玻璃体内注射抗血管内皮生长因子药物在糖尿病性黄斑水肿治疗中的应用

糖尿病性黄斑水肿（DME）是由糖尿病引起的黄斑中心区2倍于视盘直径范围内的视网膜增厚、局部的或弥漫性水肿,有或无硬性渗出。其临床表现为视力减退或视物变形或症状不明显,可伴有相对或绝对性中心暗点。未经治疗的1型和2型糖尿病患者在3年内将出现25％～30％的临床显著型黄斑水肿（CSME）。黄斑功能直接影响到患者的视锐度,DME已成为糖尿病患者视力受损甚至失明的主要原因。DM E的治疗包括黄斑激光光凝术、睫状环玻璃体切割手术、玻璃体注射曲安奈德等,但是这些治疗方法又各自具有局限性。由于血管内皮生长因子（VEGF）在糖尿病性视网膜病变（DR）及DM E发病中的作用逐渐被重视,因而从抑制VEGF的角度治疗DR、DME的研究近年逐渐兴起。现对于最常见三种抗VEGF药物进行玻璃体内注射治疗DME的研究现状作一综述。     

血清Apelin APN FFA及MMP与充血性心力衰竭的关系的分析

目的：探讨血清爱帕琳肽（Apelin）、脂联素（APN）,游离脂肪酸（FFA）及基质金属蛋白酶（MMP）与充血性心力衰竭的关系。方法本资料中80例充血性心力衰竭患者设为观察组,同期的80名健康者为对照组,将两组的血清Apelin、APN、FFA及MMP水平进行检测及比较,然后将观察组中不同分级及分类患者的血清Apelin、APN、FFA及MMP水平进行分别统计及比较,并以Logistic分析处理上述血清项目与充血性心力衰竭的关系。结果观察组的血清Apelin、APN、FFA及MMP水平均高于对照组,且观察组中分级较高者高于分级较低者,收缩性心力衰竭患者则高于舒张性心力衰竭患者,经Logistic分析显示上述血清检测指标与充血性心力衰竭有密切的关系（P均＜0.05）。结论充血性心力衰竭患者的血清Apelin、APN、FFA及MMP呈现明显升高的状态,上述血清指标均与充血性心力衰竭有密切的关系。     

激光治疗糖尿病性黄斑水肿的理论与应用

目的糖尿病性黄斑水肿(diabetic macular edema,DME)是引起糖尿病患者视力恶化的主要原因.自激光应用于眼科以来,根据资料和研究表明激光治疗黄斑水肿可以稳定和提高患者的视力.回顾DME的病因分型、激光治疗的原理及治疗方法和治疗效果,表明激光是对DME的较为理想的治疗方式.资料来源应用计算机检索Medline 1980-01/2004-01期间与激光治疗糖尿病黄斑水肿内容相关文章,检索词"diabetic macular edema,laser",并限定文章语言种类为English.同时计算机检索中国期刊全文数据库1994-01/2004-01期间与激光治疗糖尿病黄斑水肿内容相关文章,限定文章语言种类为中文,检索词"糖尿病、黄斑水肿、激光".资料选择选择关于DME及其激光治疗的文献,国外文献100篇,国内文献50篇.在文献选择中,研究原著的选择未排除其研究是否采用了随机和盲法的设计方案.资料提炼对检索到的有关DME及其激光治疗的英文文章100篇,中文文章50篇,共150篇文章中相关信息进行综合整理.资料综合分析DME的病因分型,针对激光治疗的原理、治疗的方法、治疗的效果、治疗中需注意的问题、如何进行合理的应用激光逐一阐明.结论越来越多的研究结果表明,开展光凝治疗已成为防治糖尿病视网膜病变所致失明的行之有效的方法,黄斑水肿的患者通过激光治疗使得视力得到稳定和提高.     

后Tenon′s囊下注射曲安奈德联合532激光治疗弥漫性糖尿病性黄斑水肿临床观察

目的：评价后Tenon′s囊下注射曲安奈德联合532激光治疗糖尿病性黄斑水肿（DME）的临床疗效。方法：对24例39眼伴有DME的糖尿病视网膜病变（DR）的患者给予后Tenon′s囊下注射曲安奈德30 mg 1次,2周后,采用532激光进行黄斑格栅光凝以及全视网膜光凝,再间隔2周后分析患者视力、眼底荧光造影、眼压以及并发症情况。结果：随访3~18个月,39眼中22眼（56.4%）视力稳定;13眼视力提高（33.3%）,4眼视力下降（10.2%）;荧光血管造影（FFA）眼底荧光造影检查,39眼中23眼黄斑水肿消退（59.0%）,13眼部分消退（33.3%）,另外有3眼无变化或者加重（7.7%）。39眼中除有2眼出现眼压升高症状,4眼出现晶状体混浊轻度加重外,无其他并发症出现。结论：后Tenon′s囊下注射曲安奈德联合532激光治疗DME是行之有效的治疗方法,有助于黄斑水肿的消退以及视力的提高,并且有并发症少等特点。     

