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.
Antifungal Agents* ; Trichophyton*

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

No abstract available.
Child* ; Humans ; Hypertension, Portal*

It was reported that esthetic composite resin restoration reinforces the strength of remaining tooth structure with preserving the natural tooth structure. However, it is unknown how much the strength would be recovered. The purpose of this study was to compare the fracture resistance of three types of undermined cavity filled with composite resin with that of non-cavitated natural tooth. Forty sound upper molars were allocated randomly into four groups of 10 teeth. After flattening occlusal enamel, undermined cavities were prepared in thirty teeth to make three types of specimens with various thickness of occlusal structure (Group 1 ~ 3). All the cavity have the 5 mm width mesiodistally and 7 mm depth bucco-lingually. Another natural 10 teeth (Group 4) were used as a control group. Teeth in group 1 have remaining occlusal structure about 1 mm thickness, which was composed of mainly enamel and small amount of dentin. In Group 2, remained thickness was about 1.5 mm, including 0.5 mm thickness dentin. In Group 3, thickness was about 2.0 mm, including 1 mm thickness dentin. Every effort was made to keep the remaining dentin thickness about 0.5 mm from the pulp space in cavitated groups. All the thickness was evaluated with radiographic Length Analyzer program. After acid etching with 37% phosphoric acid, one-bottle adhesive (Single Bond(TM), 3M/ESPE, USA) was applied following the manufacturer's recommendation and cavities were incrementally filled with hybrid composite resin (Filtek Z-250(TM), 3M/ESPE, USA). Teeth were stored in distilled water for one day at room temperature, after then, they were finished and polished with Sof-Lex system. All specimens were embedded in acrylic resin and static load was applied to the specimens with a 3 mm diameter stainless steel rod in an Universal testing machine and cross-head speed was 1 mm/min. Maximum load in case of fracture was recorded for each specimen. The data were statistically analyzed using one-way analysis of variance (ANOVA) and a Tukey test at the 95% confidence level. The results were as follows: 1. Fracture resistance of the undermined cavity filled with composite resin was about 75% of the natural tooth. 2. No significant difference in fracture loads of composite resin restoration was found among the three types of cavitated groups. Within the limits of this study, it can be concluded the fracture resistance of the undermined cavity filled with composite resin was lower than that of natural teeth, however remaining tooth structure may be supported and saved by the reinforcement with adhesive restoration, even if that portion consists of mainly enamel and a little dentin structure.
Adhesives ; Chimera ; Collodion ; Dental Enamel ; Dentin ; Molar ; Phosphoric Acids ; Reinforcement (Psychology) ; Stainless Steel ; Tooth ; Water

We report a case of primary cutaneous cryptococcosis on the left knee of a 67 year-old woman. She had a large ulcerated and indurated plaque with yellowish purulent exudates on her left knee. A histopathological examination from the lesion showed numerous encapsulated, round spores. Cultures from the lesion showed the presence of Cryptococcus neoforrnans. This may have resulted from an immunosuppressive state due to long-term use of oral corticosteroids.
Adrenal Cortex Hormones ; Cryptococcosis* ; Cryptococcus ; Exudates and Transudates ; Female ; Humans ; Knee ; Spores ; Ulcer

We report a case of congenital giant pigmented nevus with malignant melanoma of brain in a 14-year-old male patient. He had giant pigmented nevus on the back and neck, and multiple satellite lesions over the whole body since birth. One year prior to visit to our hospital, the patient suffered from various neurologie symptoms including headache, nausea, vomiting, seizure and right side motor weakness. Flistologic findings of skin lesions were benign nevocytic nevi. Computed tomogram of brain demonstrated increased densities in the both fronto-parietal leptameninges and brain parenchyme. Histologic findings of brain parenchyme by stereotaxic long needle biopsy showed the infiltration of melanin containing atypical melanocytes. There was no evidence of malignant melanoma at other organs. All of these findings suggested that origin of malignant melanoma of brain parenchyme was leptomeninges rather than skin.
Adolescent ; Biopsy, Needle ; Brain* ; Headache ; Humans ; Male ; Melanins ; Melanocytes ; Melanoma* ; Nausea ; Neck ; Nevus ; Nevus, Pigmented* ; Parturition ; Seizures ; Skin ; Vomiting

No abstract available.
Neurofibroma*