高血压患者黄斑区视网膜脉络膜厚度变化及脉络膜厚度影响因素分析

目的:观察高血压患者黄斑区视网膜和脉络膜厚度的变化；探讨高血压性视网膜病变的危险因素。方法:采用横断面研究，收集2020-12-2022-12本院眼科门诊就诊的62例(105眼)高血压患者为高血压组，其中男30例53眼，女32例52眼。收集同期28例(56眼)无高血压的健康者作为对照组，其中男14例28眼，女14例28眼。使用SD-OCT中自带的EDI模式，以黄斑中心凹为中心，测量直径为1mm范围内(中心凹区)、1-3mm范围内(内环区：上方、下方、颞侧及鼻侧四个分区)及3-6mm范围内(外环区：上方、下方、颞侧及鼻侧四个分区)的平均视网膜厚度及脉络膜厚度，比较两组各分区平均视网膜厚度及脉络膜厚度的差异，分析黄斑中心凹下脉络膜厚度的影响因素。结果:除黄斑中心凹和内环上方外，高血压组黄斑区视网膜厚度较对照组变薄(P<0.05或P<0.01)。高血压组黄斑区脉络膜厚度较对照组变薄(P<0.01)。回归分析发现黄斑中心凹下脉络膜厚度与年龄和收缩压呈负相关关系(P<0.05或P<0.01)。结论:高血压患者年龄及血压水平影响视网膜及脉络膜微循环。     

单纯型糖尿病视网膜病变黄斑无血管区与视力

探讨了单纯型糖尿病视网膜病变(non—Prolifcrative diabtie retinopathy,NDR)患者视力与视网膜黄斑无血管区(foveal avascular zone,FAZ)大小的关系.应用微机图像处理系统,测算43只NDR患眼和20只正常眼眼底荧光血管造影负片上FAZ与视盘的面积比值.NDR视力正常组和正常对照间该比值无显著差异(P>0.05).在NDR视力下降组中,该比值显著大于上述两组(P<0.01)、且与患者视力呈显著切相关(P<0.001),其糖尿病程亦较NDR视力正常组长(P<0.05).结论:NDR患者糖尿病病程较长时,FAZ与视盘的面积比值增大到一定程度,将引起视力损害,且损害随该比值的增大而加重.     

糖尿病视网膜病变黄斑拱环形态改变的临床研究

目的客观评价糖尿病视网膜病变（DR）患者黄斑拱环结构改变的形态特征,总结黄斑拱环形态变化、荧光渗漏及黄斑区视网膜厚度对视力的影响因素。方法患者按有无眼底改变分为3组,糖尿病视网膜病变组（DR组）38例65只眼,2型糖尿病无DR眼底改变组（非DR组）16例29只眼,正常组17例33眼。三组病例均先行眼底荧光素血管造影（FFA）检查,后行光学相干断层扫描（OCT）眼底黄斑部放射状扫描检查。结果三组之间黄斑拱环形态变化比较,有显著差异（P=0．0003）,黄斑中心1mm直径视网膜厚度有显著差异（P=0．0007）。DR组患者拱环形态与荧光渗漏程度显著相关（P=0．0003）,黄斑拱环形态与黄斑中心1mm直径视网膜厚度显著相关（P=0．0063）,荧光渗漏程度与黄斑中心1mm直径视网膜厚度显著相关（P=0．0046）。DR组患者黄斑拱环形态、荧光渗漏和黄斑中心1mm直径视网膜厚度变化与最佳矫正视力无相关性（P=0．076,P=0．067,P=0．128）。结论DR患者黄斑拱环形态改变、渗漏程度及黄斑中心视网膜厚度是相互影响和互为因果,黄斑拱环形态变化特征为进一步选择和调整治疗手段提供了准确依据。     

