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Results for “Erythema Multiforme”

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At least 343 records · Page 19Linked to original sources
PubMed1994

Toxic epidermal necrolysis and erythema multiforme following therapy with terbinafine.

We report two cases with severe skin reactions following oral terbinafine (Lamisil) therapy. The first case was a 49-year-old woman with onychomycosis of the toe nails. She had suffered from diabetes for 3 years, but it was well controlled on insulin. Five days after start of terbinafine 250 mg once daily she developed erythema. The treatment was continued for 2 days, but the skin eruption progressed, and a clinical diagnosis of toxic epidermal necrolysis was confirmed histologically. The second case was a 51-year-old woman with dermatomycosis on the right foot. She developed a papular eruption in the second week after taking terbinafine 250 mg once daily. Despite this eruption she continued treatment for 6 days. Generalized erythema multiforme developed in the following days. Terbinafine is a recently introduced efficacious fungicidal drug. This is the first report of toxic epidermal necrolysis following terbinafine.

Administration, Oral↗
PubMed1986

Erythema multiforme in a patient with T cell chronic lymphocytic leukemia.

A patient with T4+ (helper-inducer) T cell chronic lymphocytic leukemia developed an erythema multiforme-like eruption, the diagnosis of which was supported by routine light microscopic findings. Immunopathologic studies using monoclonal antibodies demonstrate that despite an overwhelming majority of leukemic T4+ cells in the peripheral blood and dermal infiltrate, the predominant cells in the epidermal infiltrate are T8+ (cytotoxic-suppressor) cells. These findings are different from those seen in epidermotropic T cell leukemic infiltrates and are similar to those previously reported in erythema multiforme. Thus it is likely that the leukemic T4+ cells are participating in this cutaneous hypersensitivity reaction along with residual, normal T8+ cells.

Aged↗
PubMed1990

Erythema multiforme associated with autoreactivity to 17 alpha-hydroxyprogesterone.

We report a case of a 23-year-old woman who was afflicted with disseminated skin erythema multiforme-like eruptions that started at the menarche, relapsed at the premenstrual periods, dramatically spread during two pregnancies and cleared after abortion; the skin lesions responded dramatically to thalidomide treatment. A high-affinity binding factor to 17 alpha-hydroxyprogesterone (17-OHP) was found in the serum of this patient. Her lymphocytes did not proliferate in vitro after exposure to exogenous 17-OHP but showed significant chromatin activation. There was a decreased expression of HLA antigens at the surface of the patient's blood lymphocytes. This is a unique well-documented case of erythema multiforme most possibly due to autoreactivity to 17-OHP; the precise mechanism(s) of this autoreactivity has not been established.

17-alpha-Hydroxyprogesterone↗
PubMed1997

Expression of bcl-2 in lichen planus, acute graft-versus-host disease, and erythema multiforme.

The bcl-2 gene family plays a significant role in the propagation of cell survival and tissue modeling. Bcl-2 was originally described in follicular lymphomas and is associated with the suppresion of cellular apoptosis. Evaluation for this protein has been performed for a variety of benign and malignant cutaneous tumors but not to any significant extent on inflammatory disorders. Therefore, we stained biopsy specimens from diseases with interface inflammation (lichen planus, acute graft-versus-host disease, and erythema multiforme) for Bcl-2. Epidermal expression of this protein was minimal for all three diseases; however, lymphocytes stained prominently in lichen planus. The data suggest that Bcl-2 is not prominently involved in the epidermal changes in these diseases. The role of other members of this oncogene family in interface dermatitis still needs to be elucidated.

Erythema Multiforme↗
PubMed1992

T lymphocytes expressing HECA-452 epitope are present in cutaneous acute graft-versus-host disease and erythema multiforme, but not in acute graft-versus-host disease in gut organs.

Lymphocytes in formalin-fixed skin biopsies from patients with cutaneous acute graft-versus-host disease (aGVHD) were studied with HECA-452 (an antibody recognizing lymphocytes with skin-homing properties) and a panel of antibodies recognizing pan-B (L26 [CD20]), pan-T (L60 [CD43] and A6 [CD45RA]), and T-helper subset (OPD4) antigens in paraffin sections. Biopsies from patients with erythema multiforme (EM) were similarly studied for comparison. In both conditions, T lymphocytes stained by OPD4 were predominantly confined to the dermis, whereas those stained by HECA-452 were concentrated in the epidermis; however, there was considerable variation between cases, and overlap between findings in the dermis and epidermis. Lymphocytes similarly studied in paraffin sections of liver, salivary gland, and gut affected by aGVHD were essentially unreactive with HECA-452, although they were largely stained by pan-T markers and showed some comparable reactivity with OPD4. The findings suggest that aGVHD of the skin is mediated by a different set of lymphocytes than in gut organs, and may have a similar immunologic mechanism to EM.

Acute Disease↗
PubMed1979

Abnormal root development, probably due to erythema multiforme (Stevens-Johnson syndrome).

A case report is presented of a patient in whom nearly all teeth of the permanent dentition still present had short roots, while some teeth had never been formed at all. It may be concluded from the typical differences in length between the roots of the various teeth that this condition must be due to complete cessation of the growth of the teeth at the age of 7 or 8 years. Since the patient suffered a fulminant attack of erythema multiforme (STEVENS-JOHNSON syndrome) at this age, and since no other possible explanation of the short roots has been found, it is concluded that this clinical condition may have been the reason for the short root anomaly found. Damage or even destruction of the epithelial root sheath during the disease may be assumed to be the direct cause of the failure of full root development.

Adult↗
PubMed1994

Localization of perforin in viral vesicles and erythema multiforme.

BACKGROUND: Perforin (Pf), a pore-forming protein, is a cytolytic protein of killer cells. Its deposition in lesioned skin has not been studied. OBJECTIVE: The purpose of this study is to show Pf deposition in the lesioned skin and Pf expression in the dermal infiltrates of various inflammatory skin diseases. METHODS: Frozen specimens obtained from 29 patients with 5 different diseases were immunohistochemically stained. RESULTS: Granular deposition of Pf was found in the lesioned skin in 2 out of 5 cases of viral vesicles and in 3 out of 7 cases of erythema multiforme. In the cases with Pf deposition, the percentages of Pf+ cells in the dermis were higher than in those without deposition. CONCLUSION: Pf released from natural killer cells or cytotoxic T lymphocytes may play a role in tissue damage.

Adolescent↗