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Peizeng Yang - One of the best experts on this subject based on the ideXlab platform.
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Advances in treatment of Vogt-Koyanagi-Harada Syndrome
Press of International Journal of Ophthalmology (IJO PRESS), 2017Co-Authors: Guo Huang, Peizeng YangAbstract:Vogt-Koyanagi-Harada(VKH)Syndrome is an autoimmune disease attacking against pigmented cells, resulting in blindness and usually affecting multiple organs including ears, meninges, hair and skin. Correct diagnosis and immediate treatment in the early stage is vital to visual prognosis. Currently, corticosteroids is first-line drug. In addition, VKH patients refractory to corticosteroids can choose other treatment such as immunosuppressive agents and biological agents
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copy number variations and gene polymorphisms of complement components in ocular behcet s disease and vogt koyanagi harada Syndrome
Scientific Reports, 2015Co-Authors: Shengping Hou, Aize Kijlstra, Jun Zhang, Yanni Jiang, Peizeng YangAbstract:Complement is involved in many immune-mediated diseases. However, the association of its copy number variations (CNVs) and polymorphisms with Behcet’s disease (BD) and Vogt-Koyanagi-Harada Syndrome (VKH) is unknown. We examined copy number and mRNA expression by real-time PCR. Cytokine production by stimulated peripheral blood mononuclear cells (PBMCs) in genotyped individuals was measured by ELISA. The frequencies of having more than two copies of C3 were significantly increased in BD and VKH, whereas CNV of C5 was only associated with BD. Increased frequencies of the GG genotype of C3 rs408290 and C5 rs2269067 were found in BD. No association was observed between C3 and C5 SNPs and VKH. mRNA expression in the high CNV group and GG cases of C3 and C5 was significantly higher compared to other genotypes. Increased interleukin-17 and IFN-γ was observed in the high CNV group and GG genotype cases of C3. Interleukin-17 but not IFN-γ was increased in the high CNV group and GG genotype cases of C5. No effect of C3 or C5 genetic variants was seen on the production of TNF-α, IL-10, IL-1β, MCP-1, IL-6 and IL-8. Our study thus provides further evidence for a role of complement in the pathogenesis of uveitis.
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Copy Number Variants and Genetic Polymorphisms in TBX21 , GATA3 , Rorc , Foxp3 and Susceptibility to Behcet's Disease and Vogt-Koyanagi-Harada Syndrome
Scientific reports, 2015Co-Authors: Dan Liao, Aize Kijlstra, Shengping Hou, Jun Zhang, Jing Fang, Yunjia Liu, Lin Bai, Qingfeng Cao, Peizeng YangAbstract:Copy Number Variants and Genetic Polymorphisms in TBX21 , GATA3 , Rorc , Foxp3 and Susceptibility to Behcet's Disease and Vogt-Koyanagi-Harada Syndrome
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a variant of clec16a gene confers protection for vogt koyanagi harada Syndrome but not for behcet s disease in a chinese han population
Experimental Eye Research, 2015Co-Authors: Shengping Hou, Aize Kijlstra, Peizeng YangAbstract:Abstract Vogt–Koyanagi–Harada (VKH) Syndrome and Behcet's disease (BD) are two common form of uveitis in China. The aim of this study was to investigate the association of C-type lectin domain family 16, member A ( CLEC16A ) gene polymorphisms with Vogt–Koyanagi–Harada Syndrome and Behcet's disease in a Chinese Han population. A two-stage association study was carried out in 988 VKH Syndrome patients，400 BD patients and 976 healthy controls. Eight single nucleotide polymorphisms of CLEC16A gene were determined with the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The data were analyzed by χ 2 test or Fisher's exact test and corrected for multiple comparisons by the Bonferroni method. The first stage study showed that the frequency of the A allele of rs6498169 was significantly decreased in VKH Syndrome patients ( Pc = 1.1 × 10 −2 , OR = 0.7, 95%CI = 0.6–0.9). No significant association was observed in the other 7 SNPs between VKH Syndrome patients and controls. No association was found with BD for the 8 SNPs tested. We further confirmed the association of single nucleotide polymorphism rs6498169 with VKH Syndrome in another cohort. Consistent with the first stage study, the combined study showed significantly lower frequencies of the AA genotype and the A allele of rs6498169 in VKH Syndrome patients ( Pc = 3.5 × 10 −4 , OR = 0.6, 95%CI = 0.5–0.7; Pc = 8.2 × 10 −4 , OR = 0.8, 95%CI = 0.7–0.9, respectively). In conclusion, the study suggested that a CLEC16A polymorphism may be protective against VKH Syndrome in a Chinese Han population.
