A case of cutaneous cartilaginous tumor was diagnosed from solitary nadular skin lesion on a toe of 59-year old female. Lack of information about cartilage tumors in the dermatologic literature suggest that they rarely develop as supeficial lesions. General clinico-pathologic feature of the tumor is reviewed.
Cartilage ; Chondroma ; Female ; Humans ; Middle Aged ; Skin ; Toes

BACKGROUND: Monofunctional psoralens plus UVA radiation are not severely phototoxic and have less mutagenic activity than bifunctional psoralens plus UVA radiation. OBJECTIVE: The purpose of this study was to evaluate pigment producing effect using various concentrations(0.02%, 0.1%, 0.5%) of monofunctional psoralens such as angelicin, khellin and comparing it's effect with TMP in topical photochemotherapy. METHOD: Ninty three C57BL mice were painted with either angelicin, khellin or TMP solution in concentrations of 0.02%, 0.1% and 0.5% each and were UVA irradiated. Skin biopsies were performed at 1,3,5 weeks after UVA irradiation. The pigment producing effects were measured by the number, area and perimeter of the melanocytes after topical PUVA. RESULTS: The comparison of melanocyte numbers between different psoralens after five weeks of photochemotherapy showed a significant difference in decreasing order of TMP, khellin and angelicin. The area and perimeter of melanocytes were larger in the TMP group after five weeks photochemotherapy than the other group. However in the khellin and angelicin group, the area and perimeter of melanocytes were not increased by increasing the frequency of the UVA irradiation. CONCLUSION: The number, area and perimeter of melanocytes after topical PUVA increased in the TMP group compared to angelicin or khellin group. We expect the clinical application of angelicin and khellin in vitiligo is possible considering the result of the study of pigment producing effect with a higher concentration and higher dose of UVA.
Animals ; Biopsy ; Ficusin* ; Furocoumarins ; Khellin ; Melanocytes* ; Methods ; Mice* ; Mice, Inbred C57BL ; Paint ; Photochemotherapy* ; Skin ; Thymidine Monophosphate ; Vitiligo

Since 1856, Mayer13) coined the term “osteotomy” for a tibial resection for an angular deformity, various shapes and designs of osteotomies in long bone or pelvis have been popularized to treat the malunion, osteoarthritis of hip and knee, bow leg, L.C.P., or C.D.H. etc. The purpose of corrective osteotomy for tibia is so different from that of upper extremity because it must be restored the weight bearing alignment, and equalize or minimize the leg length discrepancy. We respectively reviewed 14 cases with various angular deformities on tibia who were treated at Dept. of Orthopaedic Surgery, Catholic Medical College from Jan. 1976 to Dec. 1984. The results obtained were as follows: 1. Causes of angular or rotational deformities of tibia were malunion in 11, bow leg in 2 and partial closure of distal tibial epiphysis in l. 2. Ten cases of tibial deformities exceeded over the 10° of medial or lateral angulation and 15° of anterior or posterior bowing were corrected for normal weight-bearing alignment in lower leg. And a rotational deformity may be so disabling to walk as to require surgery. So four cases of tibial angular deformities combined with more than 20° of external rotation and 5° of internal rotation were corrected for normal good looking walks. 3. The maximum length that can be gained by an opening wedge osteotomy was near the point of maximum angluation, but it could be changed by the cause of deformity and patient's age. We've done 4 cases of opening and 10 cases of closing wedge osteotomy. 4. Angular deformity in one plane due to fracture in children under 10 years of age may be corrected spontaneously by growth, but deformities due to bow leg or epiphyseal injury cann't be expected any spontaneous correction of deformity by growth. So three cases of tibial deformities due to bow leg or epiphyseal injury in children were corrected in earlier after recognition of that deformities because of possible damage to articular cartilage and the combined rotational deformities. 5. A slight deformity if the angulation involves near a joint, knee or ankle could be seriously disabling and so must be correctcd earlier. 6. Functional results of the corrective wedge osteotomy in angular and rotational deformities of tibia were excellent, good, fair in 4, 7 and 3, respectively.
Ankle ; Cartilage, Articular ; Child ; Congenital Abnormalities ; Epiphyses ; Genu Varum ; Humans ; Knee ; Knee Joint ; Leg ; Numismatics ; Osteoarthritis, Hip ; Osteotomy ; Pelvis ; Tibia ; Upper Extremity ; Weight-Bearing