OCT测量分析视网膜中央静脉阻塞黄斑囊样水肿时 黄斑区视网膜厚度变化研究

目的 研究频域光学相干断层扫描仪Cirrus HD-OCT对视网膜中央静脉阻塞黄斑囊样水肿（CRVO-CME）时黄斑区视网膜厚度的变化情况。方法 纳入我院2017年11月~2019年2月收治的45例（60眼）CRVO-CME患者作为研究组,另选取45例（60眼）来我院进行体检的健康志愿者作为对照组。所有患者均行HD-OCT检查,根据早期糖尿病视网膜病变治疗研究（ETDRS）视力表对黄斑区进行分区,观察两组眼黄斑区视网膜厚度情况,分析黄斑区视网膜厚度与最佳矫正视力（BCVA）的关系。结果 研究组F、IT、II、IN、IS、OT、OI、ON以及OS黄斑区9个分区的视网膜厚度均大于对照组,差异有统计学意义（P＜0.05）。IT、II、IN、IS黄斑区4个内分区厚度组间比较,差异无统计学意义（P＞0.05）;OT、OI、ON以及OS黄斑区4个外分区厚度组组间比较,差异无统计学意义（P＞0.05）。CRVO-CME患者FT以及Fmax与BCVA存在负相关性（P＜0.05）。结论 CRVO-CME患者视网膜各分区均比正常人视网膜更厚,对CRVO-CME患者进行HD-OCT测量对视网膜厚度的判断较准确,为临床诊治CRVO-CME提供了有力依据。     

Hd-OCT测量正常青少年黄斑部视网膜厚度的研究

目的 应用频域OCT（Hd-OCT）测量正常青少年黄斑部视网膜厚度范围。方法 选择2018年1月~2019年1月我院眼科门诊查体的青少年345例（528眼）,均行光学相干断层成像仪（Zeiss Hd-OCT）进行测量,比较不同性别和眼别黄斑区分区视网膜厚度（A1~A9）。结果 Hd-OCT扫描检查的345例青少年黄斑区的OCT扫描形态呈两边高,中间低的特点。不同性别相同区域视网膜厚度比较,差异无统计学意义（P＞0.05）。不同眼别相同区域视网膜厚度比较,差异无统计学差异（P＞0.05）。黄斑中心区域内（直径1 mm）最薄,黄斑的内环区域（直径1~3 mm）最厚,外环区域（直径3~6 mm）较内环区域（直径1~3 mm）薄。在直径为1~3 mm的内环区,黄斑区视网膜厚度值依次为A5＞A4＞A2＞A3。在直径为3~6 mm的外环区,黄斑区视网膜厚度值依次是A9＞A6＞A8＞A7。结论 Hd-OCT测量青少年黄斑区视网膜厚度有一定临床意义,可以建立青少年黄斑视网膜厚度的正常值数据库,为青少年黄斑发育的评估、黄斑疾病的定量检查、治疗后随访提供参考依据。     

糖尿病视网膜病变患者检测糖化血红蛋白的临床意义

目的探讨糖尿病视网膜病变 (DR)患者检测糖化血红蛋白 (HbA1c)的临床意义。方法对154例2型糖尿病患者DR情况和HbA1c水平进行检测。并对71例、病程5～10年的糖尿病患者正常眼底 (NDR)或单纯型糖尿病视网膜病变 (BDR)患者进行1年的随访 ,检测DR进展情况和HbA1c水平。结果DR组HbA1c高于NDR组。增殖型糖尿病视网膜病变 (PDR)组HbA1c高于BDR组。随访1年 ,视网膜病变进展组(A组)平均HbA1c高于视网膜病变稳定组(B组),差异具有统计学意义 (P<0.01)。结论DR的程度和进展与HbA1c增高有关     

