Toxic epidermal necrolysis is a reactive erythema of nonstaphylococcal origin characterized by a scalded appearance of the skin. The TEN is widely regarded as a variant of severe erythema multiforme because of its acute course, its freguent common cause, its freguent overlap with Stevens-Johnson disease, and its histologic identity. I present a case of TEN with severe mucosal involvement resembled Stevens-Johnson disease.
Erythema ; Erythema Multiforme ; Skin ; Stevens-Johnson Syndrome*

Lichenoid drug eruption is lichenoid skin eruptions caused by certain drugs and compounds, and can be identical or similiar to lichen planus. A 75-year-old woman who had taken antituberculosis medication(INH, ethambutol, rifampin) for 4 months developed pruritic generalized erythematous papular eruptions on the trunk and extremities, alopecia and nail dystropy. Histopathologic findings were hyperkeratosis, hypergranulosis, hyc rophic degenaration of basal layer, band like lymphohistiocytic infiltration in the upper dermis and perivascular lymphohistiocytic infiltration in the deep dermis. She was treated with systemic corticosteroid, and then skin lesion were slightly improved. After termination of antituberculosis medication, skin lesions were markedly improved with residual hyperpigmentation. Alopecia and nail dystrophy were also improved.
Aged ; Alopecia ; Dermis ; Drug Eruptions* ; Ethambutol ; Extremities ; Female ; Humans ; Hyperpigmentation ; Lichen Planus ; Skin

BACKGROUND: In tinea pedis, the response of treatment and prognosis are different according to clinical types. Positivity in KOH mount and causative agent in culture are also different. OBJECTIVE: Our purpose was to evaluate the clinical characteristics and mycologic findings of tinea pedis according to the clinical type. METHODS: A clinical and mycological study was conducted with 97 cases of tinea pedis among out patients examined for 7 months from June 1994 to December 1994 at Yeungnam University Hospital and Catholic Skin Clizic, Taegu, Korea. RESULTS: 1. Age distribution showed patients in their fourth decade to be most common. The ratio of male to female was 1.2: 1. The distribution of patients by clinical type was interdigital type, interdigital combined with hyperkeratotic type, interdigital combined with vesicular type, hyperkeratotic type, and hyperkeratotic combined with vesicular type, in descending order. One to five years was the most comrrion duration of tinea pedis. Duration of tinea pedis was the shortest in the vesicular type, otherwis was longer in hyperkeratotic type. Rate of family history of tinea pedis was 54.6%. The larger the size of family was, the higher the positivity in family history. The rate of coexistent dermatiophytosis with tinea pedis was 39.1%, and tinea unguium was the most common one. 2. The isolated dermatophytis were T. rubrum, 90.7%, T. mentagrophytes, 7.2%, and T. rubrum rnixed with T. mentagrophytes, 2.1%. T. rubrum showed an even distribution in all clinical types of tinea pedis whereas T. mentanophytes was isolated only in the interdigital type, vesicular type, and interdigital combined with vesicular type. T. rubrum mixed with T. mentagrophytes was isolated in the interdigital combine with vesicular type. Distribution of dermatophytes was relatively even arnong the age groups. T. rubrum showed a relatively even distribution in duration of tinea pedis, but T. mentagrophytes was isolated in tinea pedis with shorter duration.
Age Distribution ; Arthrodermataceae ; Daegu ; Female ; Humans ; Korea ; Male ; Onychomycosis ; Outpatients ; Prognosis ; Skin ; Tinea Pedis* ; Tinea*

Angiosarcoma is a rare malignant vascular tumor of endothelial cell origin, Cutaneous angiosarcoma usually occurs on the scalp and face of the elderly and most frequently in the sixth and seventh decade. We presented a case of angicisarcoma in a 70 year old woman. The patient had a well-demarcated, 3 x 3cm sized, dark brownish-colored, ulcerative nodule on the vertex with hemorrhagic bulla on the right. temporal scalp. Histopathologic examination of the nodule showed a well differentiated tumor with irregular anastomosing scular channels lined by atypical endothelial cells in the dermis and subcutaneous fat. Immunohistochenlical study for factorVlll-related antigen was partially positive in tumor channels. She was treated by wide surgical excision but she expired 5 months after discharge from the hospital.
Aged ; Dermis ; Endothelial Cells ; Female ; Hemangiosarcoma* ; Humans ; Scalp ; Subcutaneous Fat ; Ulcer

No abstract available.

No abstract available.
Temperament*

We report a case of kerion celsi caused by Trichophyton verrucosum in a 4-year-old male. He presented painful, tender, indurated, boggy masses discharing pus on the vertex and occiput. Kerion celsi caued by T. verrucosum was diagnosed by the characteristic gross and microscopic findings of the colony on the Sabourauds glucose. agar. The possible source of infection was searched and wq found that he raised the cattles in his house. They had multiple, scaly, whitish plaques on the skin and T. verrucosum was identified from the hairs of the lesions. He had been treated with griseofulvin and prednisolone, and all lesions were cleared leaving partial alopecia in 2 months.
Agar ; Alopecia ; Child, Preschool ; Glucose ; Griseofulvin ; Hair ; Humans ; Male ; Prednisolone ; Skin ; Suppuration ; Tinea Capitis* ; Trichophyton*

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

No abstract available.
Appointments and Schedules* ; Erythrocytes*