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Clinical features of the investigated BD and VKH Syndrome patients.
2014Co-Authors: Lin Bai, Aize Kijlstra, Shengping Hou, Jing Fang, Qingyun Zhou, Peizeng YangAbstract:BD, Behcet's disease; VKH, Vogt–Koyanagi–Harada Syndrome.
Narsing A Rao - One of the best experts on this subject based on the ideXlab platform.
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utility of existing vogt koyanagi harada Syndrome diagnostic criteria at initial evaluation of the individual patient a retrospective analysis
Ocular Immunology and Inflammation, 2000Co-Authors: Russell W Read, Narsing A RaoAbstract:The diagnosis of Vogt-Koyanagi-Harada Syndrome is hampered by its variable manifestations and the lack of unique ancillary and laboratory findings. In this study, the diagnostic criteria established in 1978 by the American Uveitis Society (AUS) are retrospectively analyzed via their application to a population of 71 consecutive patients, using only those features present at the initial evaluation. All patients were previously diagnosed with Vogt-Koyanagi-Harada Syndrome based on the clinical features and course of the disease combined with fluorescein angiography with or without ultrasonography in selected cases. Mean age of all patients was 36.7 years ± 15.1 years. Fifty (70%) were female and 45 (65%) were Hispanic. Patients presenting acutely, subacutely, and in the chronic stages met the AUS criteria for Vogt-Koyanagi-Harada Syndrome in 56%, 48%, and 58% of cases, respectively. Allowance for variation in features, incomplete cases, and modification of the disease by treatment might increase the sensiti...
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simultaneous onset of vogt koyanagi harada Syndrome in monozygotic twins
American Journal of Ophthalmology, 1995Co-Authors: Allan R Rutzen, Gabriela Ortegalarrocea, Ivan R Schwab, Narsing A RaoAbstract:Purpose/Methods We examined monozygotic twins of Vietnamese ancestry in whom the Vogt-Koyanagi-Harada Syndrome developed. Results/Conclusions Both patients demonstrated typical clinical findings of the Vogt-Koyanagi-Harada Syndrome, and HLA typing disclosed HLA-DR4, an antigen that is present in a disproportionate number of patients with the Vogt-Koyanagi-Harada Syndrome. Although familial cases of the Vogt-Koyanagi-Harada Syndrome are rare, associations with HLA antigens may indicate that genetic factors play a role in this disease.
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vogt koyanagi harada Syndrome
Survey of Ophthalmology, 1995Co-Authors: Ramana S Moorthy, Hajime Inomata, Narsing A RaoAbstract:The Vogt-Koyanagi-Harada Syndrome (VKH) is a bilateral, diffuse granulomatous uveitis associated with poliosis, vitiligo, alopecia, and central nervous system and auditory signs. These manifestations are variable and race dependent. This inflammatory Syndrome is probably the result of an autoimmune mechanism, influenced by genetic factors, and appears to be directed against melanocytes. On histopathologic examination typical cases show nonnecrotizing diffuse granulomatous panuveitis with initial sparing and late involvement of the choriocapillaris and formation of Dalen-Fuchs' nodules. Fluorescein angiography, lumbar puncture, and echography are useful adjuncts in the diagnosis and management of VKH Syndrome. Patients with this Syndrome are treated generally with high dose systemic corticosteroids or, when necessary, with cyclosporine or cytotoxic agents. The prognosis of patients with VKH Syndrome is fair, with nearly 60% of patients retaining vision of 20/30 or better. The complications of VKH Syndrome that lead to visual loss include cataracts in about 25% of patients, glaucoma in 33%, and subretinal neovascular membranes (SRNVMs) in about 10%; the latter, however, are an important cause of late visual loss. These complications usually require medical and/or surgical intervention, including photocoagulation. The major risk factor for the development of cataracts, SRNVMs, and, to some extent, glaucoma, is chronic recurrent intraocular inflammation that may be resistant to corticosteroid therapy. It appears that initial treatment with high dose corticosteroids, combined with prolonged corticosteroid therapy at appropriate dosage, may minimize these complications and may improve visual prognosis.
