8 research outputs found
Common variants near CAV1 and CAV2 are associated with primary openangle glaucoma.
l e t t e r s We conducted a genome-wide association study for primary open-angle glaucoma (POAG) in 1,263 affected individuals (cases) and 34,877 controls from Iceland. We identified a common sequence variant at 7q31 (rs4236601[A], odds ratio (OR) = 1.36, P = 5.0 × 10 −10 ). We then replicated the association in sample sets of 2,175 POAG cases and 2,064 controls from Sweden, the UK and Australia (combined OR = 1.18, P = 0.0015) and in 299 POAG cases and 580 unaffected controls from Hong Kong and Shantou, China (combined OR = 5.42, P = 0.0021). The risk variant identified here is located close to CAV1 and CAV2, both of which are expressed in the trabecular meshwork and retinal ganglion cells that are involved in the pathogenesis of POAG. Glaucoma is the leading cause of irreversible blindness worldwide, affecting approximately 70 million people 1 . It is a chronic degenerative optic neuropathy with progressive loss of retinal ganglion cells and axons resulting in a corresponding thinning of the neuroretinal rim of the optic nerve and a characteristic visual field defect. It is distinct from other forms of optic neuropathy in that the neuro retinal rim of the optic nerve retains its normal pink color as it becomes progressively thinner, leading to an enlarged opticnerve cup. POAG is the most common form of glaucoma. Excluding rare primary juvenile glaucoma with age of onset between 10 and 35 years, POAG is arbitrarily divided into highpressure glaucoma (defined as ≥22 mmHg) and normalpressure glaucoma. POAG is thought to have a multifactorial etiology, with the main risk factors being age, elevated intraocular (IOP) pressure, family history, race, central corneal thickness (CCT), hypertension, diabetes and myopia. The familiality of POAG has been known for decades, and studies have revealed three to ninefold greater risk of POAG in firstdegree relatives of POAG cases than in the population in general 2 . Common variants near CAV1 and CAV2 are associated with primary openangle glaucom
18 Eye Clinic
We conducted a genome-wide association study for primary open-angle glaucoma (POAG) in ,263 affected individuals (cases) and 34,877 controls from Iceland. We identified a common sequence variant at 7q3 (rs423660[A], odds ratio (OR) = .36, P = 5.0 × 0 −0 ). We then replicated the association in sample sets of 2,75 POAG cases and 2,064 controls from Sweden, the UK and Australia (combined OR = .8, P = 0.005) and in 299 POAG cases and 580 unaffected controls from Hong Kong and Shantou, China (combined OR = 5.42, P = 0.002). The risk variant identified here is located close to CAV1 and CAV2, both of which are expressed in the trabecular meshwork and retinal ganglion cells that are involved in the pathogenesis of POAG. Glaucoma is the leading cause of irreversible blindness worldwide, affecting approximately 70 million people 1 . It is a chronic degenerative optic neuropathy with progressive loss of retinal ganglion cells and axons resulting in a corresponding thinning of the neuroretinal rim of the optic nerve and a characteristic visual field defect. It is distinct from other forms of optic neuropathy in that the neuro retinal rim of the optic nerve retains its normal pink color as it becomes progressively thinner, leading to an enlarged opticnerve cup. POAG is the most common form of glaucoma. Excluding rare primary juvenile glaucoma with age of onset between 10 and 35 years, POAG is arbitrarily divided into highpressure glaucoma (defined as ≥22 mmHg) and normalpressure glaucoma. POAG is thought to have a multifactorial etiology, with the main risk factors being age, elevated intraocular (IOP) pressure, family history, race, central corneal thickness (CCT), hypertension, diabetes and myopia. The familiality of POAG has been known for decades, and studies have revealed three to ninefold greater risk of POAG in firstdegree relatives of POAG cases than in the population in general 2 . Common variants near CAV1 and CAV2 are associated with primary openangle glaucom
Visual field loss in eyes undergoing minimally invasive glaucoma surgery in Iceland
Ágrip Inngangur Gláka er sjúkdómur sem lýsir sér með hrörnun á sjóntaug augans og er ein helsta ástæða blindu. Eina viðurkennda meðferð sjúkdómsins er lækkun augnþrýstings með lyfjum, lasermeðferð eða skurðaðgerðum. Undanfarið hafa orðið stórstígar framfarir með komu MIGS (minimally invasive glaucoma surgery) glákuaðgerða sem taka styttri tíma og eru með lægri fylgikvillatíðni samanborið við hefðbundnar glákuaðgerðir. Því ætti að vera lægri þröskuldur til að vísa sjúklingum í aðgerð. Tilgangur rannsóknarinnar var að kanna sjónsviðsskerðingu við tilvísun í MIGS-aðgerð. Efni og aðferðir Afturskyggn rannsókn sem náði til allra sjúklinga sem undirgengust MIGS-aðgerð á tímabilinu janúar 2019 til júní 2020. Meðal þess sem var skoðað var glákugerð, sjónsviðsskerðing, og augnþrýstingur. Hópnum var skipt í tvo undirhópa eftir því hvort MIGS var framkvæmt með