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Vitamin B12 decreases, but does not normalize, homocysteine and methylmalonic acid in end-stage renal disease: a link with glycine metabolism and possible explanation of hyperhomocysteinemia in end-stage renal disease.
Metabolism 2003; 52(2):168-72M

Abstract

The genetic and environmental factors influencing catabolism of homocysteine in end-stage renal disease (ESRD) patients remain poorly understood. This study investigated how genetic and nutritional influences affect the response to high-dose vitamin B(12) and folate treatment in ESRD patients with hyperhomocysteinemia. We studied 81 hemodialysis patients with hyperhomocysteinemia (> 16 micromol/L) on varied doses of a multivitamin containing 1 mg of folic acid per day. After screening blood work, all patients were switched to daily multivitamin therapy including 1 mg of folic acid for 4 weeks. Vitamin B(12), 1 mg/d, was added for an additional 4 weeks. Patients were then randomized to receive folic acid or placebo. The influence of the 3 methylenetetrahydrofolate reductase (MTHFR) 677 C-->T genotypes on the efficacy of vitamin therapy was assessed. In addition, we investigated how the metabolic complications of ESRD, including the relationship between methylmalonic acid (MMA) and circulating glycine, may contribute to hyperhomocysteinemia. There was no significant difference in total homocysteine (tHcy) levels between the MTHFR 677 C-->T genotypes during the screening phase of the trial. Treatment with a daily multivitamin containing 1 mg folate significantly lowered tHcy levels in all patients by 19.2%. Further supplementation with 1 mg vitamin B(12) resulted in greater tHcy reduction among subjects with the MTHFR 677 T/T genotype (P<.01, T/T v C/C or C/T) while lowering MMA equally in all MTHFR genotypes. There was a significant positive correlation between plasma glycine levels and MMA (P <.05). High-dose vitamin therapy significantly lowers, but does not normalize, MMA and tHcy levels. The MTHFR genotype, while influencing homocysteine levels, was not responsible for the majority of the elevation in plasma tHcy.

Authors+Show Affiliations

Division of Nephrology, Department of Medicine, University of Calgary, Calgary, Alberta, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12601627

Citation

Hyndman, Matthew Eric, et al. "Vitamin B12 Decreases, but Does Not Normalize, Homocysteine and Methylmalonic Acid in End-stage Renal Disease: a Link With Glycine Metabolism and Possible Explanation of Hyperhomocysteinemia in End-stage Renal Disease." Metabolism: Clinical and Experimental, vol. 52, no. 2, 2003, pp. 168-72.
Hyndman ME, Manns BJ, Snyder FF, et al. Vitamin B12 decreases, but does not normalize, homocysteine and methylmalonic acid in end-stage renal disease: a link with glycine metabolism and possible explanation of hyperhomocysteinemia in end-stage renal disease. Metab Clin Exp. 2003;52(2):168-72.
Hyndman, M. E., Manns, B. J., Snyder, F. F., Bridge, P. J., Scott-Douglas, N. W., Fung, E., & Parsons, H. G. (2003). Vitamin B12 decreases, but does not normalize, homocysteine and methylmalonic acid in end-stage renal disease: a link with glycine metabolism and possible explanation of hyperhomocysteinemia in end-stage renal disease. Metabolism: Clinical and Experimental, 52(2), pp. 168-72.
Hyndman ME, et al. Vitamin B12 Decreases, but Does Not Normalize, Homocysteine and Methylmalonic Acid in End-stage Renal Disease: a Link With Glycine Metabolism and Possible Explanation of Hyperhomocysteinemia in End-stage Renal Disease. Metab Clin Exp. 2003;52(2):168-72. PubMed PMID: 12601627.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vitamin B12 decreases, but does not normalize, homocysteine and methylmalonic acid in end-stage renal disease: a link with glycine metabolism and possible explanation of hyperhomocysteinemia in end-stage renal disease. AU - Hyndman,Matthew Eric, AU - Manns,Braden J, AU - Snyder,Floyd F, AU - Bridge,Peter J, AU - Scott-Douglas,Nairne W, AU - Fung,Ernest, AU - Parsons,Howard G, PY - 2003/2/26/pubmed PY - 2003/3/15/medline PY - 2003/2/26/entrez SP - 168 EP - 72 JF - Metabolism: clinical and experimental JO - Metab. Clin. Exp. VL - 52 IS - 2 N2 - The genetic and environmental factors influencing catabolism of homocysteine in end-stage renal disease (ESRD) patients remain poorly understood. This study investigated how genetic and nutritional influences affect the response to high-dose vitamin B(12) and folate treatment in ESRD patients with hyperhomocysteinemia. We studied 81 hemodialysis patients with hyperhomocysteinemia (> 16 micromol/L) on varied doses of a multivitamin containing 1 mg of folic acid per day. After screening blood work, all patients were switched to daily multivitamin therapy including 1 mg of folic acid for 4 weeks. Vitamin B(12), 1 mg/d, was added for an additional 4 weeks. Patients were then randomized to receive folic acid or placebo. The influence of the 3 methylenetetrahydrofolate reductase (MTHFR) 677 C-->T genotypes on the efficacy of vitamin therapy was assessed. In addition, we investigated how the metabolic complications of ESRD, including the relationship between methylmalonic acid (MMA) and circulating glycine, may contribute to hyperhomocysteinemia. There was no significant difference in total homocysteine (tHcy) levels between the MTHFR 677 C-->T genotypes during the screening phase of the trial. Treatment with a daily multivitamin containing 1 mg folate significantly lowered tHcy levels in all patients by 19.2%. Further supplementation with 1 mg vitamin B(12) resulted in greater tHcy reduction among subjects with the MTHFR 677 T/T genotype (P<.01, T/T v C/C or C/T) while lowering MMA equally in all MTHFR genotypes. There was a significant positive correlation between plasma glycine levels and MMA (P <.05). High-dose vitamin therapy significantly lowers, but does not normalize, MMA and tHcy levels. The MTHFR genotype, while influencing homocysteine levels, was not responsible for the majority of the elevation in plasma tHcy. SN - 0026-0495 UR - https://www.unboundmedicine.com/medline/citation/12601627/Vitamin_B12_decreases_but_does_not_normalize_homocysteine_and_methylmalonic_acid_in_end_stage_renal_disease:_a_link_with_glycine_metabolism_and_possible_explanation_of_hyperhomocysteinemia_in_end_stage_renal_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0026049502052381 DB - PRIME DP - Unbound Medicine ER -