We investigated the clinical aspect and immunologic parameters of childhood and adult vitiligo in our clinics and made a comparative study. The childhood vitiligo showed the following results : similar incidence of clinical patterns with adults except for the lower incidence of the acrofacial type than in adults ; less involvement in the extent of lesion of disease than in adults ; higher incidence of family history than with adults ; of the precipitating factors, trauma is the main one whereas emotional stress is for adults ; higher association with halo nevi than adults ; and lower incidence of serum autoantibodies than adults. We have ascertained that childhood vitiligo is a distinct subset of vitiligo, showing the above features which will be studied in more patients in a long term follow-up clinical study.
Adult ; Autoantibodies ; Clinical Study ; Follow-Up Studies ; Humans ; Incidence ; Nevus, Halo ; Precipitating Factors ; Stress, Psychological ; Vitiligo

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es 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 t,he 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* ; 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 treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es 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 t,he 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* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

Several observation suggest that the antimelanocyte autoantibodies could play a role in melanocyte destruction. Some experiments indicate that melanocyte antibodies from patients with vitiligo can kill melanocyte in vitro. In these experiments, we demonstrated that vitiligo patient's sera containing antimelanocyte antibodies can lyse cultured human melanocytes by complement activation. Melanocyte cytotoxicity was measured using the ethidium bromide/ acridine orange viability assay. Significant melanocyte cytotoxicity was seen in sera from patients with both active and inactive vitiligo(p<0.01). Melanocyte cytotoxicity measured with complement-mediated cytotoxicity decreased after systemic steroid treatment(p<0.05) ; however melanocyte cytotoxicity showed no significant change with systemic PUVA therapy.
Acridine Orange ; Antibodies ; Autoantibodies* ; Complement Activation ; Ethidium ; Humans ; Melanocytes ; PUVA Therapy ; Vitiligo*

BACKGROUND: It is reported by rnany t,hat UVB and large coses of UVA damage epidermal Langerhans cells. UVA irradiated skin produces reactive oxygen soecies such as superoxide anion(O ), hydrogen peroxide(H O), hydroxyl radical( OH) and singlet oxigen(O ). Reactive oxygen species such as O are invnlved in the process of decreasing the number if epidermal Langerhans cells after irradiation with UVB. However, no well established studies have been carried out after irradiation with UVA. OBJECTIVES: We wished to find out whether the UVA-induced decrease in the number of Ia Langerhans cells would be protected by scavengers of reactive oxiygen species. METHODS: We irradiated 200J/cm and 400J/cm of UVA on thi ears of C3H mice with or without intravenous injectior. of SOD, catalase, and sodium azide which are the scavengers of O , HO and O, respectively. We biopsied the ears of mice 2 days after irradiaion, stained them with immunope-roxidase technique, and counted the number of Langerhans cells. RESULTS: 1, There was significant decrease in the number of Ia Langerhans cells in the 200J/cm or 400J/cm of UVA irradiated group compared to the normal control group. 2. The pretreatment groups with SOD, catalase, and sodium to before irradiation with 200J/cm or 400J/cm of UVA showed less decrease in the number of la Langerhans cells compared to the 200J/cm or 400J/cm irradiated group with UVA only. CONCLUSION: Frorn the above result, we can deduce that reactive oxygen species are involved in the decrease in the number of Ia Langerhans cells induced by 200J/cm. or 400J/cm of UVA irradiation.
Animals ; Catalase ; Ear ; Hydrogen ; Langerhans Cells* ; Mice ; Mice, Inbred C3H ; Oxygen ; Reactive Oxygen Species* ; Skin* ; Sodium ; Sodium Azide ; Superoxides

This study was undertaken to investigate the recovery of epidermal Langerhans cells in relation to time after UVA irradiation through different amounts and ways of exposure in CH mice. We irradiated the ears of C2H mice with UVA 200J/cm2 and 400J/cm2 in a single dose at one time or 5 fractionated doses for 5 days and performed biopsies on the ears of the control and experimental groups after 2, 7, 14, 21days of irradiation and stained them with immunoperoxidase method. The results are summarized as follows, l. We observed a significant decrease in the number of the Ia-positive epidermal Langerhans cells in the single-dose-exposed group compared to the fractionated- dose-exposed group on 7th and 14th days irradiated with UVA 200J/cm. 2. There was no significant difference in the change in the number of the Ia- positive epidermal Langerhans cells until 21 days of exposure between the single- dose-exposed group and the fractionated-dose-exposed group irradiated with UVA 400 J/cm 3. In the group irradiated with UVA 2003/cm, the reduced number of the Ia-positive epidermal Langerhans cells returned to normal on the 14th day after irradiation in the fractionated-dose-exposed group and on the 21st day in the single- dose-exposed group. In the group irradiated with 400J/cm, the number returned to normal on the 21st day of irradition both in the fractionated-dose-exposed group and in the single-dose-exposed group.
Animals ; Biopsy ; Ear ; Langerhans Cells* ; Mice ; Mice, Inbred C3H*

No abstract available.
Hyperplasia