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作 者:庞燕华[1] 赵桂玲[1] 谭志[2] 李瑞庄[1] 朱敏怡[1] 魏进芬[1]
机构地区:[1]广东医学院附属医院眼科,湛江524023 [2]广东医学院附属医院放射科
出 处:《中国实用眼科杂志》2014年第6期701-704,共4页Chinese Journal of Practical Ophthalmology
摘 要:目的 前瞻性研究三维光学相干断层扫描仪(three dimensional optical coherence tomography,3D-OCT)检测急性闭角型青光眼发作眼(经药物降眼压缓解后1d内)黄斑区视网膜厚度,并与正常眼黄斑区视网膜厚度进行比较,初步探讨青光眼黄斑区视网膜厚度改变的可能机制.方法 临床病例对照研究.对2013年1~8月在广东医学院附属医院眼科应用TOPCON 3D-OCT确诊急性闭角型青光眼26例30只眼进行黄斑区视网膜厚度检测,此为病例组.同时对40名健康者(40只正常眼)进行检测作为对照组,并对比两组的差异.结果 急性闭角型青光眼发作眼测得黄斑中心凹、黄斑中心1 mm视网膜厚度分别为(238.38±51.77) μm、(248.31±40.79) μm;正常眼分别为(195.73±16.38)μ.m、(220.15±18.61) μm,两组对比差异有统计学意义P<0.05(t=4.07、3.30,均P =0.00).而黄斑内环、外环各象限视网膜厚度(上、颞、下、鼻)及黄斑区视网膜体积对比两组,差异均无统计学意义(均P >0.05).结论 急性闭角型青光眼发作眼经历急性高眼压后黄斑区中心凹及中心1 mm视网膜增厚,推测与黄斑水肿有关.Objective To measure macular retinal thickness parameters in acute primary angle-closure glaucoma (APACG) patients and to compare them to normal subjects using three dimensional Optical Coherence Tomography (3D-OCT) and discuss the possible mechanism.Methods The prospective analysis included 26 participants with APACG affected 30 eyes (including 22 patients with unilateral affected eyes and 4 patients with bilateral eyes) and 40 healthy subjects in control group.3D-OCT was used to measure and compared the macular retinal thickness in both two groups' eyes.Results Comparison of the macular retinal thickness between the groups showed that the thickness in the APACG eyes were significantly greater than in healthy eyes at fovea and at lmm from the fovea (t =4.07,3.30; both P =0.00),while there were no statistic difference in macular inner-ring retinal thickness and outer-ring retinal thickness (both P 〉0.05).The retinal thickness at fovea and at lmm from the fovea in APACG eyes were (238.38±51.77)μm,(248.31±40.79)μm,while in healthy eyes were (195.73±16.38)μm,(220.15±-18.61)μm.Conclusions Macular retinal thickness in the APACG eyes is significantly greater than in healthy eyes at fovea and at lmm from the fovea,presumably because of macular edema.The innovation of OCT technology may probably help us to learn more about the pathogenesis of acute angle-closure glaucoma.
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