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首页> 外文期刊>Journal of the Royal Society of Medicine >Severe visual loss secondary to central serous chorioretinopathy following prolonged immune suppression with oral prednisolone
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Severe visual loss secondary to central serous chorioretinopathy following prolonged immune suppression with oral prednisolone

机译:口服泼尼松龙延长免疫抑制后,继发于中央浆液性脉络膜视网膜病变继发的严重视力丧失

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DECLARATIONSCompeting interestsNone declaredEthical approvalWritten informed consent to publication has been obtained from the patient or next of kinGuarantorSPContributorshipSP and AH wrote the case report. SP was the patient's ophthalmic consultant and obtained the images. KA was the renal consultant involved in the patient's care and editor the report prior to submission. SP was the supervising author for the paperReviewerBalini BalasubramaniamCentral serous chorioretinopathy (CSCR) is often self-limiting but can have serious ocular complications. We present a case of severe visual loss secondary to chronic CSCR in a renal transplant patient on long-term corticosteriods.Case history Section:A 50-year-old man presented to the eye clinic with a 12-month history of a gradual loss of vision in the right eye. He had no significant past ocular history but had been diagnosed at the age of 10 years with Henoch-Schonlein nephritis. He had a renal transplant in 1997 and had been taking oral prednisolone for the past 12 years as part of his immunosuppression regime. He also suffered from hyperparathyroidism and had recently been diagnosed with type 2 diabetes. At the time of presentation his medication included immunosuppression with cyclosporin 50 mg twice daily, azothiaprine 100 mg and prednisolone 7.5 mg. He was also on candesartan, atenolol, furosemide, simvastatin, alfacalcidol, darbepoetin alfa and cinacalcet.On examination his visual acuities were 2/60 in the right eye and 6/4 in the left eye. The anterior segments, intraocular pressures and crystalline lenses were normal in both eyes. A dilated ophthalmic examination revealed diffuse nonspecific retinal pigment epithelial (RPE) changes in both eyes. There were no clinical signs of subretinal fluid or neurosensory or pigment epithelial retinal detachments in either eye although the ocular coherence tomogram (OCT) detected shallow extrafoveal subretinal fluid in the left eye. The OCT, fundus autofluorescence (FA) and fundus fluorescein angiogram (FFA) findings are shown in Figure 1. The optic discs were healthy.DownloadOpen in new tabDownload in PowerPointFigure 1 Showing the OCT, fundus autofluorescence and angiographic findings in the right and left eyes at presentation. A and B: OCT images captured on the Topcon 3D OCT 1000. No subretinal fluid seen in the right eye (1A). Left eye shows disruption of the retinal pigment epithelium associated with shallow subretinal fluid localized to the superotemporal macular area (red arrow) (1B). C and D: Fundus autofluorescence images captured on the Heidelberg retina angiograph 2 (HRA 2). There is an area of mottled reduced autofluorescence with bright margins, a gravitational distribution and extensive foveal involvement in the right eye (1C). The left eye shows a localized and relatively uniform area of increased autofluorescence, sparing the macula (1D). E and F: Fundus fluorescein angiogram images captured on HRA 2. There is mottled hyperfluorescence in the right eye at 1 minute corresponding to the area of abnormal fundus autofluorescence (1E). The left eye at 45 seconds shows a triangular area of hypofluorescence (corresponding to a similar shaped area of increased fundus autofluorescence) surrounded by mottled hyperfluorescence (1F). Neither eye showed any area of focal hyperfluorescence or choroidal neovascularizationA diagnosis of steroid-induced chronic central serous retinopathy was made. The right eye had inactive end-stage disease. However, the presence of shallow subretinal fluid in the left eye indicated residual disease activity in this eye. If left untreated there remained the threat of foveal involvement and loss of vision. After discussion with the treating renal physician and the patient it was decided to reduce the oral prednisolone while jointly monitoring both the renal function and the ophthalmic condition. His oral prednisolone has been gradually reduced over three months from 7.5 mg to 2 mg. Both his transplant
机译:声明竞争利益未宣告伦理批准已从患者或近亲GuarantorSPContributorshipSP和AH的亲属处获得书面公开知情同意,并且AH撰写了病例报告。 SP是患者的眼科顾问并获得了图像。 KA是参与患者护理的肾脏顾问,并在提交前编辑报告。 SP是本文的指导作者。审阅者Balini Balasubramaniam中央浆液性脉络膜视网膜病变(CSCR)通常是自限性的,但可能会引起严重的眼部并发症。我们在长期使用皮质类固醇的肾移植患者中出现一例继发于慢性CSCR的严重视力丧失病例案例历史部分:一名50岁的男子被送往眼科诊所,有12个月的逐渐消失史右眼的视力。他没有明显的既往眼病史,但在10岁时被诊断出患有Henoch-Schonlein肾炎。他于1997年进行了肾脏移植,并且在过去的12年中一直服用口服泼尼松龙作为其免疫抑制方案的一部分。他还患有甲状旁腺功能亢进症,最近被诊断出患有2型糖尿病。在介绍时,他的药物包括免疫抑制,每日两次,环孢素50 mg,硫唑嘌呤100 mg,泼尼松龙7.5 mg。他还接受坎地沙坦,阿替洛尔,速尿,辛伐他汀,阿法骨化醇,达贝泊汀α和西那卡塞治疗。检查时,他的视力在右眼为2/60,在左眼为6/4。两只眼的前节,眼压和晶状体均正常。散瞳检查发现两只眼睛的弥漫性非特异性视网膜色素上皮(RPE)改变。尽管眼相干断层扫描(OCT)在左眼中发现浅凹的视网膜下视网膜下液,但两眼都没有视网膜下液或神经感觉或色素上皮视网膜脱离的临床体征。图1显示了OCT,眼底自发荧光(FA)和眼底荧光素血管造影(FFA)的结果。视盘是健康的。下载在新标签中打开在PowerPoint中下载图1显示左右眼的OCT,眼底自发荧光和血管造影结果在演示中。 A和B:在Topcon 3D OCT 1000上捕获的OCT图像。右眼(1A)中未见视网膜下液。左眼显示视网膜色素上皮的破坏与浅颞叶黄斑区域的浅视网膜下液有关(红色箭头)(1B)。 C和D:在海德堡视网膜血管造影仪2(HRA 2)上捕获的眼底自发荧光图像。右眼有一处斑驳的自发荧光减少,边缘明亮,有重力分布,中央凹广泛受累(1C)。左眼显示出局部和相对均匀的自发荧光增加区域,保留了黄斑(1D)。 E和F:在HRA 2上捕获的眼底荧光血管造影图像。右眼在1分钟处有斑驳的高荧光,与异常的眼底自发荧光(1E)区域相对应。左眼在45秒处显示出一个呈斑点状的高荧光(1F)包围的三角形低荧光区域(相当于眼底自发荧光增加的类似形状区域)。两只眼睛均未显示任何区域的局灶性高荧光或脉络膜新血管形成。诊断为类固醇诱发的慢性中枢性浆液性视网膜病变。右眼患有非活动性晚期疾病。但是,左眼中浅视网膜下液的存在表明该眼中残留疾病活动。如果不及时治疗,则仍然存在中央凹受累和视力丧失的威胁。与主治肾脏医生和患者讨论后,决定减少口服泼尼松龙,同时联合监测肾功能和眼科疾病。他的口服泼尼松龙在三个月内逐渐从7.5 mg减少至2 mg。都是他的移植

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