Aleksandra Krasińska, J. Mamczur, Manuela Pajdowska, A. Brązert
{"title":"Difficulties in Treatment of Iridocorneal Endothelial Syndrome - Case Report","authors":"Aleksandra Krasińska, J. Mamczur, Manuela Pajdowska, A. Brązert","doi":"10.2478/acb-2022-0009","DOIUrl":null,"url":null,"abstract":"Abstract The iridocorneal endothelial syndrome manifests in three clinical types: Chandler syndrome, progressive iris atrophy, and Cogan-Reese syndrome. It is caused by the presence of abnormal corneal endothelium on the iris stroma and anterior chamber angle leading to usually unilateral, progressive iris atrophy, glaucoma, and/or corneal edema. The etiology is yet unclear. It affects mostly young adults, mostly females. Management of iridocorneal endothelial syndrome is complex: conservative and surgical, depending on the stage of the disease and intensity of present symptoms. A 30-year-old female with a medical history of the iridocorneal endothelial syndrome was reported to the Ophthalmology Department for consultation. Slit-lamp examination revealed iris atrophy and superior-nasal corectopia in the left eye. On gonioscopy, the angle was wide open in the right eye, but there were iridocorneal adhesions and incomplete angle-closure in the left eye. The patient was provided with maximum local therapy consisting of three anti-glaucoma medications. On later check-ups, the patient presented corneal edema and increased intraocular pressure. She was qualified to ExPress mini shunt trabeculectomy with mitomycin C. Two years later, a patient came to the clinic because of increased values of intraocular pressure (up to 59 mmHg), slit-lamp examination showed that the ExPress implant was congested with fragments of the corneal endothelial cells. Thanks to YAG iridotomy the implant was recanalized.","PeriodicalId":18329,"journal":{"name":"Medical Journal of Cell Biology","volume":"10 1","pages":"56 - 60"},"PeriodicalIF":0.0000,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Journal of Cell Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2478/acb-2022-0009","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0
Abstract
Abstract The iridocorneal endothelial syndrome manifests in three clinical types: Chandler syndrome, progressive iris atrophy, and Cogan-Reese syndrome. It is caused by the presence of abnormal corneal endothelium on the iris stroma and anterior chamber angle leading to usually unilateral, progressive iris atrophy, glaucoma, and/or corneal edema. The etiology is yet unclear. It affects mostly young adults, mostly females. Management of iridocorneal endothelial syndrome is complex: conservative and surgical, depending on the stage of the disease and intensity of present symptoms. A 30-year-old female with a medical history of the iridocorneal endothelial syndrome was reported to the Ophthalmology Department for consultation. Slit-lamp examination revealed iris atrophy and superior-nasal corectopia in the left eye. On gonioscopy, the angle was wide open in the right eye, but there were iridocorneal adhesions and incomplete angle-closure in the left eye. The patient was provided with maximum local therapy consisting of three anti-glaucoma medications. On later check-ups, the patient presented corneal edema and increased intraocular pressure. She was qualified to ExPress mini shunt trabeculectomy with mitomycin C. Two years later, a patient came to the clinic because of increased values of intraocular pressure (up to 59 mmHg), slit-lamp examination showed that the ExPress implant was congested with fragments of the corneal endothelial cells. Thanks to YAG iridotomy the implant was recanalized.