Apelin在糖尿病心血管病变中的研究进展

研究表明Apelin．APJ系统参与了糖尿病心血管并发症的病理生理过程，但其具体机制目前仍不甚明了。目前已有报道Apelin与肥胖、胰岛素抵抗有关，并通过一氧化氮（N0）系统扩张血管，在糖尿病血管病变中发挥一定作用。此外，Apelin作为一种血管生成因子可能参与了糖尿病视网膜血管生成和糖尿病心肌病的心室重构。本文试就Apelin在糖尿病心血管病变中的研究进展作一综述。     

雷珠单抗联合曲安奈德玻璃体注射治疗弥漫性糖尿病黄斑水肿的临床研究

目的探讨雷珠单抗（Lucentis）联合曲安奈德（TA）玻璃体腔注射治疗弥漫性糖尿病黄斑水肿（DME）所致视力受损患者的临床疗效。 方法收集2017年1月至2018年10月在南方医科大学附属花都医院眼科确诊为DME患者78例（90眼）,采用双盲随机均分为Lucentis组（Lu组）、TA组、Lucentis＋TA组（Lu＋TA组）,3组分别以玻璃体腔单次注射Lucentis（0.5 mg/0.05 ml）、TA（2 mg/0.05 ml）和2种联合注射。检测治疗前及治疗后1 d、1周、1个月、3个月最佳矫正视力、黄斑中心视网膜厚度、眼压、眼底黄斑水肿程度和渗漏类型的变化,同时在各时间点取桡静脉血,应用酶联免疫吸附试验方法检测血清血管内皮生长因子（VEGF）、肿瘤坏死因子（TNF）-α和白介素（IL）-1β水平,采用流式细胞分析外周血中性粒细胞的凋亡情况。采用单因素方差分析和t检验比较各组最佳矫正视力、黄斑中心视网膜厚度、眼压、眼底黄斑水肿程度、VEGF、TNF-α和IL-1β水平的组内和组间差异。 结果各组治疗前平均最佳矫正视力差异无统计学意义（P<0.05）,治疗后1 d、1周、1个月、3个月最佳矫正视力明显好转,与治疗前比较差异具有统计学意义（P<0.05）,不同时间点Lu+TA组与TA组、Lu组比较,差异均具有统计学意义（P<0.05）。各组治疗前黄斑中心视网膜厚度比较差异无统计学意义（P>0.05）,治疗后1 d、1周、1个月、3个月与治疗前相比均显著降低,差异具有统计学意义（P<0.05）,不同时间点Lu＋TA组与TA组、Lu组比较,差异均具有统计学意义（P<0.05）。各组治疗前眼压、眼底黄斑水肿程度和渗漏类型比较,差异无统计学意义（P>0.05）,治疗后3个月眼压、眼底黄斑水肿程度和渗漏类型与治疗前比较,差异具有统计学意义（P<0.05）。各组治疗前血清VEGF、TNF-α和IL-1β及外周血中性粒细胞凋亡比较,差异无统计学意义（P>0.05）,治疗后1 d、1周、1个月、3个月血清VEGF、TNF-α和IL-1β外周血中性粒细胞凋亡与治疗前比较,差异具有统计学意义（P<0.05）,不同时间点Lu＋TA组与TA组、Lu组比较,差异均具有统计学意义（P<0.05）。 结论Lucentis联合TA治疗对控制糖尿病黄斑水肿以及提高DME患者最佳矫正视力、改善黄斑厚度及降低黄斑水肿程度优于Lucentis和TA单一治疗,且Lucentis与TA玻璃体腔注射有协同治疗作用,同时可以降低DME患者术后VEGF和炎性因子的水平。     

糖尿病性黄斑水肿及其检查

糖尿病性黄斑水肿(DME)是引起糖尿病患者视力恶化的主要原因,故早期诊断尤为重要。随着眼科检查技术的更新,尤其是眼底荧光血管造影(FFA)、光学相干断层成像(OCT)等的出现,增加了DME的检出率,提高了准确度,且各检查方法对DME的分型也不尽相同。因此,熟练掌握各检查手段及其各自分型,对临床上诊断、治疗DME并判断其预后具有重要意义。     

糖尿病视网膜病变的治疗

随着糖尿病发病率增高,糖尿病视网膜病变（diabetic retinopathy,DR）的发病率也日益增加,已成为发达国家致盲人数最多的眼病.既往糖尿病所引起的黄斑水肿（diabetic macular edema,DME）和增殖性糖尿病视网膜病变（proliferative diabetic retinopathy,PDR）主要通过眼底激光进行治疗.近年来,在药物治疗方面也有令人鼓舞的进展.本文着重对这些不同的治疗方案及其疗效比较进行综述.     

