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      Increased Uric Acid and Glucose Concentrations in Vitreous and Serum of Patients with Diabetic Macular Oedema

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          Abstract

          Background: Diabetic retinopathy (DR) is characterized by blood-retina barrier breakdown induced by local changes in the retina and systemic factors. We investigated vitreous and serum levels of glucose and uric acid (UA) in patients with DR and aimed to describe their correlation with the grade of DR. Methods: Prospective study of 81 patients with DR and 48 non-diabetic controls. Biochemical analysis of vitreous and serum samples was performed. Results: UA and glucose concentrations in vitreous and serum were significantly higher in diabetic patients than in controls. Absolute ratios (vitreous level/serum level) of UA and glucose were higher in proliferative compared with non-proliferative DR. Conclusions: The results suggest that, apart from glucose, increased levels of UA in diabetic patients may also be involved in the pathogenesis and progression of DR.

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          Most cited references11

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          Molecular understanding of hyperglycemia's adverse effects for diabetic complications.

          Diabetic complications are the major cause of morbidity and mortality in persons with diabetes. Chronic hyperglycemia is a major initiator of diabetic microvascular complications (eg, retinopathy, neuropathy, nephropathy). Glucose processing uses a variety of diverse metabolic pathways; hence, chronic hyperglycemia can induce multiple cellular changes leading to complications. Several predominant well-researched theories have been proposed to explain how hyperglycemia can produce the neural and vascular derangements that are hallmarks of diabetes. These theories can be separated into those that emphasize the toxic effects of hyperglycemia and its pathophysiological derivatives (such as oxidants, hyperosmolarity, or glycation products) on tissues directly and those that ascribe pathophysiological importance to a sustained alteration in cell signaling pathways (such as changes in phospholipids or kinases) induced by the products of glucose metabolism. This article summarizes these theories and the potential therapeutic interventions that may prevent diabetic complications in the presence of hyperglycemia, control of which is often difficult with current therapeutic options.
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            Diabetic Retinopathy

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              Risk of developing retinopathy in Diabetes Control and Complications Trial type 1 diabetic patients with good or poor metabolic control.

              The study goal was to assess and predict the risk of developing retinopathy in type 1 diabetic patients with extreme metabolic control. Based on material from the Diabetes Control and Complications Trial (DCCT) study (n = 1,441 patients), patients without retinopathy at baseline (DCCT primary cohort) were considered under good or poor metabolic control if the mean HbA(1c) level (until the last visit) fell in the lower or upper 20% of the overall HbA(1c) distribution, respectively. Retinopathy was recorded as either absent or present. Logistic regression was used to predict retinopathy from covariates used in the DCCT retinopathy study. Among the 153 DCCT patients with "good metabolic control" (mean HbA(1c) or = 9.49%), the complication did not develop in 71 (43%) and did develop in 95 (57%). Whereas occurrence of diabetic retinopathy was primarily due to metabolic control (P 40% of patients with type 1 diabetes remain free of retinopathy despite poor metabolic control. After adjusting for metabolic control and duration of participation in the study, it was found that previous glycemic exposure (HbA(1c)) and BMI may provide a possible explanation to such paradoxical clinical situations.
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                Author and article information

                Journal
                ORE
                Ophthalmic Res
                10.1159/issn.0030-3747
                Ophthalmic Research
                S. Karger AG
                0030-3747
                1423-0259
                2011
                July 2011
                14 January 2011
                : 46
                : 2
                : 73-79
                Affiliations
                aDepartment of Ophthalmology, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague and bInstitute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, and cFaculty of Pharmacy, Charles University in Prague, Hradec Kralove, Czech Republic
                Author notes
                *Prof. Tomas Zima, MD, PhD, Institute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University in Prague, U. Nemocnice 2, CZ–128 08 Prague 2 (Czech Republic), Tel. +420 224 962 841, Fax +420 224 962 848, E-Mail zimatom@cesnet.cz
                Article
                322994 Ophthalmic Res 2011;46:73–79
                10.1159/000322994
                21242702
                fbbb51ec-da72-49da-a133-27057364ebab
                © 2011 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 23 May 2010
                : 24 November 2010
                Page count
                Figures: 4, Tables: 3, Pages: 7
                Categories
                Original Paper

                Vision sciences,Ophthalmology & Optometry,Pathology
                Uric acid,Diabetic retinopathy,Glucose,Diabetic macular oedema,Vitreous

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