers' nodules--after a hematopoietic stem cell transplantation for multiple myeloma. The infection was complicated by erythema multiforme and acute exacerbation of graft-versus-host disease. Parapoxvirus was confirmed by electron microscopy. The natural history of milker's nodules in immunocompetent hosts is described and compared to that in our immunocompromised patient.
The polymerase chain reaction (PCR) was used to detect HSV DNA in genomic DNA extracted from skin biopsies obtained from healed skin of five patients with hyperpigmented macules following recurrent cutaneous HSV infections and from eight patients with HSV-associated erythema multiforme (EM). A 92-bp HSV-1 DNA fragment was found in all the skin biopsies from the site of recurrent HSV infection and in five of eight (62%) biopsies from the EM patients. Virus DNA was not found in tissues distant from the site of HSV recurrence or from a patient without a history of HSV infection. These findings confirm the presence of HSV in healed skin from the site of recurrent HSV disease and are consistent with the concept that HSV is involved in EM pathogenesis.
The demonstration of circulating autoantibodies directed against the constitutive desmosomal plaque proteins desmoplakin (dp) I and II in mucocutaneous lesions in a subset of patients with erythema multiforme major, suggests that humoral immune mechanisms may play a role in the pathogenesis of this severe skin disease. In this study we identified a specific peptide sequence--YSYSYS--representing an antigenic binding site for the human autoantibodies. This epitope is localized at the extreme carboxy terminal domain of dp thought to be responsible for the assembly of keratin filaments with desmosomes. To test the possibility whether these antibodies may exert any pathologic effects in vivo, human autoantibodies were affinity purified on a corresponding synthetic peptide matrix and peptide-specific antibodies were raised in rabbits. After repeated subcutaneous injections into newborn mice, affinity-purified human autoantibodies and anti-peptide rabbit IgG were detected on desmosomal plaques of keratinocytes overlying the injection site. Histologic and electron microscopic examinations showed hydropic degeneration of basal and suprabasal keratinocytes, dyskeratosis, signs of suprabasal acantholysis, and keratin filaments detached from the desmosomal plaques clumping around the nucleus. We demonstrate that autoantibodies are directed to an epitope within a dp domain crucial for the interaction of keratin filaments with desmosomes, and, when injected subcutaneously into newborn mice, produce pathologic changes. These findings imply that autoantibodies to dp could impair the function of desmosome-keratin filament complexes suggesting a pathogenic role in vivo.
The preventive effect of low concentrations of zinc sulphate solution in recurrent herpes simplex of the skin and oral mucous membrane is reported. Treatment with zinc sulphate solution of the skin at the site of the herpetic infection also prevents relapse of post-herpetic erythema multiforme. For the skin, 0.025-0.05%, and for the oral mucous membrane, 0.01-0.025% zinc sulphate solution was used.
A case report is presented in which a respiratory tract infection with M. pneumoniae appears to have provoked a generalised mucocutaneous disease, described as Stevens Johnson syndrome. The patient possessed complement-fixing antibodies to M. pneumoniae to a titre of 1/2048 compared with the general population titre of 1/32. The oral mucosal lesions are described in particular and a likely pathogenesis of erythema multiforme is discussed.
Cutaneous larva migrans is an intensely pruritic serpiginous eruption caused by the dog or cat hookworm. Often, the disease is self-limiting and no other significant pathology develops; however, a significant localized inflammatory response to the nematode is extremely common. We present a case of cutaneous larva migrans in which a systemic inflammatory process ensued that was characteristic of erythema multiforme. We discuss possible mechanisms of this complication and review the literature.
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As reliable data on prevalence rates of drug-induced oral mucosa side effects are scarce in the medical literature, a retrospective analysis of drugs as possible inducers in 173 in-patients with either minor or major type of erythema multiforme (EM) admitted to the Erlangen University Department of Dermatology from 1970 through 1981 was carried out. In 62 of these cases precipitation by drugs was suspected by history, in 31 of them with oral mucosa involvement. In 11 out of 19 patients with mucocutaneous EM drug testing either in vivo or in vitro provided evidence for drug induction of EM.
A 5-month old female domestic shorthair cat developed lethargy and severe ulcerative skin lesions that covered more than half of its body after routine administration of rabies vaccine, anthelmintic, and ear medication. Clinical and histologic findings were consistent with a severe cutaneous drug reaction or erythema multiforme. The cat's condition continued to deteriorate despite drug withdrawal and supportive care. Administration of human intravenous immunoglobulin was well tolerated by the cat and led to rapid resolution of ulcerative cutaneous lesions, accompanied by substantial improvement in the cat's demeanor within 8 days. Human intravenous immunoglobulin appears to be a novel promising treatment for life-threatening cutaneous drug reactions.
Kikuchi disease, or histiocytic necrotizing lymphadenitis, is a benign illness characterized by fever and cervical lymphadenopathy predominantly in young women. It has a self-limiting course. Skin changes occur in about one-third of patients and are of a nonspecific nature. A case of Kikuchi disease with cutaneous involvement in the guise of erythema multiforme and a facial rash is reported. The differential diagnosis with systemic lupus erythematosus and Rowell syndrome is discussed.
A 5-year-old female border collie presented with erythematous skin lesions at the axillae, groin, mucocutaneous junctions, and pinnae. Biopsy revealed lymphocytic interface dermatitis with hydropic degeneration of basal cells and keratinocyte apoptosis. Based on gross and histological features, diagnosis of erythema multiforme was made. The disease was resolved by treatment with azathioprine, prednisolone, and a hypoallergenic diet. Finally, the skin lesion was controlled without drug therapy but recurred easily every time commercial foods except the hypoallergenic diet were used, suggesting that food substances triggered this outbreak.
Recently, it has been suggested that reactive oxygen species (ROS) produced by activated polymorphonuclear leukocytes (PMNs) exert auto-oxidative tissue damage at the site of inflammation. In the present study, a possible role of ROS in the pathogenesis of erythema multiforme (EM) was investigated by determining the capacity of the sera from patients for generating ROS from PMNs. Significantly increased hydroxyl radical production was observed, which is one of the most potent ROS capable of causing tissue damage. This change was not observed when PMNs were incubated with sera from patients with bullous pemphigoid (BP) or inflammatory acne, indicating that this finding was not a common feature of immunologically mediated and/or inflammatory cutaneous disorders. Elevated C1q activities and depositions of immunoreactants in the blood vessels were also noticed in some patients. These findings suggest that ROS generated by PMNs are involved in the formation of cutaneous lesions of EM and that immune complexes (ICs) may provide an important mechanism in PMN activation.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.