激光治疗糖尿病性黄斑水肿的理论与应用

目的：糖尿病性黄斑水肿(diabetic macular edema，DME)是引起糖尿病患视力恶化的主要原因。自激光应用于眼科以来，根据资料和研究表明激光治疗黄斑水肿可以稳定和提高患的视力。回顾DME的病因分型、激光治疗的原理及治疗方法和治疗效果，表明激光是对DME的较为理想的治疗方式。资料来源：应用计算机检索Medline 1980—01／2004—01期间与激光治疗糖尿病黄斑水肿内容相关章，检索词“diabetic macular edema，laser”，并限定章语言种类为Endish。同时计算机检索中国期刊全数据库1994—01／2004—01期间与激光治疗糖尿病黄斑水肿内容相关章，限定章语言种类为中，检索词“糖尿病、黄斑水肿、激光”。资料选择：选择关于DME及其激光治疗的献，国外献100篇，国内献50篇。在献选择中，研究原的选择未排除其研究是否采用了随机和盲法的设计方案。资料提炼：对检索到的有关DME及其激光治疗的英章100篇，中章50篇，共150篇章中相关信息进行综合整理。资料综合：分析DME的病因分型，针对激光治疗的原理、治疗的方法、治疗的效果、治疗中需注意的问题、如何进行合理的应用激光逐一阐明。结论：越来越多的研究结果表明，开展光凝治疗已成为防治糖尿病视网膜病变所致失明的行之有效的方法，黄斑水肿的患通过激光治疗使得视力得到稳定和提高。     

激光治疗糖尿病性黄斑水肿的疗效观察

目的探讨激光治疗糖尿病性黄斑水肿的疗效。方法对糖尿病性视网膜病变伴黄斑水肿的38例（56眼）患者行焦点光凝或格栅样光凝,观察治疗前后的视力、眼底荧光血管造影及视野的改变。结果治疗后视力提高者占37．50％,视力不变者占43．75％。黄斑水肿完全消退者占53．57％,部分消退者占28．57％,未消退者占17．85％,出血、渗出均有不同程度的提高;黄斑阈值视野检测无明显改变。结论激光可以有效治疗糖尿病性黄斑水肿,减少渗出,促进出血吸收,稳定和提高视力。     

2型糖尿病肾病患者血清visfatin、Apelin的变化及其临床意义

目的检测2型糖尿病肾病患者血清visfatin、Apelin水平,探讨其在2型糖尿病肾病发生发展中的作用及临床意义。方法根据24 h尿微量白蛋白排泄率(UAER)将105例2型糖尿病患者分为正常白蛋白尿组(NA组,39例)、微量白蛋白尿组(MA组,36例)、临床白蛋白尿组(CP组,30例),选取健康者作为对照组(NC组,35例)。采用酶联免疫吸附法(ELISA)测定血清visfatin、Apelin水平,同时测定患者空腹血糖(FPG)、糖化血红蛋白(HbA1c)、血脂、血尿素氮、血肌酐(Scr)、BMI,计算UAER,比较各组间的差异。结果与NC组比较,3组糖尿病患者血清visfatin、Apelin水平显著升高(P<0.01),3组糖尿病患者之间血清visfatin、Apelin逐渐升高(P<0.05或P<0.01)。相关分析显示,visfatin与BMI、FPG、HbA1c、HOMA-IR、TG、LDL-C、Scr、UAER、Apelin呈正相关(P<0.05);Apelin与BMI、收缩压、FPG、HbA1c、HOMA-IR、LDL-C、Scr、UAER、visfatin呈正相关(P<0.05);visfatin、Apelin均与HDL-C呈负相关(P<0.05)。多元线性回归分析显示:Scr、UAER是糖尿病组患者血清visfatin的独立相关因素(r2分别为0.325、0.267,P<0.05)。HOMA-IR、UAER是糖尿病组患者血清Apelin的独立相关因素(r2分别为0.256、0.487,P<0.05)。结论血清visfatin、Apelin随UAER升高而逐渐升高,其可能参与了糖尿病肾病的发生和发展。     