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incidence and management of cataracts in vogt koyanagi harada Syndrome
American Journal of Ophthalmology, 1994Co-Authors: Ramana S Moorthy, Ronald E Smith, Buddi Rajeev, Narsing A RaoAbstract:Of 65 consecutive patients (130 eyes) with Vogt-Koyanagi-Harada Syndrome, 26 (40%) developed cataracts (49 eyes, 38%). Twenty-eight cataracts were posterior subcapsular, six nuclear, 14 combined nuclear and posterior subcapsular, and one anterior cortical. Risk factors for the development of cataracts included age (P = .003), long-standing recurrent anterior segment inflammation (P
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subretinal neovascular membranes in vogt koyanagi harada Syndrome
American Journal of Ophthalmology, 1993Co-Authors: Ramana S Moorthy, Lawrence P Chong, Ronald E Smith, Narsing A RaoAbstract:Subretinal neovascular membranes cause late visual loss and are important determinants of final visual acuity in patients with Vogt-Koyanagi-Harada Syndrome. The purpose of this study was to determine the prevalence and risk factors associated with the development of subretinal neovascular membranes in Vogt-Koyanagi-Harada Syndrome. We reviewed the charts of 58 patients (116 eyes) with Vogt-Koyanagi-Harada Syndrome. We separated patients into two groups, one with and one without subretinal membranes. Demographic characteristics, namely age, gender, and race, initial and final visual acuities, duration and method of treatment, anterior chamber and vitreous cell, presence of fundus pigmentary disturbances, and phase of inflammation, were evaluated for each group. Overall, ten eyes (9%) of seven patients developed the subretinal neovascular membranes. Demographic characteristics among the two groups of patients were not markedly different (P
Aize Kijlstra - One of the best experts on this subject based on the ideXlab platform.
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copy number variations and gene polymorphisms of complement components in ocular behcet s disease and vogt koyanagi harada Syndrome
Scientific Reports, 2015Co-Authors: Shengping Hou, Aize Kijlstra, Jun Zhang, Yanni Jiang, Peizeng YangAbstract:Complement is involved in many immune-mediated diseases. However, the association of its copy number variations (CNVs) and polymorphisms with Behcet’s disease (BD) and Vogt-Koyanagi-Harada Syndrome (VKH) is unknown. We examined copy number and mRNA expression by real-time PCR. Cytokine production by stimulated peripheral blood mononuclear cells (PBMCs) in genotyped individuals was measured by ELISA. The frequencies of having more than two copies of C3 were significantly increased in BD and VKH, whereas CNV of C5 was only associated with BD. Increased frequencies of the GG genotype of C3 rs408290 and C5 rs2269067 were found in BD. No association was observed between C3 and C5 SNPs and VKH. mRNA expression in the high CNV group and GG cases of C3 and C5 was significantly higher compared to other genotypes. Increased interleukin-17 and IFN-γ was observed in the high CNV group and GG genotype cases of C3. Interleukin-17 but not IFN-γ was increased in the high CNV group and GG genotype cases of C5. No effect of C3 or C5 genetic variants was seen on the production of TNF-α, IL-10, IL-1β, MCP-1, IL-6 and IL-8. Our study thus provides further evidence for a role of complement in the pathogenesis of uveitis.