视网膜中央动脉阻塞性缺血对黄斑区视网膜神经上皮的影响

目的:应用光学相干断层扫描(OCT)探讨视网膜中央动脉阻塞(CRAO)性缺血对黄斑区视网膜组织结构的影响。方法:用OCT对单眼CRAO 2-3d,黄斑区视网膜血液循环未完全恢复的患者 14例(14眼 )和 11例(11眼 )对侧健眼进行经中心小凹的水平和垂直扫描,分别测量及计算中心小凹、中心凹及黄斑的平均视网膜神经上皮层(RNL)厚度。结果:正常眼中心小凹、中心凹及黄斑平均RNL厚度分别为(169.91± 10.96) μm、(176.36± 11.74) μm、(256.45± 16.95) μm;CRAO黄斑区RNL明显增厚,中心小凹、中心凹及黄斑平均RNL厚度分别为(235.64± 47.02) μm、(241.84± 49.36) μm、(401.57± 54.53) μm,与正常眼比较有显著性差异(P <0.05,P <0.01)。 结论:CRAO性缺血明显地改变了黄斑区正常视网膜组织结构,使视网膜神经上皮层细胞水肿.     

2型糖尿病视网膜病变患者血清sVCAM-1水平的变化和意义

研究糖尿病视网膜病变不同时期血清可溶性血管内皮细胞粘附分子-1(sVCAM-1)与视网膜病变严重程度、诊断病程、血清胰岛素和血糖的相关性.采用ELISA法检测85例2型糖尿病视网膜病变患者血清sVCAM-1含量, 由同一眼科医师通过眼底镜或荧光造影检查, 将患者分为无视网膜病变组(NDR)、背景期视网膜病变组(BDR)和增殖期视网膜病变组(PDR).结果显示, 三组糖尿病患者血清sVCAM-1水平均高于对照组, 其中PDR组、BDR组血清sVCAM-1水平与对照组和NDR组比较, 均有显著性差异(P＜0.01), NDR组与对照组比较也存在显著性差异(P＜0.01).糖尿病患者血清sVCAM-1水平与血糖、血清胰岛素、诊断病程均无相关性(P＞0.05).研究表明, 糖尿病视网膜病变不同时期血清sVCAM-1水平的变化可作为判断视网膜病变发展和严重程度的指标, 为临床早期发现和治疗糖尿病视网膜病变提供较好的依据.     

血清胱抑素C及同型半胱氨酸与2型糖尿病 视网膜病变的相关性分析

目的 探讨CysC与Hcy与2型糖尿病视网膜病变的相关性。方法 选取我院2017年1月~12月收治的2型糖尿病患者160例,根据眼底照相结果分为糖尿病视网膜病变组（DR组）和糖尿病无视网膜病变组（NDR组）,每组80例,同时选取健康受试者80例作为对照组。观察各组患者血糖、血脂、血清CysC及Hcy水平。结果 ①DR组和NDR组SBP、DBP、FBG、2hBG、TG、TC、LDL-C、BUN、SCr、HbA1C、CysC和Hcy水平均高于对照组,差异具有统计学意义（P＜0.05）;DR组和NDR组HDL-C水平低于对照组,差异具有统计学意义（P＜0.05）;DR组SBP、TG、SCr、CysC和Hcy水平高于NDR组,差异具有统计学意义（P＜0.05）。②CysC与病程、TG、SCr、Hcy呈正相关（r=0.428、0.490、0.479、0.215,P＜0.05）,与BMI、SBP、LDL-C、FBG无明显相关性。③Logistic多元回归分析显示:TG、SBP、CysC和Hcy为影响2型糖尿病视网膜病变发生的危险因素。结论 高CysC及Hcy水平是发生糖尿病视网膜病变的危险因素,CysC联合Hcy检测对2型糖尿病视网病变的诊治有一定指导意义。     

532激光联合曲安奈德治疗糖尿病视网膜病变的临床观察

目的评价倍频532激光联合曲安奈德治疗伴有黄斑水肿的糖尿病视网膜病变的疗效。方法对52例87眼伴有弥漫性黄斑水肿的糖尿病视网膜病变患者采用532激光进行黄斑格栅样光凝联合全视网膜光凝，同时球后注射曲安奈德20mg，1～3次，间隔1周，分析患者视力、黄斑水肿及并发症情况。结果激光治疗后随访6～18个月，87眼中51（59％）眼视力稳定，视力提高者30（35％）眼，视力下降者6（7％）眼；眼底荧光血管造影检查，光凝后水肿完全消退者50（57％）眼，部分消退者32（37％）眼，不变者5（6％）眼，晶状体混浊加重者5眼，4只眼眼压升高。结论532倍频激光联合曲安奈德治疗糖尿病视网膜病变有助于黄斑水肿消退，提高视力。     

Early diagnosis of diabetic retinopathy in primary care

Objective:

To evaluate the impact of a strategy for early detection of diabetic retinopathy in patients with type 2 diabetes mellitus (DMT2) in Quintana Roo, México.