糖尿病视网膜病变患者黄斑厚度测量方法对比研究

目的评价光学相干断层扫描(OCT)和海德堡断层扫描(HRT-Ⅱ)对背景期糖尿病视网膜病变患者黄斑水肿的诊断价值。方法40例背景期糖尿病视网膜病变患者(80眼)分成黄斑水肿组和非黄斑水肿组,用OCT测量黄斑区厚度,HRT-Ⅱ测量黄斑水肿指数,对结果进行统计学分析。结果对背景期糖尿病视网膜病变患者黄斑水肿的诊断,OCT检查的Kappa值高于HRT-Ⅱ。以眼底荧光血管造影(FFA)检查作为黄斑水肿的诊断标准,OCT检查P=0.0001,HRT-Ⅱ检查P=0.0856。结论OCT和HRT-Ⅱ均可用于定量检测糖尿病黄斑水肿,但OCT检查对黄斑水肿的确诊比HRT-Ⅱ检查更有优势;HRT-Ⅱ对黄斑水肿的误诊率高但漏诊率低,可以作为对糖尿病视网膜病变患者黄斑水肿进行筛查的手段。     

The vitreous and vitreoretinal interface: natural history and associated retinal diseases

Such significant correlations have been found between vitreal changes and retinal breaks that retinal detachment is now considered as a vitreoretinal disease. Concerning this issue, not only the posterior vitreous detachment seems to play an important role in the occurrence of rhegmatogenous retinal detachment but also the vitreoretinal interactions themself seem to be important in the pathogenesis of cystoid and diabetic macular edema, proliferative diabetic retinopathy, age-related macular degeneration, macular pucker, idiopathic macular hole and macular disease associated with optic disk pit. It seemed therefore useful to the author an updated review on alterations of the vitreoretinal interface and associated ocular diseases.     

椎管内麻醉与Apelin对血压和血糖影响的研究进展

椎管内麻醉由于阻滞了交感神经,故能抑制机体对手术牵拉等刺激的应激反应,同时肾上腺皮质激素、甲状腺素、儿茶酚胺等分泌均减少,血糖也会出现波动。交感神经阻滞会引起外周静脉血管扩张,回心血量减少,导致血压降低。Apelin是血管紧张素Ⅱ1型受体相关蛋白（APJ）的内源性配体,在体内分布广泛,在许多器官和组织中通过不同的方式参与血压和血糖的调节。Apelin在糖尿病、高血压等代谢综合征的发生发展中起着重要作用。该文就Apelin的功能及椎管内麻醉下Apelin与血压和血糖的关系进行了综述。     

玻璃体切割联合黄斑部内界膜撕除治疗糖尿病性黄斑水肿

目的观察玻璃体切割联合黄斑部内界膜撕除治疗糖尿病性黄斑水肿（ME）的疗效。方法选择增殖期糖尿病性视网膜病变（PDR）合并ME患者40例42眼,所有患者接受玻璃体切割联合黄斑部内界膜撕除术,观察术后1、3、6个月的视力、眼底荧光血管造影、光学相干断层扫描等资料以及手术并发症,术后随访6个月以上。结果本组40例（42只眼）均未发生手术并发症,视力提高31只眼,视力不变8只眼,下降3只眼。结论严重PDR伴黄斑水肿患者行璃体切割联合黄斑部内界膜撕除,有利于改善黄斑水肿,提高患者视力。     

Apelin表达与结直肠癌发生发展的关系及意义

目的 研究Apelin在人结直肠癌组织中的表达情况与临床病理参数的关系.方法 采用免疫组织化学SP法检测Apelin在45例新鲜结直肠癌及36例正常癌旁黏膜组织中的表达.结果 免疫组织化学结果显示Apelin在结直肠癌组织中表达均高于对照组（P＜0.05）.在45例结直肠癌组织中,Apelin表达与分化程度、淋巴结转移、TNM分期有关（P＜0.05）,与性别、年龄、肿瘤大小、组织学类型无明显相关（P＞0.05）.结论 Apelin在大肠癌组织以及正常癌旁黏膜组织中普遍表达,且在结直肠癌组织中的表达上调.Apelin的表达与患者肿瘤的分化程度、淋巴结转移情况以及TNM分期有关.Apelin有可能成为结直肠癌治疗的一个新靶点.     

