No abstract available.
Colorectal Neoplasms*

No abstract available.
Anal Canal* ; Leiomyosarcoma*

No abstract available.
Urticaria*

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: Today, patients with fatty liver have increased by several factors. Some patients with fatty liver have abnormal liver function tests, by the way they have interpreted unwisely and made wrong therapeutic approach about abnoimal liver function tests. So we conducted this study to evaluate the factors related to patients with fatty liver and make basic concept for management. METHODS: We selected 96 patients(71 men, 25 women) who were diagnosed as fatty liver by ultrasound in Asan Medical Health Examination Center, also selected 91 controls(68 men, 23 women) who had similar sex and age distribution from January to December, 1993. We excluded toxic and viral hepatitis cases or patients. We surveyed by questionnaires that composed of 3 day-dietary diary and life style. Nutrient and alcohol intakes were analyzed by nutrient-analysis program that was derivated from Food Composition Table, and we analyzed several biochemical variables. RESULTS: There were 71 men and 25 women with fatty liver, 68 men and 23 women in controls. In cases of men, the mean age was 47 years-old in patient group, 44 years-old in control group. The obesity index was 112.7% in patients, 102.6% in controls, the mean level of triglyceride was 205mg/dl in patients, 150mg/dl in controls. The mean level of serum HDL-C was 46mg/dl in patients, 50mg/dl in controls(p<0.05). The frequency of obesity was 66.2% in patients, 27.9% in controls, hypertriglyceridemia was 42.3% in patients, 22.1% in controls(p<0.05). The frequency of patients who had increased AST was 26.8% in patients, 11.8% in controls, and the frequency of patients or cases who had increased ALT was 26.8%, in patients, 7.4% in controls(p<0.05). There were no significant statistical differences in the nutrient intakes, alcohol drinking and exercise between the male patients and controls. In cases of women, the mean age was 53 years in patient gr oup or among patients, 51 years in controls. The obesity index was 112.2% in patients, 102.1% in controls, and the mean level of serum triglyceride was 198.3mg/dl in patients, 136.4mg/dl in controls(p<0.05). The frequency of obesity was 76.0% in patients, 30.4% in controls, and the frequency of hypertriglyceridemia was 36.0% in patients, 13.0% in controls. There were statistically significant differences in the frequency of obesity and hypertriglyceridemia between patients and controls(p<0,05). There were no statistically significant differences in the frequency of increased AST and ALT, nutrient intakes, alcohol drinking, and excercise between patients and controls. CONCLUSIONS: The fatty liver disease was attributed either to obesity or hypertriglyceridemia. Therefore, it is very important to control of weight and hypertriglyceridemia in the management of patients with fatty liver.
Adult ; Age Distribution ; Alcohol Drinking ; Chungcheongnam-do ; Fatty Liver* ; Female ; Hepatitis ; Humans ; Hypertriglyceridemia ; Life Style ; Liver Function Tests ; Male ; Middle Aged ; Obesity ; Triglycerides ; Ultrasonography ; Surveys and Questionnaires

Sunlight is one of the well-established factors which play key roles in the induction and exacerbation of lupus erythematosus. In two patients of discoid lupus erythematosus, we have experimentally reproduced skin lesions by provocative phototesting. Both UVA (100 joules/cm²) and UVB (80 millijoules/cm²) radiation induced the skin lesions. The reproduced skin lesions were clinically and histopathologically consistent with lupus erythematosus.
Humans ; Lupus Erythematosus, Discoid ; Reproduction* ; Skin ; Sunlight

BACKGROUND: The clinical behavior of vitiligo has not been clearly understood and hypothesis concerning the pathogenesis of the disease has been confusing and contradictory though autoimmune mechanisms have been considered important by many authors. OBJECTIVE: The purpose of this study was to develop a better understanding of the clinical features and pathogenesis of vitiligo. METHODS: We investigated clinical features of vitiligo in 1315 patients, and also compared the clinical course and features of non-segmental type(type A) and segmental type(type B) vitiligo patients to see whether the two types of vitiligo have a different pathogenic mechanism. RESULTS: Previously reported clinical patterns of the disease were reviewed and compared with our data, and the different clinical findings between the two types which supported the hypothesis of Koga et al. that type A and type B vitiligo had a different pathogenesis and autoimmune mechanisms played a role only in type A were shown. CONCLUSION: We investigated the clinical characteristics of vitiligo in Korea and showed that the type A vitiligo might have a different pathogenic mechanism with type B.
Clinical Study* ; Humans ; Korea ; Vitiligo*

BACKGROUND: Combined spinal epidural anesthesia (CSE) often produces a more extensive spinal block than expected. This study was designed to evaluate the effects of CSE on subarachnoid block in patients undergoing lower extremity surgery. METHODS: Thirty-three patients who undergone lower extremity surgeries were randomly allocated to three groups of 11 patients each. Using needle through needle technique, all patients received a subarachnoid injection of hyperbaric 0.5% bupivacaine 1.6~2.0 ml through a 25G Whitacre spinal needle. Group 1 received no extradural injection for 25min, but group 2 and 3 received extradural saline 10 ml and bupivacaine 10 ml 5min after the subarachnoid injection, respectively. Levels of sensory and motor block were assessed at 4, 6, 8, 10, 15, 20, and 25 min after subarachnoid injection. RESULTS: The median values of maximum sensory block level were T7 in all groups. Levels of sensory blockade and the time to onset of maximum sensory blockade were similar among the three groups. There was no significant difference in the degree of motor block among three groups. CONCLUSIONS: This study suggests that extradural saline 10 ml or 0.5% bupivacaine 10 ml which injected 5min after subarachnoid injection does not significantly influence the level of subarachnoid block in lower extremity surgical patients. However, further study is required to declare the safety or optimal dose of extradural injection during CSE.
Anesthesia, Epidural* ; Bupivacaine ; Humans ; Injections, Epidural ; Lower Extremity* ; Needles

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*