Methods:

Study transversal, observational, prospective, analytical, eight primary care units from Mexican Social Security Institute in the northern delegation of the State of Quintana Roo, Mexico were included. A program for early detection of diabetic retinopathy (DR) in adult 376,169 was designed. Were diagnosed 683 cases of type 2 diabetes, in 105 patients randomized was conducted to direct ophthalmoscopy were subjected to a secondary hospital were assigned. Will determine the degree of diabetic retinopathy and macular edema was performed.

Results:

In population were 55.2% female, mean age 48+11.1 years, 23.8 % had some degree of DR, 28.0% with mild non- proliferative diabetic retinopathy 48.0 % moderate 16.0% and severe and 8.0% showed proliferative diabetic retinopathy. Those over age 30 are 2.8 times more risk of developing DR, OR= 2.8; 95%CI: 0.42-18.0, and OR= 1.7; 95%CI: 1.02-2.95 women.

Conclusions:

The implementation of programs aimed at the early detection of debilitating conditions such as diabetic retinopathy health impact beneficiaries, effective links between primary care systems and provide second level positive health outcomes for patient diseases.     

基于改进SOLO＿v2的糖尿病黄斑水肿分割模型

糖尿病黄斑水肿（DME）是导致糖尿病患者视力损害的常见原因。光学相干断层扫描技术（OCT）有助于增强对糖尿病视网膜病变的早期检测和预防。目前,OCT图像中的DME区域存在大量散斑噪声及小目标区域,现有的实例分割方法存在漏分割等问题。针对上述问题,本文利用特征金字塔转换器（FPT）改进SOLO＿v2模型,提出了一种新的DME分割模型（SOLO-OCT）,包括：（1）利用基于双域滤波去噪算法去除图像上存在的大量散斑噪声,提高输入图像质量;（2）引入FPT,提高模型对小目标的识别能力和学习能力;（3）改进非极大值抑制（NMS）算法,缓解对小目标区域的漏分割问题。将SOLO-OCT模型与其他实例分割模型（包括Mask R-CNN、SOLO和SOLO＿v2）进行了比较,以评估其对DME区域的分割性能。与Mask R-CNN、SOLO和SOLO＿v2模型相比,SOLO-OCT模型对DME区域的分割精度（mAP）提高了3.1%,对小目标DME区域的分割精度（APs）提高了2.2%,而单幅图像的处理时间（Fps）只增加了0.009 9 s。本文提出的DME分割模型（SOLO-OCT）可用于大规模糖尿病...     

Cirrus OCT、Stratas OCT、HRT-Ⅱ检测糖尿病黄斑水肿的可行性分析

目的探讨蔡司第3代及第4代光学相干断层成像（OCT）和海德堡视网膜断层扫描（HRT-Ⅱ）检测糖尿病黄斑水肿（DME）的可行性。方法采用Cirrus OCT、Stratas OCT和HRT-Ⅱ对41只糖尿病视网膜病变（DR）患眼及24只正常对照眼进行黄斑容积512×128组合扫描（Cirrus OCT）、快速黄斑地形图扫描（Stratas OCT）、线性扫描（Stratas OCT）和HRT-Ⅱ检查。结果以上述4种检测方式的正常对照组95%可信区间上限分界值判断DR组患眼是否存在DME,4种检测方式的灵敏度依次为73.68%、36.84%、73.68%、73.68%,特异度依次为100.00%、100.00%、90.91%、36.36%。以荧光素眼底血管造影及眼底检查结果为＂金标准＂,绘制上述4种检测方法的接受者操作特性曲线（ROC曲线）,其ROC曲线面积依次为0.937、0.935、0.908、0.554,以ROC曲线最佳界值判断DR组患眼是否存在DME,此时其灵敏度依次为89.47%、89.47%、89.47%、36.84%,特异度依次为81.82%、81.82%、81.82%、90.91%。结论 Cirrus OCT、Stratas OCT和HRT-Ⅱ均能够量化测量DME。两种OCT能比较客观地评价DME,且在量化评价DME时,两代OCT的价值相差不大。HRT-Ⅱ检测DME仅能顾及灵敏度和特异度之一,其量化评价DME时的临床价值要劣于第3代及第4代OCT。     

