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

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

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*

No abstract available.

KOH examination is a simple, rapid and diagnostic procedure to confirm dermatophytic infections. It is important to select a proper examination site of the lesion. To determinate the proper examination site of the lesion, mycologic studies were done with multiple specimens collected from the center, margin and out of margin of the ring-shaped dermatophytic skin lesion on the 58 patients. The results were as follows. Positive rate of KOH wet smear was 94.8% at the center and 100% at the margin of the lesions, 22.4% at the 1 cm and 5.2% at the 2 cm out of the lesions. The more hyphae were found in the lesion, the more hyphae were found out of the lesion. Culture was done on the Sabouraud's glucose agar from the highest KOH positive area and the positive culture was 48 strains (82.8%) of 58 patients. These findings suggested that the ring-shaped active margin was the best site to examine mycologic studies.
Agar ; Glucose ; Humans ; Hyphae ; Skin*

No abstract available.
Temperament*

BACKGROUND: thermotherapy has been shown to be effective in the treatment of some fungal infections. Dermatophyte are well grown at 25degrees C rather than 37degrees C or high temperature. OBJECTIVE: An vitro test was done to assess the complemental effect and optimal conditions of local heating on the susceptability of t. rubrum to systemic antifungal agents. METHODS: Microdilution susceptability test to ketoconazole and itraconazole was done using 96 well microplate. Eight strains of T. rubrum were isolated from patients withtinea pedis and were cultured at 25degrees C, 37degrees C and 42degrees C for 1, 8 or 24 hours per day. MIC were checked at 4th, 7th, 9th day after inoculution. RESULTS: The growth without antifungal agents at 37degrees C and 42degrees C were decreased by 805 and 50% of the growth at 25degrees C respectively. Seven day after inoculation was the proper time to check the MIC. MIC50 of ketoconazole was the lowest at 42degrees C for 24hours per day in value of 0.006microgram/ml, and 0.09microgram/ml at 37degrees C for 24hours per day, 0.37microgram/mlat 42degrees C, for 8hours per day and 37degrees C for 8hours per day. MIC at 42degrees C for 1 hours er day, 37degrees C for 1 hyours and 25degrees C for 24hours per ady MIC were the same in value of 0.05microgram/ml. MIC50 of itraconazole was the lowest at 42degrees C for 24hours per day in value of 0.006microgram/ml, 0.01microgram/ml at 37degrees C for 24hours per day, 0.02microgram/ml at 37degrees C for 8hours per day. MIC at 42degrees C for 8hours per day, 42degrees C for 1hours per day, 37degrees C for 24hours per day MIC were the same in value of 0.05microgram/ml. CONCLUSION: Incubation at 37degrees C for 24 hours per day or 42degrees C for 24 hours per day increased the susceptability of T. rubrum to ketoconazole and itraconazole.
Antifungal Agents* ; Arthrodermataceae* ; Complement System Proteins ; Heating ; Hot Temperature ; Humans ; Hyperthermia, Induced ; Itraconazole ; Ketoconazole

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