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      Effect of Usual Doses of Folate Supplementation on Elevated Plasma Homocyst(e)ine in Hemodialysis Patients: No Difference between 1 and 5 mg Daily

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          Abstract

          Hyperhomocyst(e)inemia is a probable contributor to the excess atherosclerosis of patients with chronic renal failure on dialysis. Although treatment with folate 2 mg daily is usually effective in normalizing plasma homocyst(e)ine (H(e)) in patients with normal renal function, higher doses of folate or other approaches to treatment may be necessary in renal failure. There is no agreement among dialysis units regarding the ‘correct’ dose of folate supplementation; routine doses range from 1 to 5 mg daily. To determine whether one of these doses is more effective, we compared H(e) in 55 hemodialysis taking 1 mg folate versus 73 patients taking 5 mg folate daily at two dialysis units. In the group as a whole, mean H(e) was 28.23 ± 17.49, significantly higher than in a group of 290 volunteers with normal renal function 12.31 ± 6.17 (p = 0.0001). H(e) levels were 28.93 ± 16.79 μmol/l on 5 mg folate and 27.31 ± 18.49 on 1 mg; p = 0.61. There was no significant relationship between adequacy of dialysis (K<sub>t</sub>/V) and H(e). In a small group of peritoneal dialysis patients, H(e) was significantly lower at 18.8 ± 7.89 (p = 0.026), but further study is required in a larger sample to confirm that observation. It appears that routine doses of folate in use in dialysis units are not sufficient to reduce H(e) to levels associated with average cardiovascular risk; new approaches to treatment of hyperhomocyst(e)inemia in dialysis patients are required.

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          Plasma homocysteine levels and mortality in patients with coronary artery disease.

          Elevated plasma homocysteine levels are a risk factor for coronary heart disease, but the prognostic value of homocysteine levels in patients with established coronary artery disease has not been defined. We prospectively investigated the relation between plasma total homocysteine levels and mortality among 587 patients with angiographically confirmed coronary artery disease. At the time of angiography in 1991 or 1992, risk factors for coronary disease, including homocysteine levels, were evaluated. The majority of the patients subsequently underwent coronary-artery bypass grafting (318 patients) or percutaneous transluminal coronary angioplasty (120 patients); the remaining 149 were treated medically. After a median follow-up of 4.6 years, 64 patients (10.9 percent) had died. We found a strong, graded relation between plasma homocysteine levels and overall mortality. After four years, 3.8 percent of patients with homocysteine levels below 9 micromol per liter had died, as compared with 24.7 percent of those with homocysteine levels of 15 micromol per liter or higher. Homocysteine levels were only weakly related to the extent of coronary artery disease but were strongly related to the history with respect to myocardial infarction, the left ventricular ejection fraction, and the serum creatinine level. The relation of homocysteine levels to mortality remained strong after adjustment for these and other potential confounders. In an analysis in which the patients with homocysteine levels below 9 micromol per liter were used as the reference group, the mortality ratios were 1.9 for patients with homocysteine levels of 9.0 to 14.9 micromol per liter, 2.8 for those with levels of 15.0 to 19.9 micromol per liter, and 4.5 for those with levels of 20.0 micromol per liter or higher (P for trend=0.02). When death due to cardiovascular disease (which occurred in 50 patients) was used as the end point in the analysis, the relation between homocysteine levels and mortality was slightly strengthened. Plasma total homocysteine levels are a strong predictor of mortality in patients with angiographically confirmed coronary artery disease.
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            Insulin-dependent diabetes mellitus in Sardinian-heritage children living in Lombardy.

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              Clinical significance of pharmacological modulation of homocysteine metabolism.

              The metabolic fate of homocysteine is linked to vitamin B12, reduced folates, vitamin B6 and sulfur amino acids. Clinical and experimental data suggest that elevated plasma homocysteine is an independent risk factor for premature vascular disease. This is particularly significant because plasma homocysteine levels are altered in several diseases, including folate and vitamin B12 deficiencies, and because many commonly used drugs have now been shown to interfere with homocysteine metabolism. In summarizing the data, Helga Refsum and Per Ueland highlight the clinical implications for these metabolic changes.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                1999
                June 1999
                18 June 1999
                : 19
                : 3
                : 405-410
                Affiliations
                Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute, London, Ont., Canada
                Article
                13486 Am J Nephrol 1999;19:405–410
                10.1159/000013486
                10393379
                © 1999 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: 2, References: 49, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/13486
                Categories
                Clinical Study

                Cardiovascular Medicine, Nephrology

                Homocysteine, Atherosclerosis, Dialysis, Homocyst(e)ine, Renal failure

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