augasteinaskiptum eða ekki. Niðurstöður Gögn fengust frá 112 augum. Meðalaldur var 74,5 ára. Meðaltal sjónsviðsskerðingar var 8,8±6,4 dB og fjöldi glákulyfja var 2,3±1,2 fyrir allan hópinn. Marktækur munur (p<0,01) var á aldri, sjónsviðsskerðingu og fjölda glákulyfja milli þeirra sem fóru í glákuaðgerð með augasteinaskiptum og þeirra sem fóru í glákuaðgerð án augasteinakipta. Meðaltal sjónsviðsskerðingar fyrir augu með frumgleiðhornsgláku sem fóru ekki í augasteinaskipti var 11,2±6,5 dB samanborið við 6,0±3,3 dB fyrir flögnunargláku (p<0,05). Ályktanir Sjúklingar sem fóru einnig í augasteinaskipti voru með vægari gláku, á færri glákudropum og eldri en þeir sem fóru í MIGS-aðgerð án augasteinaskipta. Sjónsviðsskerðing og fjöldi augndropa var lægri samanborið við íslenska rannsókn þar sem sjúklingar gengust undir hefðbundna gláku-hjáveituaðgerð. Þetta bendir til þess að verið sé að senda sjúklinga fyrr í skurðaðgerð en áður. Augu með flögnunargláku voru með marktækt lægri sjónsviðsskerðingu heldur en gleiðhornsgláka. Þetta er vísbending um að íslenskir augnlæknar sendi sjúklinga með flögnunargláku fyrr í aðgerð en flögnunargláka er illvígari sjúkdómur en gleiðhornsgláka. INTRODUCTION: Glaucoma is a degenerative disease of the optic nerve and is marked by visual field defects (VFD). The only approved treatment is IOP lowering, either with eye drops, laser or surgery. Minimally invasive glaucoma surgery (MIGS) has become an appealing treatment modality, offering IOP lowering effect without the complication rates of trabeculectomy or the patient adherence required for pharmacologic therapy. In this study we aim to describe the severity of VFD in patients undergoing their first MIGS surgery. METHODS: Retrospective study reviewing the medical records of all patients that underwent MIGS surgery at the University Hospital of Iceland from January 2019 to June 2020. Eyes with previous glaucoma surgeries and secondary glaucomas were excluded. The results were divided into two groups, MIGS with phacoemulsification and standalone MIGS. RESULTS: 112 eyes included in the study. Mean age 74.5 ± 10.6 years. The mean defect (MD) score was 8.8 ± 6.4 and the number of glaucoma medications 1.8 ± 1.0 for the group as a whole. Significant difference (p<0.01) was between the age, MD score and the number of glaucoma medications between the two groups. Looking at the eyes that did not undergo phacoemulsification a significant difference (p<0.05) was between the MD score of primary open angle glaucoma eyes, 11.2 ± 6.5 dB and pseudoexfoliation glaucoma, 6.0 ± 3.3 dB. CONCLUSION: Visual field defect and the number of glaucoma medications at referral to surgery was markedly less compared to a trabeculectomy study done in Iceland 3 years prior. Few comparable studies include MD score in their results, most focus on changes in intraocular pressure. Comparing the MD score to three studies from Germany and Austria the MD score seems to be similar. In our study a lower MD score for pseudoexfoliation glaucoma implies that Icelandic ophthalmologists send pseudoexfoliation eyes earlier for an operation.Peer reviewe
Can postoperative dexamethasone nanoparticle eye drops replace mitomycin C in trabeculectomy?
Purpose: Compare (a) nonmitomycin C (MMC) trabeculectomy and 1.5% dexamethasone nanoparticle (DexNP) eye drops postoperatively with (b) trabeculectomy with MMC and Maxidex® eye drops postoperatively. Methods: Randomized prospective single masked clinical trial with 20 patients with primary open‐angle glaucoma undergoing primary trabeculectomy. The study group consisted of 10 patients without MMC intraoperatively and postoperative DexNP eye drops, and the control group consisted of 10 patients treated with MMC intraoperatively and postoperative Maxidex®. The drops were tapered out over 8 weeks. The main outcome measures were as follows: rates of complete success, that is intraocular pressure (IOP) within target pressures at different time‐points without IOP‐lowering medication, or reoperation. Secondary outcome measures included the following: relative success rate (with IOP‐lowering medications), number of glaucoma medications and reoperations. Patients were followed for 36 months. Results: Both groups showed similar postoperative course and IOP reduction. Intraocular pressures (IOPs) in the DexNP group and in the control group were 25.6 and 24.4 mmHg, respectively, at baseline. Intraocular pressures (IOPs) were reduced to 13.2 and 14.5 mmHg at 12 months, 11.7 and 12.6 mmHg at 24 months and 11.7 and 12.1 mmHg at 36 months, respectively. There were no statistically significant differences between the groups in absolute (p = 0.36) or relative (p = 1.0) success rates, number of medications (p = 0.71) or reoperations (p = 1.0) between the groups at any time‐point. Conclusions: DexNP eye drops are effective postoperative treatment following trabeculectomy. The potent anti‐inflammatory and antifibrotic effect of DexNP may offer an alternative to mitomycin C in glaucoma surgery
Retinal oximetry in primary open-angle glaucoma.