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Copy Number Variants and Genetic Polymorphisms in TBX21 , GATA3 , Rorc , Foxp3 and Susceptibility to Behcet's Disease and Vogt-Koyanagi-Harada Syndrome
Scientific reports, 2015Co-Authors: Dan Liao, Aize Kijlstra, Shengping Hou, Jun Zhang, Jing Fang, Yunjia Liu, Lin Bai, Qingfeng Cao, Peizeng YangAbstract:Copy Number Variants and Genetic Polymorphisms in TBX21 , GATA3 , Rorc , Foxp3 and Susceptibility to Behcet's Disease and Vogt-Koyanagi-Harada Syndrome
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a variant of clec16a gene confers protection for vogt koyanagi harada Syndrome but not for behcet s disease in a chinese han population
Experimental Eye Research, 2015Co-Authors: Shengping Hou, Aize Kijlstra, Peizeng YangAbstract:Abstract Vogt–Koyanagi–Harada (VKH) Syndrome and Behcet's disease (BD) are two common form of uveitis in China. The aim of this study was to investigate the association of C-type lectin domain family 16, member A ( CLEC16A ) gene polymorphisms with Vogt–Koyanagi–Harada Syndrome and Behcet's disease in a Chinese Han population. A two-stage association study was carried out in 988 VKH Syndrome patients，400 BD patients and 976 healthy controls. Eight single nucleotide polymorphisms of CLEC16A gene were determined with the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The data were analyzed by χ 2 test or Fisher's exact test and corrected for multiple comparisons by the Bonferroni method. The first stage study showed that the frequency of the A allele of rs6498169 was significantly decreased in VKH Syndrome patients ( Pc = 1.1 × 10 −2 , OR = 0.7, 95%CI = 0.6–0.9). No significant association was observed in the other 7 SNPs between VKH Syndrome patients and controls. No association was found with BD for the 8 SNPs tested. We further confirmed the association of single nucleotide polymorphism rs6498169 with VKH Syndrome in another cohort. Consistent with the first stage study, the combined study showed significantly lower frequencies of the AA genotype and the A allele of rs6498169 in VKH Syndrome patients ( Pc = 3.5 × 10 −4 , OR = 0.6, 95%CI = 0.5–0.7; Pc = 8.2 × 10 −4 , OR = 0.8, 95%CI = 0.7–0.9, respectively). In conclusion, the study suggested that a CLEC16A polymorphism may be protective against VKH Syndrome in a Chinese Han population.
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Clinical features of the investigated BD and VKH Syndrome patients.
2014Co-Authors: Lin Bai, Aize Kijlstra, Shengping Hou, Jing Fang, Qingyun Zhou, Peizeng YangAbstract:BD, Behcet's disease; VKH, Vogt–Koyanagi–Harada Syndrome.
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decreased microrna 155 expression in ocular behcet s disease but not in vogt koyanagi harada Syndrome
Investigative Ophthalmology & Visual Science, 2012Co-Authors: Qingyun Zhou, Aize Kijlstra, Xiang Xiao, Chaokui Wang, Xuedong Zhang, Yan Zhou, Peizeng YangAbstract:Purpose MicroRNAs (miRNAs) have emerged as a class of gene expression regulators involved in immune regulation. In the present study, we investigated the role of miRNA in two uveitis entities: Behcet's disease (BD) and Vogt Koyanagi Harada Syndrome (VKH). Methods The expression of five miRNAs was studied in PBMCs, DCs, and CD4(+) T cells from BD patients with active and inactive uveitis, VKH patients with active uveitis, and healthy controls using real-time PCR. MiR-155 mimics and inhibitor were transfected to DCs to evaluate the effect on DC maturation and cytokine production by these cells and CD4(+) T cells. Luciferase reporter assays and Western blotting were performed to identify the target gene of miR-155. Results Only miR-155 expression was significantly decreased in PBMCs and DCs from BD patients with active uveitis and no differences were observed in the miRNA expression in cells from patients with VKH as compared with controls. Overexpression of miR-155 in DCs was shown to inhibit the production of IL-6 and IL-1β, and to promote the expression of IL-10 by these cells. MiR-155 transfected DCs significantly inhibited intracellular IL-17 expression in allogeneic CD4(+) T cells; however, it did not influence the expression of cell surface markers CD80, CD40, CD83, CD86, and HLA-DR. Luciferase reporter assays revealed that TAB2 was a target gene of miR-155, which was confirmed by Western blotting. Conclusions The present results suggest that miR-155 expression is decreased in active BD but not in VKH patients. Downregulated miR-155 may be involved in BD pathogenesis by targeting TAB2.
