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PubMed2003

[Folic acid and prevention of anomalies of foetal neural tube closing in women treated for epilepsy].

Anomalies of neural tube closing are serious malformations which are encountered most often in babies of epileptic women treated with anti-epileptic drugs during pregnancy. Dietary supplementation of folic acid has been suggested as a preventive measure in these cases, based on the long suspected association between folic acid deficiency and congenital malformations. Folic acid deficiency usually results from insufficient dietary intake, or increased requirements during pregnancy. Moreover, certain anti-epileptic drugs can reduce the availability of folic acid. In secondary prevention, the protective effect of folic acid has been clearly demonstrated, whilst epidemiological data suggest that such treatment is also useful in primary prevention. With respect to women with epilepsy, there is a clear consensus as to the interest of dietary supplementation with folic acid before conception and during the first three months of pregnancy (the period of organogenesis), particularly given the fact that side-effects are extremely rare. Apart from recurrence prevention, where a dose of 4mg/day is recommended, no standard dosing guidelines exist. We would suggest that this same dose be used for epileptic patients in pregnancy, particularly if they are treated with barbamazepine or valproic acid.

Adult↗
PubMed2000

Clinical and laboratory features and sequelae of deficiency of folic acid (folate) and vitamin B12 (cobalamin) in pregnancy and gynecology.

Classically, deficiency of folic acid (folate) or vitamin B12 (cobalamin) was recognized by the presence of a macrocytic anemia resulting from megaloblastic changes in the bone marrow. A markedly changing paradigm has identified both new mechanisms for altered folate and cobalamin status and new sequelae and clinical interrelationships that include altered mechanisms of absorption, a changing pattern of neurologic deficits, an increased risk of vascular occlusive lesions, and an important relationship with the mechanisms of neoplastic transformation. Several of these newer characterizations relate to issues of neoplasia in the nonpregnant woman and to issues in pregnancy, such as the potential for developmental abnormalities of the fetal nervous system.

Anemia, Megaloblastic↗
PubMed1997

The role of folic acid in deficiency states and prevention of disease.

Folic acid, a water-soluble vitamin, has been used since the 1940s to treat some cases of macrocytic anemia without neurologic disease. Folate deficiency is best diagnosed with red blood cell folate levels along with macrocytosis and/or megaloblastic anemia. In addition to reversing overt deficiency, the vitamin may reduce the incidence of neural tube defects by 45% in women who receive 400 micrograms per day. It is recommended that all women of childbearing age take 400 micrograms of folate per day. Elevations in homocysteine levels, a metabolite intimately associated with folate, are also being found with increasing regularity in those with cardiovascular diseases. Homocysteine levels are reduced by folic acid administration. Therefore, there is some biologic plausibility, but not currently direct proof, for the assumption that folate supplements may prevent heart disease, stroke, and peripheral arterial disease. Controlled trials should take place before widespread food supplementation with folate is carried out on a large scale because of the possibility of outbreaks of permanent B12-related neurologic damage in those with undiagnosed pernicious anemia. However, if a patient has a premature cardiovascular event and has minimal risk factors, ordering a test to determine homocysteine level may be advisable, and if elevated, treating with folic acid supplement as long as B12 deficiency does not coexist.

Anemia, Macrocytic↗
PubMed1987

Intestinal absorption, liver uptake, and excretion of 3H-folic acid in folic acid-deficient, alcohol-consuming nonhuman primates.

Nonhuman primates fed folic acid-deficient diets +/- 30% kcal ethanol were used to determine alcohol effects on megaloblastic anemia development and folate bioavailability. Lower hemoglobin (Hb) and red blood cell (RBC) counts and higher mean corpuscular volume (MCV) occurred after 13 wk in alcohol-fed monkeys, later in controls. Plasma, RBC, and liver folate declined and urinary formiminoglutamic acid (FIGLU) was elevated in both groups with FIGLU increasing more among alcohol-fed monkeys at 38 wk. After 40 wk, the bioavailability of oral 3H-folic acid was investigated and showed increased fecal and reduced urinary tritium excretion in alcohol-fed monkeys compared with controls while plasma uptake and liver and whole body tritium retention were similar in both groups. These observations demonstrate that chronic alcohol consumption impairs folate coenzymes, accelerates appearance of hematologic indices of megaloblastic anemia, and causes possible malabsorption of enterohepatically circulated folates in folate deficiency even when other essential nutrients are provided.

Alcohol Drinking↗
PubMed1976

[Folic acid determination in the serum and erythrocytes by means of a competitive binding method with 125 iodine labeling].

Folic acid concentration in serum and erythrocytes was measured by radio assay according to the principle of competitive binding to proteins with 125I as marker. The method yielded a linear regression with readily reproducible results. The mean value in controls was 7.05 -+/ 3.4 ng/ml in serum and 386.8 -+/ 215.1 ng/ml in erythrocytes. In chronic alcoholics the respective values were significantly lower: 4.79 -+/ 2.02 ng/ml for serum and 344.4 -+/ 198.9 ng/ml for erythrocytes. The clinical importance of folic acid estimations arises from the general frequency of folic aicd deficits. Latent folic acid deficiency is associated with lowered folic acid concentrations in serum and normal values in red cells. In manifest folic acid deficiency both concentrations are decreased.

Alcoholism↗
PubMedDate not supplied

[Iron deficiency anemia in childhood. A case with associated deficiency of folic acid (author's transl)].

The case of a six year and ten months old girl with an iron deficiency anemia of long duration is reported. The lack of iron was associated with folic acid deficiency, which disguished the hematologic pattern, presenting a normocromic and aniso-poiquilocytic anemia. Long duration of iron deficiency allowed for evaluation of the iron deficiency effects on weight and height growth which were diminished as well as on the functioning and morphology of the gastrointestinal system, showing malabsorption syndrome which improve with iron supply.