Linkage studies of Best''s macular dystrophy

Genetic linkage studies are presented for nine kindreds with Best's vitelliform macular dystrophy (BVMD). This condition is an autosomal dominant macular dystrophy with reduced penetrance and highly variable expressivity. Asymptomatic carriers were identified with electro-oculography, fundus photographs and fluorescein angiography. Blood and saliva specimens were obtained from informative family members and genotyped for 26 polymorphic genetic traits. No firm evidence was found for linkage between BVMD and 18 informative markers; the highest positive lod score was z = 0.57 for GPT1 at a recombination fraction of theta = 0.30. An atypical form of vitelliform macular dystrophy (VMD-1) is linked to GPT1 (theta less than 0.05) and is provisionally assigned to chromosome 16pter-p11. Our data are not sufficient to rule out loose linkage for GPT1 and BVMD. Thus we were not able to determine whether BVMD and VMD-1 are allelic mutations or separate genetic disorders. Additional linkage and gene mapping studies of these loci and BVMD (as well as other atypical forms of macular dystrophy) would be useful to further delineate these disorders.     

Unique noncoding variants upstream of PRDM13 are associated with a spectrum of developmental retinal dystrophies including progressive bifocal chorioretinal atrophy

The autosomal dominant progressive bifocal chorioretinal atrophy (PBCRA) disease locus has been mapped to chromosome 6q14–16.2 that overlaps the North Carolina macular dystrophy (NCMD) locus MCDR1. NCMD is a nonprogressive developmental macular dystrophy, in which variants upstream of PRDM13 have been implicated. Whole genome sequencing was performed to interrogate structural variants (SVs) and single nucleotide variants (SNVs) in eight individuals, six affected individuals from two families with PBCRA, and two individuals from an additional family with a related developmental macular dystrophy. A SNV (chr6:100,046,804T>C), located 7.8 kb upstream of the PRDM13 gene, was shared by all PBCRA‐affected individuals in the disease locus. Haplotype analysis suggested that the variant arose independently in the two families. The two affected individuals from Family 3 were screened for rare variants in the PBCRA and NCMD loci. This revealed a de novo variant in the proband, 21 bp from the first SNV (chr6:100,046,783A>C). This study expands the noncoding variant spectrum upstream of PRDM13 and suggests altered spatio‐temporal expression of PRDM13 as a candidate disease mechanism in the phenotypically distinct but related conditions, NCMD and PBCRA.     

Adult vitelliform macular dystrophy is frequently associated with mutations in the peripherin/RDS gene

Mutations in the peripherin/RDS gene, which encodes a photoreceptor-specific membrane glycoprotein, have been identified in a variety of retinal phenotypes. However, the mechanisms by which specific mutations in this gene can cause typical features of retinal dystrophies clinically as distinct as retinitis pigmentosa or macular degeneration are still unknown. Recently, a single case of adult vitelliform macular dystrophy (AVMD) has been associated with a Y258Stop mutation. To assess the frequency of peripherin/RDS mutations in the clinically heterogeneous group of AVMD, we analyzed the entire coding region of the gene in 28 unrelated patients. We identified five novel mutations including two presumed null allele mutations. Thus, our results demonstrate that a significant portion of AVMD patients (18%) carry point mutations in peripherin/RDS, suggesting that this gene is frequently involved in the pathogenesis of this macular disorder. In addition, this study shows that the variable phenotypes in AVMD are due, at least in part, to genetic heterogeneity and are likely to be caused by mutations in disease genes thus far unknown. Hum Mutat 10:301–309, 1997. © 1997 Wiley-Liss, Inc.     

