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      Glycemic Pattern in Diabetic Patients on Hemodialysis: Continuous Glucose Monitoring (CGM) Analysis

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          Abstract

          Background/Aims: Recent evidences suggest that hemodialysis (HD) induces glycemic variations in diabetic patients. Continuous glucose monitoring (CGM) devices measure interstitial glucose in a ‘Holter-like' manner thereby improving the glycemic control assessment method. Methods: A CGM device (Medtronic iPRO) was used on 12 diabetic patients with chronic HD for 6 days to assess intra- and extra-dialytic interstitial glucose. Results: In all enrolled patients, HD was associated with a decrease of interstitial glucose values. Intradialytic glucose nadir was 79 mg/dl and it was reached at the third hour after the beginning of the session. At the end of HD, interstitial glucose increased in all patients and a glycemic peak (187 mg/dl) occurred after an average time of 2.5 h. No episodes of nocturnal hypoglycemia occurred. Conclusion: HD is associated with significant intradialytic reduction of glycemia and postdialytic hyperglycemia. CGM devices result in better monitoring of glycemic trends in diabetic patients on chronic HD and could improve insulin management.

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          Most cited references 15

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          Association of Clinical Symptomatic Hypoglycemia With Cardiovascular Events and Total Mortality in Type 2 Diabetes

          OBJECTIVE Hypoglycemia is associated with serious health outcomes for patients treated for diabetes. However, the outcome of outpatients with type 2 diabetes who have experienced hypoglycemia episodes is largely unknown. RESEARCH DESIGN AND METHODS The study population, derived from the National Health Insurance Research Database released by the Taiwan National Health Research Institutes during 1998–2009, comprised 77,611 patients with newly diagnosed type 2 diabetes. We designed a prospective study consisting of randomly selected hypoglycemic type 2 diabetic patients and matched type 2 diabetic patients without hypoglycemia. We investigated the relationships of hypoglycemia with total mortality and cardiovascular events, including stroke, coronary heart disease, cardiovascular diseases, and all-cause hospitalization. RESULTS There were 1,844 hypoglycemic events (500 inpatients and 1,344 outpatients) among the 77,611 patients. Both mild (outpatient) and severe (inpatient) hypoglycemia cases had a higher percentage of comorbidities, including hypertension, renal diseases, cancer, stroke, and heart disease. In multivariate Cox regression models, including diabetes treatment adjustment, diabetic patients with hypoglycemia had a significantly higher risk of cardiovascular events during clinical treatment periods. After constructing a model adjusted with propensity scores, mild and severe hypoglycemia still demonstrated higher hazard ratios (HRs) for cardiovascular diseases (HR 2.09 [95% CI 1.63–2.67]), all-cause hospitalization (2.51 [2.00–3.16]), and total mortality (2.48 [1.41–4.38]). CONCLUSIONS Symptomatic hypoglycemia, whether clinically mild or severe, is associated with an increased risk of cardiovascular events, all-cause hospitalization, and all-cause mortality. More attention may be needed for diabetic patients with hypoglycemic episodes.
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            Glycemic variability: the third component of the dysglycemia in diabetes. Is it important? How to measure it?

            THE dysglycemia of diabetes includes two components: (1) sustained chronic hyperglycemia that exerts its effects through both excessive protein glycation and activation of oxidative stress and (2) acute glucose fluctuations. Glycemic variability seems to have more deleterious effects than sustained hyperglycemia in the development of diabetic complications as both upward (postprandial glucose increments) and downward (interprandial glucose decrements) changes activate the oxidative stress. For instance, the urinary excretion rate of 8-iso-PGF2alpha, a reliable marker of oxidative stress, was found to be strongly, positively correlated (r = 0.86, p < .001) with glycemic variability assessed from the mean amplitude of glycemic excursions (MAGE) as estimated by continuous glucose monitoring systems (CGMS). These observations therefore raise the question of whether we have the appropriate tools for assessing glycemic variability in clinical practice. From a statistical point of view, the standard deviation (SD) around the mean glucose value appears as the "gold standard." By contrast, the MAGE index is probably more appropriate for selecting the major glucose swings that are calculated as the arithmetic mean of differences between consecutive peaks and nadirs, provided that the differences be greater than the SD around the mean values. Furthermore, calculating the MAGE index requires continuous glucose monitoring, which has the advantage to detect all isolated upward and downward acute glucose fluctuations. In conclusion, the increasing use of CGMSs will certainly promote better assessment and management of glycemic variability.
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              Postprandial hyperglycemia on vascular endothelial function: mechanisms and consequences.

              Vascular endothelial dysfunction precedes atherosclerosis and contributes to cardiovascular disease (CVD), which accounts for one-third of all deaths in the United States. Chronic hyperglycemia, such as that associated with diabetes, is well known to impair vascular function. However, recent evidence demonstrates that acute or postprandial hyperglycemia (PPH) not only exacerbates vascular endothelial dysfunction in individuals with chronic hyperglycemia but also transiently impairs vascular function in healthy individuals. Postprandial hyperglycemia has been shown to better predict future CVD mortality compared with fasting glucose in both diabetic and normoglycemic individuals. Compelling evidence exists suggesting that PPH-mediated insults to the vascular endothelium contribute to CVD, especially in pathophysiologic conditions whereby vascular recovery is compromised. Although the mechanisms by which PPH induces vascular dysfunction is not fully understood, oxidative stress-mediated disruptions in nitric oxide homeostasis are implicated as key events leading to vascular dysfunction associated with PPH. This review aims to highlight the findings of clinical studies using functional indices of vascular function to demonstrate that PPH impairs vascular function. We will also discuss the evidence showing the central involvement of oxidative stress in dysregulating nitric oxide homeostasis and contributing to PPH-mediated vascular endothelial dysfunction. Lastly, this review will identify areas of knowledge that remain limited and will provide recommendations for future investigation to more fully define PPH as an important risk factor for CVD.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                0253-5068
                1421-9735
                2014
                November 2014
                07 October 2014
                : 38
                : 1
                : 68-73
                Affiliations
                aSCU Nephrology, Dialysis and Transplantation, bSCDU Endocrinology, Diabetology and Metabolism, Azienda Ospedaliera Città della Salute e della Scienza di Torino, Presidio ‘Molinette', Torino, Italy
                Author notes
                *Massimo Gai, MD, Azienda Ospedaliera S. Giovanni Battista di Torino, S.C.U. Nefrologia, Dialisi e Trapianto, Corso Bramante 88, IT-10126 Torino (Italy), E-Mail massimogai@gmail.com
                Article
                362863 Blood Purif 2014;38:68-73
                10.1159/000362863
                25300368
                © 2014 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.

                Page count
                Figures: 2, Tables: 1, Pages: 6
                Categories
                Original Paper

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