No abstract available.

No abstract available.
Angiokeratoma* ; Hypertrophy*

PURPOSE: The purpose of this study was to determine the role of CT and MR imagings in the diagnosis aortic dissection and differentiation between the true and false lumen. MATERIALS AND METHODS: We retrospectively studied forty patients with aortic dissection(AD) diagnosed imagings or surgery. Of the forty patients, 19 were examined with only CT, 14 with CT and MR, and 7 with MI~: Our points of view were(1) the classification of AD according to configuration of intimal flap by cross-sectional imaging, (2) differentiation between the true and false lumens, (3) the course of the false lumen, and (4)! detectability of the origin of major branch vessels of the abdominal aorta. RESULTS: The classification by corss-sectional imaging were crescentic(65%), circumferential(15%), flat(12%), and irregular(8%) type, in which false negative diagnosis was made in 1 case of crescentic and circumferential type, respectively. In 2 case of flat type and 1 case of irregular type, the differentiation between the true and false lumen was impossible with CT. The course of the false lumen in descending thoracic aorta revealed countrclock wise rotation(66%), clockwise rotation(5%) or fixed(29%) apperance. MR imaging was superior to CT in the detection of the origin of major branch vessels of the abdominal aorta. The determination of the origin of major branches of abdominal aorta arising from the true and false lumen were impossible in 2 cases in which only CT was done. CONCLUSION: Diagnosis of crescentic and circumferential types of AD with narrow and thrombosed false lumen was problematic in both CT and MR with no difference of diagnostic accuracy between the two modalities. The differentiation between the true and false lumen was difficult in flat and irregular types with only CT. Therefore, when surgical treatment is considered as in type B aortic dissection, MR imaging is recommended in order to determine the origin of major branch vessels.
Aorta, Abdominal ; Aorta, Thoracic ; Classification ; Diagnosis* ; Humans ; Magnetic Resonance Imaging ; Retrospective Studies

Purpose: We report two cases of exudative retinal detachment with a characteristic distribution of subretinal fluid (SRF) on optical coherence tomography (OCT) after vitrectomy for proliferative diabetic retinopathy (PDR).Case summary: A 54-year-old woman diagnosed with PDR and vitreous hemorrhage (VH) was treated with pars plana vitrectomy combined with endolaser photocoagulation and cataract surgery. Based on a diagnosis of PDR and VH, a 66-year-old man underwent vitrectomy and endolaser photocoagulation. In both cases, exudative retinal detachment was observed on OCT a few days after surgery. On OCT vertical section, the SRF was mainly distributed in the inferior and superior regions of the fovea, while sparing the foveal center.The patients were followed via observation, and SRF resolved spontaneously. Conclusions Our two cases suggest that excessive endolaser photocoagulation during vitrectomy may cause exudative retinal detachment.

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*

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

No abstract available.
Urticaria*

No abstract available.
Fallopian Tubes* ; Female ; Mucous Membrane* ; Sterilization*

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*