No abstract available.
Antifungal Agents* ; Trichophyton*

PURPOSE: Lower caliceal stones treated with ESWL do fail to pass more frequently than middle or upper caliceal stones. We analyzed the results of ESWL of renal caliceal stones according to the location of calix. MATERIALS AND METHODS: We reviewed the stone-free rate in 119 caliceal stone patients treated with 3rd generation lithotriptor, EDAP LT-02 according to the caliceal location of the stone. Location of the stones were upper calix in 30, middle calix in 30, and lower calix in 59 patients. RESULTS: Stone-free rate was 90.0%(27/30 patients) in middle caliceal stones, 74.6%(44/59 patients) in lower caliceal stones, and 66.7%(20/30 patients) in upper caliceal stones. CONCLUSIONS: Stone-free rate of lower caliceal stones is higher than upper caliceal stones.
Humans ; Lithotripsy* ; Shock*

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*

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

Extramammary paget's disease is uncommon intraepithelial carcinoma of the skin and frequently associated with a subjacent or a regionally proximate carcinoma. We have experienced a case of extramammary Paget's disease affecting 71 year-old man. The patient has been suffered from a well demarcated, and slowly growing erythematous plaque on the left suprapubic area of 3 years. A biopsy specimen reveals infiltration of typical Paget's cells within the epidermis and the adnexa. We review the literature briefly.
Biopsy ; Carcinoma in Situ ; Epidermis ; Humans ; Paget Disease, Extramammary* ; Skin

No abstract available.
Drug Therapy*

A case of sporotrichosis misdiagnosed as lupus vulgaris was presented. A 56-year-old woman had been to pea sized, nontender pustules and a hypertrophic-scar-like nodule on the right thigh. She denied any trauma before the lesions developed. Histopathologic findings from the lesion showed tuberculosis-like granulomatous changes. And she was diagnosed as lupus vulgaris. She also had pulmonary tuberculosis and had been treated with antituberculous drugs for 1 year. But skin lesions was not cleared. We suspected the lesions as one of deep mycoses and could confirm sporotrichosis by mycologic studies. They showed characteristic gross colonies and microscopic findings of Sporothrix schenckii..
Female ; Humans ; Lupus Vulgaris* ; Middle Aged ; Mycoses ; Peas ; Skin ; Sporothrix ; Sporotrichosis* ; Thigh ; Tuberculosis, Pulmonary

We report a case of piroxicam-induced photosensitive dermatitis in a 54-year-old female. She had taken oral piroxicam and was exposed to the sunlight on her way home for a few minutes. Several hours after the sun-exposure she developed well-defined, confluent, erythematous plaques and numerous vesicobullae with pruritus and prickling sensation on the sun-exposed areas. A phototest was done on her first visit. The minimal erythemogenic dose (2 J/cm²) of ultraviolet (UV) A was markedly decreased whereas that of UVB was within a normal limit. Visible light irradiation for 30 minutes did not cause skin lesions. Six months after the initial skin lesions, a photopatch test with 1% and 10% piroxicam solution followed by UVA (10 J/cm²) irradiation showed positive responses on both concentrations.
Dermatitis* ; Female ; Humans ; Light ; Middle Aged ; Piroxicam ; Pruritus ; Sensation ; Skin ; Sunlight

No abstract available.
Humans* ; Interleukin-10*