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      Randomized Trial of Methylcobalamin and Folate Effects on Homocysteine in Hemodialysis Patients

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          Abstract

          Background: There are no data available on the effects of intravenous (i.v.) methylcobalamin (Me-Cbl), the coenzymatically active form of vitamin B<sub>12</sub> that acts as a cofactor for methionine synthase in the conversion of total homocysteine (tHcy) to methionine, with or without oral folic acid (FA) supplementation, on fasting tHcy levels in hemodialysis (HD) patients. Methods: We performed a prospective randomized trial in which 62 chronic HD patients without previous vitamin supplementation were divided into four groups. Group A received Me-Cbl 500 µg twice/week plus FA 10 mg/day; group B received FA 10 mg/day alone; group C received no vitamin supplementation, and group D was on Me-Cbl 500 µg twice/week alone. Fasting tHcy, vitamin B<sub>12</sub>, serum (s) FA and erythrocytic (e) FA were measured predialysis before and after 4 months of therapy. Results: Final tHcy levels were significantly lower in group A (10.2 ± 3.1 µmol/l) compared to groups C (27.3 ± 9.7 µmol/l, p < 0.001) and group D (24.3 ± 11.8 µmol/l, p < 0.001) and similar to group B (11.2 ± 1.9 µmol/l, p = n.s.). Mean tHcy levels showed a significant decrease in group A from 22.5 ± 15.6 to 10.2 ± 3.1 µmol/l (p = 0.003) and in group B from 19.9 ± 4.0 to 11.2 ± 1.9 µmol/l (p = 0.012), while no significant changes were observed in groups C (25.9 ± 9.3 vs. 27.3 ± 9.7 µmol/l, p = n.s.) and D (26.6 ± 14.3 vs. 24.3 ± 11.8 µmol/l, p = n.s.). Conclusion: Oral FA (10 mg/day) supplementation appears to be an effective approach to normalize plasma tHcy in chronic HD patients; the addition of i.v. Me-Cbl (500 µg twice/week) to this regimen showed no benefit. Separately, FA corrected hyperhomocysteinemia (HtHcy), while Me-Cbl showed no change.

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          Most cited references 4

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          Hyperhomocysteinemia as a risk factor for deep-vein thrombosis.

          Previous studies have suggested that hyperhomocysteinemia may be a risk factor for venous thrombosis. To assess the risk of venous thrombosis associated with hyperhomocysteinemia, we studied plasma homocysteine levels in patients with a first episode of deep-vein thrombosis and in normal control subjects. We measured plasma homocysteine levels in 269 patients with a first, objectively diagnosed episode of deep-vein thrombosis and in 269 healthy controls matched to the patients according to age and sex. Hyperhomocysteinemia was defined as a plasma homocysteine level above the 95th percentile in the control group (18.5 micromol per liter). Of the 269 patients, 28 (10 percent) had plasma homocysteine levels above the 95th percentile for the controls, as compared with 13 of the controls (matched odds ratio, 2.5; 95 percent confidence interval, 1.2 to 5.2). The association between elevated homocysteine levels and venous thrombosis was stronger among women than among men and increased with age. The exclusion of subjects with other established risk factors for thrombosis (e.g., a deficiency of protein C, protein S, or antithrombin; resistance to activated protein C; pregnancy or recent childbirth; or oral-contraceptive use) did not materially affect the risk estimates. High plasma homocysteine levels are a risk factor for deep-vein thrombosis in the general population.
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            Homocyst(e)ine and coronary artery disease. Clinical evidence and genetic and metabolic background.

            Many studies have demonstrated a strong association between elevated plasma total homocyst(e)ine levels and vascular diseases. Consequently, hyperhomocyst(e)inemia is now generally accepted as an independent risk factor for coronary artery disease. We critically reviewed the results of 35 human studies in which the levels of plasma total homocysteine were measured in patients with atherosclerotic diseases (n = 4338) and in controls (n = 22,593). Total homocysteine levels were consistently higher in patients than in controls. The average of this increment among 23 case-control studies was 26%. New insights into the biochemical pathways of total homocysteine metabolism, the factors that influence total homocysteine levels, genetic contributions to hyperhomocyst(e)inemia, the pathogenesis of homocyst(e)ine-induced vascular damage, and current recommendations for treatment of hyperhomocyst(e)inemia were also reviewed. Various lines of evidence now link hyperhomocyst(e)inemia with vascular diseases. Although there are no data from double-blind, placebo-controlled clinical trials of treatment for hyperhomocyst(e)inemia, the strong epidemiologic and experimental evidence argues for treatment of hyperhomocyst(e)inemia; in fact, its treatment with low doses of vitamins is thought to be safe and is inexpensive.
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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

              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 t /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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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2002
                May 2002
                02 May 2002
                : 91
                : 1
                : 58-63
                Affiliations
                Departments of aNephrology and bNuclear Medicine, Hospital Británico de Buenos Aires, Argentina
                Article
                57605 Nephron 2002;91:58–63
                10.1159/000057605
                12021520
                © 2002 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: 1, Tables: 3, References: 39, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/57605
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