Anemia, Hypochromic↗
PubMed1979

Polyglutamate forms of folate in liver of folic acid-deficient rats.

In view of role played by pteroylpolyglutamates as actual folate coenzymes in single-carbon unit metabolism, the effect of folic acid deficiency on the distribution of these compounds in rat liver has been studied. In deficient rats the liver levels of pteroylpolyglutamates and in particular of those containing a higher number of glutamyl residues are more decreased as compared with monoglutamates. In fact penta- and other higher polyglutamates: mono-, di- and tri-glutamates ratio is lower in deficient rats than that in control rats. The decreased amount of these coenzymic forms observed in this condition may be considered as the consequence of the severe alterations of process which adds glutamate moieties to monoglutamate forms.

Animals↗
PubMed2001

Methylenetetrahydrofolate reductase C677T polymorphism does not alter folic acid deficiency-induced uracil incorporation into primary human lymphocyte DNA in vitro.

Methylenetetrahydrofolate reductase (MTHFR) is an enzyme which converts 5,10-methylene tetrahydrofolate (5,10-MnTHF) to 5-methyl tetrahydrofolate. A common C to T transition (C677T) in the MTHFR gene is reported to reduce the risk for colorectal cancer and acute lymphocytic leukemia in homozygotes (TTs). It is hypothesized that because TTs have reduced MTHFR activity, more 5,10-MnTHF is available to provide methyl groups for the conversion of uracil to thymidine. Folic acid deficiency causes the intracellular accumulation of dUMP and the subsequent incorporation of uracil into DNA. The removal of uracil from DNA may result in double-stranded DNA breaks, the accumulation of which is a putative risk factor for cancer. We tested whether human lymphocytes taken from TTs (n = 10) were more able to resist uracil incorporation into DNA than controls (n = 14 CCs and 6 CTs) when cultured in medium containing 12-120 nM folic acid for 9 days. DNA uracil content of these lymphocytes was measured by CG-MS. TTs and controls showed a dose-dependent increase in DNA uracil content during folic acid deficiency (P < 0.0001, R2 = 0.23 for TTs and P < 0.0001, R2 = 0.19 for controls). DNA uracil content was not different between the two groups at any of the folic acid concentrations (two-way ANOVA: media [folic acid], P < 0.0001; genotype, P = 0.4). The results show that, in this in vitro system, the MTHFR C677T polymorphism does not affect the cell's ability to resist uracil incorporation into DNA. Chromosome breakage, as measured by micronuclei, was also shown to correlate with folic acid concentration in a preliminary experiment (P < 0.0001). Although the results appear not to support the hypothesis that a reduced risk for certain cancers in TTs is due to diversion of folic acid to thymidine synthesis, differences between the in vivo and in vitro situation make this conclusion not definitive.

DNA↗
PubMed2004

[Relationship of plasma homocysteine and folic acid levels and 5,10-methylenetetrahydrofolate reductase gene mutation with venous thromboembolism].

OBJECTIVE: To investigate the association between concentrations of plasma homocysteine and folic acid, 5,10-methylenetetrahydrofolate reductase (MTHFR) C667T mutation and venous thromboembolism (VTE) and to analyze the effect of MTHFR C667T mutation on concentrations of plasma homocysteine and folic acid. METHODS: In 58 patients with VTE and 58 sex and age matched controls, epidemiological risk factors were surveyed. The concentration of plasma homocysteine was measured by high performance liquid chromatography, and the concentration of plasma folic acid was measured by radioimmunoassay. MTHFR C667T genotype was measured by PCR-RFLP. RESULTS: The concentrations of plasma homocysteine and folic acid showed significant difference between the case group and the control group (OR = 1.5, 95% CI: 1.216 - 2.213 and OR = 0.396, 95% CI: 0.149 - 0.709, respectively). There was no significant difference in the frequency of mutant alleles in site 667 of MTHFR gene between the cases and the controls (P > 0.05). The concentration of plasma folic acid was associated with the concentration of plasma homocysteine (multiple correlation coefficient = -2.061, P < 0.05). The MTHFR C667T polymorphism was associated with the concentration of plasma folic acid but not with the concentration of plasma homocysteine in both the case group and the control group. The multiple correlation coefficient between the MTHFR C667T polymorphism and the concentration of plasma folic acid is 0.5856 (P < 0.01). CONCLUSIONS: The results of our study demonstrate that hyperhomocysteinemia and folic acid deficiency are independent risk factors for VTE. Folic acid deficiency is a cause of hyperhomocystinemia while the MTHFR C667T mutation is one of the possible genetic factors causing folic acid deficiency in this Chinese population.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed1986

Enhanced sensitivity of lymphoblastoid cells from individuals carrying the mutation for the fragile X syndrome to the clastogenic effects of FUdR.

Individuals known to carry the mutation for the fragile X syndrome can sometimes be identified cytogenetically by the presence of a fragile site on the X chromosome at q27.3. The frequency of cells bearing this fragile site is known to be enhanced by culturing the cells in folic acid deficient medium and/or by introducing folic acid metabolism inhibitors such as FUdR. In this study FUdR induction of chromosomal aberrations other than the fragile X was investigated. Lymphoblastoid cells from an obligate carrier, a mentally retarded male and a control were cultured in folic acid deficient medium in the presence of FUdR and harvested at various times after culture initiation. The frequency of chromosome and chromatid breaks was found to be higher in cells from the individuals carrying the mutation for the fragile X syndrome. The frequency of micronuclei, an indirect index of chromosome breakage, was also more elevated in cells from these individuals than in cells from the control. These findings are of potential importance to carrier detection of this common genetic disorder.

Cell Nucleus↗