Hajime Inomata - One of the best experts on this subject based on the ideXlab platform.
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ultrasound biomicroscopic analysis of transient shallow anterior chamber in vogt koyanagi harada Syndrome
American Journal of Ophthalmology, 1996Co-Authors: Yohichi Kawano, Akihiko Tawara, Yuko Nishioka, Yayoi Suyama, Hidehisa Sakamoto, Hajime InomataAbstract:Purpose To evaluate the mechanism of formation of the transient shallow anterior chamber in Vogt-Koyanagi-Harada Syndrome. Methods Two patients with Vogt-Koyanagi-Harada Syndrome with shallow anterior chambers were examined with an ultrasound biomicroscope. Results A ciliochoroidal detachment, which was not obvious on ophthalmoscopic examination, was clearly demonstrated in both patients by ultrasound biomicroscopy. The detachment disappeared after systemic corticosteroid therapy. Conclusion The shallowing of the anterior chamber in two patients with Vogt-Koyanagi-Harada Syndrome was caused by suprachoroidal effusion secondary to inflammation of the uvea.
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vogt koyanagi harada Syndrome
Survey of Ophthalmology, 1995Co-Authors: Ramana S Moorthy, Hajime Inomata, Narsing A RaoAbstract:The Vogt-Koyanagi-Harada Syndrome (VKH) is a bilateral, diffuse granulomatous uveitis associated with poliosis, vitiligo, alopecia, and central nervous system and auditory signs. These manifestations are variable and race dependent. This inflammatory Syndrome is probably the result of an autoimmune mechanism, influenced by genetic factors, and appears to be directed against melanocytes. On histopathologic examination typical cases show nonnecrotizing diffuse granulomatous panuveitis with initial sparing and late involvement of the choriocapillaris and formation of Dalen-Fuchs' nodules. Fluorescein angiography, lumbar puncture, and echography are useful adjuncts in the diagnosis and management of VKH Syndrome. Patients with this Syndrome are treated generally with high dose systemic corticosteroids or, when necessary, with cyclosporine or cytotoxic agents. The prognosis of patients with VKH Syndrome is fair, with nearly 60% of patients retaining vision of 20/30 or better. The complications of VKH Syndrome that lead to visual loss include cataracts in about 25% of patients, glaucoma in 33%, and subretinal neovascular membranes (SRNVMs) in about 10%; the latter, however, are an important cause of late visual loss. These complications usually require medical and/or surgical intervention, including photocoagulation. The major risk factor for the development of cataracts, SRNVMs, and, to some extent, glaucoma, is chronic recurrent intraocular inflammation that may be resistant to corticosteroid therapy. It appears that initial treatment with high dose corticosteroids, combined with prolonged corticosteroid therapy at appropriate dosage, may minimize these complications and may improve visual prognosis.
Shaohong Qian - One of the best experts on this subject based on the ideXlab platform.
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bilateral acute angle closure glaucoma as a presentation of vogt koyanagi harada Syndrome in four chinese patients a small case series
Ocular Immunology and Inflammation, 2013Co-Authors: Jing Yao, Yuhong Chen, Tingting Shao, Zhihong Ling, Wenji Wang, Shaohong QianAbstract:Purpose: To report the clinical features of Vogt-Koyanagi-Harada Syndrome presented with bilateral acute angle closure glaucoma in 4 Chinese patients.Methods: The medical records were retrospectively reviewed.Results: Visual acuity ranged from counting fingers before the eye to 6/30. Intraocular pressure ranged from 22.2 to 29.7 mmHg with or without anterior chamber inflammation. Mild vitritis and massive exudative retinal detachment were seen. B scan and fundus fluorescein angiography supported the diagnosis. After corticosteroid treatment, the increased intraocular pressure was resolved with deepened anterior chamber and open angle. Inflammation was controlled and visual acuity was improved.Conclusions: Bilateral acute angle closure glaucoma could be the initial symptom of Vogt-Koyanagi-Harada Syndrome. Mild increased intraocular pressure in association with moderate to severe visual disturbance in both eyes is an important sign of this diagnosis. Careful fundus examination and B scan are helpful in dia...
