Homocysteinemia due to folate deficiency

Kang, Seok Seon; Wong, Paul; Norušis, Marija J.

doi:10.1016/0026-0495(87)90043-6

Cited by 390 publications

(159 citation statements)

References 22 publications

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“…To compensate for the lack of red-cell specimens in our study, we measured serum homocysteine, which has been proposed as a sensitive indicator of functional folate deficiency that is distinguishable from low serum folate concentrations following shortterm decreases in dietary intake (Kang et al, 1987;Stabler et al, 1988;Ubbink et al, 1993;Jacob et al, 1994;O'Keefe et al, 1995). Our data show that the variability of serum homocysteine in the population was much narrower than that of folate, suggesting that homocysteine levels are more tightly regulated by metabolism.…”

Section: Discussionmentioning

confidence: 99%

Serum folate, homocysteine and colorectal cancer risk in women: a nested case–control study

et al. 1999

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Summary Accumulating evidence suggests that folate, which is plentiful in vegetables and fruits, may be protective against colorectal cancer. The authors have studied the relationship of baseline levels of serum folate and homocysteine to the subsequent risk of colorectal cancer in a nested case-control study including 105 cases and 523 matched controls from the New York University Women's Health Study cohort. In univariate analyses, the cases had lower serum folate and higher serum homocysteine levels than controls. The difference was more significant for folate (P < 0.001) than for homocysteine (P = 0.04). After adjusting for potential confounders, the risk of colorectal cancer in the subjects in the highest quartile of serum folate was half that of those in the lowest quartile (odds ratio, OR = 0.52, 95% confidence interval, CI = 0.27-0.97, P-value for trend = 0.04). The OR for the highest quartile of homocysteine, relative to the lowest quartile, was 1.72 (95% CI = 0.83-3.65, P-value for trend = 0.09). In addition, the risk of colorectal cancer was almost twice as high in subjects with belowmedian serum folate and above-median total alcohol intake compared with those with above-median serum folate and below-median alcohol consumption (OR = 1.99, 95% CI = 0.92-4.29). The potentially protective effects of folate need to be confirmed in clinical trials.

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Section: Discussionmentioning

confidence: 99%

Serum folate, homocysteine and colorectal cancer risk in women: a nested case–control study

et al. 1999

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“…Several investigators have demonstrated that subjects who are homozygous for the TT polymorphism have an elevated tHcY only when plasma folate is low (Kang et al, 1987;Harmon et al, 1996;Christensen et al, 1997;Kluijtmans et al, 1997). Plasma folate levels in the group of patients with TT polymorphism were relatively low compared to folate levels in the CC group.…”

Section: Genotype Of the Patient And Homocysteine Levelsmentioning

confidence: 99%

Pharmacokinetic study on the utilisation of 5‐methyltetrahydrofolate and folic acid in patients with coronary artery disease

Willems

Boers²,

Blom³

et al. 2004

British J Pharmacology

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1 Methylenetetrahydrofolate reductase (MTHFR) is a regulating enzyme in folate-dependant homocysteine remethylation, because it catalyses the reduction of 5,10 methylenetetrahydrofolate to 5-methyltetrahydrofolate (5-MTHF). 2 Subjects homozygous for the 677C-T mutation in the MTHFR enzyme suffer from an increased cardiovascular risk. It can be speculated that the direct administration of 5-MTHF instead of folic acid can facilitate the remethylation of homocysteine in methionine. 5 All pharmacokinetic parameters demonstrate that the bioavailability of 5-MTHF is higher compared to folic acid. The peak concentration of both isomers following the administration of 6[R,S] 5-MTHF is almost seven times higher compared to folic acid, irrespective of the patient's genotype. However, at 1 week after the administration of a single dosage 6[R,S] 5-MTHF, we detected 6[R] 5-MTHF following the administration of folic acid, indicating storage of this isomer in the body. 6 Our results demonstrate that oral 5-MTHF has a different pharmacokinetic profile with a higher bioavailability compared to folic acid, irrespective of the patient's genotype. Detrimental effects of the storage of high levels of the non-natural isomer 6[R] 5-MTHF cannot be excluded.

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“…In a situation with deficiency of cobalamin, methylmalonyl-CoA is converted to methylmalonic acid (MMA) rather than to succinyl-CoA [9]. In addition, cobalamin is needed to convert homocysteine (Hcy) to methionine, which means that serum MMA and serum total Hcy (tHcy) increase if there is a deficiency of cobalamin [8,10,11]. Methyltetrahydrofolate is required for homocysteine remethylation to methionine, which means that if there is a deficiency of folate, homocysteine is accumulated in spite of availability of cobalamin [10±12].…”

Section: Introductionmentioning

confidence: 99%

Elevated serum levels of methylmalonic acid and homocysteine in elderly people. A population‐based intervention study

Björkegren

Svärdsudd²

1999

Journal of Internal Medicine

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Abstract. Bjo Èrkegren K, Sva Èrdsudd K (University Hospital Uppsala; Skutska Èr Primary Health Care Center, Skurska Èr, Sweden). Elevated serum levels of methylmalonic acid and homocysteine in elderly people. A population-based intervention study. J Intern Med; 246: 317±324.Objectives. There is uncertainty amongst clinicians about the definitions of cobalamin and folate deficiency and therefore about the indications for treatment. In this report we present the results of systematic cobalamin and folic acid treatment based upon serum cobalamin, total homocysteine (tHcy) and methylmalonic acid (MMA) analyses in a population-based sample. Subjects. A 20% random sample of persons 70 years or older in a defined geographical area were invited to a survey (n = 266). Sixty-nine persons who had serum cobalamin , 300 pmol L 21 and serum MMA $0.37 mmol L 21 or serum tHcy $15 mmol L 21 and who had no cobalamin or folic acid substitution were selected for treatment.Interventions. Initially all 69 patients were given cobalamin orally or intramuscularly. Those who remained high in tHcy were in addition given folic acid treatment. Main outcome measures. Serum cobalamin, serum MMA and serum tHcy. Results. After 6 months of cobalamin treatment, serum MMA became normal in 13 out of 15 persons. Mean serum tHcy decreased but was normalized in only 15 out of 56 persons. After 3 months of folic acid treatment added to those who still had an abnormal serum tHcy, serum tHcy had normalized in all but one person. Conclusions. Cobalamin treatment normalizes increased MMA values and combined cobalamin and folic acid treatment normalizes tHcy, suggesting a pretreatment deficiency of tissue cobalamin and folate in spite of normal serum cobalamin and folate values in the majority of cases.

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Homocysteinemia due to folate deficiency

Cited by 390 publications

References 22 publications

Serum folate, homocysteine and colorectal cancer risk in women: a nested case–control study

Serum folate, homocysteine and colorectal cancer risk in women: a nested case–control study

Pharmacokinetic study on the utilisation of 5‐methyltetrahydrofolate and folic acid in patients with coronary artery disease

Elevated serum levels of methylmalonic acid and homocysteine in elderly people. A population‐based intervention study

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