Dominantly inherited macular degeneration (Best's disease) in a homozygous father with 11 children

In Sweden, more than 250 cases of hereditary macular degeneration (HMD), inherited as an autosomal dominant trait and consistent with Best's disease, have been traced to one gene source in the 17th century. In this large material an apparently homozygous father was found, who was aged 56 and had 11 affected children. One of the children, aged 24, did not show any macular degeneration, but nevertheless she was considered to be a carrier of the HMD-gene because she had pathological EOG-values. The great variations in expressivity of the disease in the 11 children reflected what has been found as a rule in large Swedish families with HMD. The homozygotic stage did not seem to differ in clinical appearance from the heterozygotic.     

Genetic susceptibility to age related macular degeneration

Age related macular degeneration (AMD) is the leading cause of visual impairment in the elderly and a major cause of blindness in the developed world. The disease can take two forms, geographic atrophy and choroidal neovascularisation. The pathogenesis of AMD is poorly understood. There are undoubtedly environmental and other risk factors involved and the adverse effect of smoking is well established. Several studies have shown that genetic factors are important but leave uncertainty about the magnitude and nature of the genetic component and whether it varies with the type of AMD. Several hereditary retinal dystrophies show similarities to AMD and these genes are potential candidate susceptibility genes. Particular interest has focused on the ABCR gene which is responsible for autosomal recessive Stargardt macular dystrophy. It has been claimed that heterozygotes for ABCR mutations are predisposed to AMD but the data are conflicting. Studies of the genes responsible for autosomal dominant Sorsby fundus dystrophy, Doyne honeycomb retinal dystrophy, and Best disease have given negative results. In one large AMD family, linkage has been reported to markers in 1q25-q31. Recent data suggest that the ApoE epsilon4 allele may be associated with reduced risk of AMD. A better understanding of the genetic factors in AMD would contribute to understanding the pathogenesis. If those at risk could be identified it may be possible to modify lifestyle or develop novel therapies in the presymptomatic stage to prevent disease or decrease its severity.     

年龄相关性黄斑变性与单核甘酸多态性相关性的研究进展

年龄相关性黄斑变性(AMD)是发达国家老年人致盲的首要疾病.遗传因素在AMD的发生、发展中起重要作用.近几年研究发现,一些单核甘酸多态性(SNP)与AMD的发病明显相关.因而对补体因子H(CFH)基因,补体因子B(CFB)基因,补体因子2(C2)基因,补体因子3(C3)基因,CX3C趋化因子受体1(CX3CR1)基因,三磷酸腺苷结合盒转运体基因亚家族A第4成员(ABCA4)在AMD形成过程中的研究具有重要意义.     

Visual impairment due to macular disciform scars in a 20-year-old man with Smith-Magenis syndrome: Another ophthalmologic complication

We describe a 20-year-old man with Smith-Magenis syndrome and a 46,XY,del(17)(p11.2p11.2) karyotype. The interstitial deletion was confirmed by metaphase analysis using the fluorescent in situ hybridization probe (D17S29) for the Smith-Magenis region. The patient had hypertelorism, exotropia, and high myopia. Examination under anesthesia showed a lacquer crack near the right macula and a disciform scar of the left macula. Six months later, the patient presented with subacute visual loss. Examination demonstrated end-stage macula degeneration with bilateral disciform scars. There was no evidence of retinal detachment. Prior reports of Smith-Magenis syndrome mention telecanthus, ptosis, strabismus, iris anomalies, cataract, microcornea, optic nerve hypoplasia, myopia, retinal detachment, and lattice retinal degeneration. Bilateral macular degeneration has not been reported previously, and it may be an additional ophthalmologic manifestation of Smith-Magenis syndrome, either as a primary manifestation or as a direct consequence of high myopia. Am. J. Med. Genet. 80:373–376, 1998. © 1998 Wiley-Liss, Inc.