To access publisher full text version of this article. Please click on the hyperlink in Additional Links field.PURPOSE. To determine whether retinal vessel oxygen saturation is affected in primary open-angle glaucoma (POAG) patients. METHODS. Retinal oxygen saturation in patients with POAG was measured in retinal vessels with a spectrophotometric retinal oximeter in darkness, and visual fields were obtained. Oxygen tension (Po(2)) was calculated from oxygen saturation values. Statistical analysis was performed using Pearson's correlation and Student's t-test. RESULTS. Mean oxygen saturation in venules was higher in persons with poor visual fields (68% ± 4%, mean ± SD) than in those with good visual fields (62% ± 3%; P = 0.0018). The mean arteriovenous difference in oxygen saturation was lower in persons with poor visual fields (30% ± 4%, n = 9) than in those with good visual fields (37% ± 4%; P = 0.0003; n = 12). No correlation was found between saturation in retinal arterioles and visual field mean defect (n = 31; r = -0.16; P = 0.38). Oxygen saturation in retinal venules correlated positively with worsening visual field mean defect (r = 0.43; P = 0.015). Arteriovenous difference in oxygen saturation decreased significantly as the visual field mean defect worsened (r = -0.55; P = 0.0013). Mean Po(2) in venules was 38 ± 3 mm Hg. It was significantly higher in persons with poor visual field fields (40 ± 3 mm Hg) than in those with good visual fields (36 ± 2 mm Hg; P = 0.0016). CONCLUSIONS. Deeper glaucomatous visual field defects are associated with increased oxygen saturation in venules and decreased arteriovenous difference in retinal oxygen saturation. The data suggest that oxygen metabolism is affected in the glaucomatous retina, possibly related to tissue atrophy.Icelandic Centre for Research (Rannis)
Icelandic Fund for Prevention of Blindness
Landspitali-University Hospita
Retinal oxygen metabolism in healthy subjects and glaucoma patients.
To test whether retinal oxygen metabolism is different in glaucoma patients compared with healthy subjects.This was a two-centre study where retinal vessel oxygen saturation was measured in glaucoma patients and healthy individuals with a non-invasive spectrophotometric retinal oximeter. Visual fields were obtained in the glaucoma patients.No statistical difference was found in retinal oxygen saturation in arterioles (p=0.16), venules (p=0.16) and arteriovenous difference (p=0.24) when all glaucoma patients (n=74) were compared with healthy individuals (n=89). When patients with advanced glaucoma (visual field mean defect (MD ≥ 10 dB, n=21)) were compared with healthy individuals, the oxygen saturation in venules was higher in glaucoma patients (58.2% ± 5.4% vs 53.8% ± 6.4%; p=0.0054, mean ± SD) and the arteriovenous difference was lower in glaucoma patients (36.4% ± 4.7% vs 39.5% ± 5.7%; p=0.021). In glaucoma patients with mild glaucoma (visual field MD ≤ 5 dB, n=33), no statistical differences were found in retinal oxygen saturation compared with healthy individuals.Glaucoma patients with advanced glaucoma have higher oxygen saturation in venules and lower arteriovenous difference in oxygen saturation compared with healthy individuals. The decreased arteriovenous difference in severe glaucoma may be related to lower oxygen consumption secondary to neuropathy.FWO 'Fonds Wetenschappelijk Onderzoek-Vlaanderen'
Icelandic Centre for Research/100429021
Merck Sharp and Dohme (MSD)
Prevention of Blindness Fund
Landspitali-University Hospital Research Fund/
A-2013-02
Common variants near CAV1 and CAV2 are associated with primary open-angle glaucoma
We conducted a genome-wide association study for primary open-angle glaucoma (POAG) in 1,263 affected individuals (cases) and 34,877 controls from Iceland. We identified a common sequence variant at 7q31 (rs4236601[A], odds ratio (OR) = 1.36, P = 5.0 × 10?10). We then replicated the association in sample sets of 2,175 POAG cases and 2,064 controls from Sweden, the UK and Australia (combined OR = 1.18, P = 0.0015) and in 299 POAG cases and 580 unaffected controls from Hong Kong and Shantou, China (combined OR =5.42, P = 0.0021). The risk variant identified here is located close to CAV1 and CAV2, both of which are expressed in the trabecular meshwork and retinal ganglion cells that are involved in the pathogenesis of POAG