Endothelial nitric oxide synthase gene is associated with diabetic macular edema in type 2 diabetes

OBJECTIVE: We examined the endothelial nitric oxide (eNOS) gene polymorphisms to assess its possible association with diabetic retinopathy and macular edema. RESEARCH DESIGN AND METHODS: A total of 226 patients with type 2 diabetes and 186 healthy subjects were studied. Type 2 diabetic patients consisted of 110 patients without retinopathy, 46 patients with nonproliferative diabetic retinopathy, and 71 patients with proliferative diabetic retinopathy. Diabetic macular edema was present in 48 patients. Three polymorphisms of the eNOS gene were determined: T-786C in the promoter region, 27-bp repeat in intron 4, and Glu298Asp in exon 7. RESULTS: Close linkage disequilibrium was observed between the T-786C polymorphism and the 27-bp repeat, as has been previously reported, but Glu298Asp was not in linkage disequilibrium with the other two polymorphisms. The eNOS gene polymorphisms were not significantly associated with the presence of retinopathy or with retinopathy severity or type 2 diabetes itself. However, by both association study and multiple logistic regression analysis, the T-786C and 27-bp repeat polymorphisms were significantly associated with a risk of developing macular edema with the -786C allele and the "a" allele increasing the risk. CONCLUSIONS: The present study suggests that the eNOS gene is a novel genetic risk factor for diabetic macular edema. The eNOS gene polymorphisms may contribute to the development of macular edema by impairing basal eNOS expression and resulting in the breakdown of the blood-retina barrier.     

A telemedical approach to the screening of diabetic retinopathy: digital fundus photography

OBJECTIVE: The importance of screening for diabetic retinopathy has been established, but the best method for screening has not yet been determined. We report on a trial of assessment of digital photographs by telemedicine compared with standard retinal photographs of the same fields and clinical examination by ophthalmologists. RESEARCH DESIGN AND METHODS: A total of 129 diabetic inpatients were screened for diabetic retinopathy by slit-lamp biomicroscopy performed by an ophthalmologist and by two-field 50 degrees non-stereo digital fundus photographs assessed by six screening centers that received the images by electronic mail. Conventional 35-mm transparencies of the same fields as the digital photographs were assessed by a retinal specialist and served as the reference method for detection of diabetic retinopathy. Slit-lamp biomicroscopy was the reference method for the detection of macular edema. RESULTS: The prevalence of any form of diabetic retinopathy was 30% (n = 35); of sight-threatening retinopathy including macular edema, the prevalence was 6% (n = 7). The assessment of digital images by the six screening centers resulted in a median sensitivity of 85% and a median specificity of 90% for the detection of moderate nonproliferative or sight-threatening diabetic retinopathy. Clinically significant macular edema (n = 4) was correctly identified in 15 of the 24 grading reports. An additional seven reports referred the patients for further investigation because of concurrent diabetic retinopathy. CONCLUSIONS: Telescreening for diabetic retinopathy by an assessment of two-field 50 degrees non-stereo digital images is a valid screening method. Although detection of clinically significant macular edema using biomicroscopy is superior to digital or standard non-stereo photographs, only few patients with sight-threatening diabetic retinopathy are missed.     

Incidence of patients presenting with exudative maculopathy and neovascular retinal disease in an urban population

PURPOSE: To determine the incidence of exudative macular and neovascular retinal disease presenting within a defined urban population. STUDY DESIGN: prospective, observational, consecutive case series. PATIENTS AND METHODS: Patients referred to ten ophthalmic centers within a defined 10-week period with a newly diagnosed exudative macular and/or neovascular retinal disease were examined fundoscopically, angiographically and quantified according to age and underlying disease. RESULTS: A total of 527 eyes of 426 patients were referred. The most frequent disease was neovascular age-related macular degeneration (AMD, 199/527, 37.8%, 184 patients), followed by diabetic maculopathy and/or proliferative diabetic retinopathy (199/527, 37.8%, 128 patients) and venous occlusive disease (67/527, 12.7%, 67 patients). The majority of neovascular AMD consisted of occult without classic choroidal neovascularization (CNV, 115/ 199, 57.8%); predominantly classic CNV was seen more often than minimally classic CNV (43/199, 21.6% vs. 27/ 199, 13.6%). The overwhelming majority of the diabetic cases had diabetic macular edema (179/199, 89.9%); only 10.1% had vasoproliferative disease. All other causes of CNV, macular edema/exudation, and retinal neovascularization were observed in < 5% of all patients. CONCLUSION: The main causes of exudative maculopathy are CNV due to neovascular AMD and diabetic macular edema. Proliferative diabetic retinopathy is the main cause of retinal neovascularization. The number of patients with neovascular AMD presents a future challenge for ophthalmologists.