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Results for “FOLIC ACID DEFICIENCY”

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PubMed2000

[Importance of proper nutrition before and during pregnancy].

Maternal nutrition before and during pregnancy may influence the course of the pregnancy, foetal development and the child's health in its early and also adult life. Maternal underweight before pregnancy (BMI<19.8 kg/m2) and low pregnancy weight gain may increase the risk of low infant birth weight. There is accumulating evidence that persons who were born with low body mass are more susceptible to insulin-independent diabetes, arterial hypertension, hypercholesterolemia and ischaemic heart disease, than those whose birth weight was normal. Recommendations concerning pregnancy weight gain are discussed. Folic acid deficiency during the periconceptional period may cause neural tube defects in the offspring. Full cover of folic acid requirement is necessary. This may be achieved only by diet supplementation or food fortification. Recommendations concerning folic acid supplementation during the periconceptional period are discussed. Folic acid deficiency during pregnancy may also contribute to the preterm delivery and low infant birth weight. The importance of antioxidant vitamins in the prevention of pregnancy hypertension and the consequences of vitamin A overdosage are discussed. Protective calcium activity against pregnancy hypertension and preterm delivery, the importance of maternal iron supplementation in the prevention of low infant birth weight, and also the problem of maternal zinc deficiency which increases the risk of the low infant birth weight, preterm delivery, malformations, post-term delivery and pregnancy hypertension were discussed as well as the consequences of deficiency of the iodine and n-3 fatty acids in the diet.

Adult↗
PubMed1998

[Hemolysis and schizocytosis, malabsorption and the "folate trap": unusual semiological peculiarities associated with vitamin B12 deficiency].

INTRODUCTION: Hemolysis and red cell fragmentation accompanying vitamin B12 deficiency may misdirect the diagnosis. Signs of malabsorption and abnormalities related to folic acid metabolism characterized by discrepancies between folic acid normal serum levels and erythrocytic folic acid levels may also exist. EXEGESIS: We report the occurrence of hemolysis and red cell fragmentation mimicking microangiopathic hemolytic anemia, malabsorption and folic acid deficiency in the course of vitamin B12 deficiency. Appropriate replacement therapy corrected all abnormalities. CONCLUSION: An association between hemolysis, malabsorption and folic acid deficiency should lead physicians to search for signs of vitamin B12 deficiency.

Adult↗
PubMed2006

Four-way calibration applied to the simultaneous determination of folic acid and methotrexate in urine samples.

First-, second- and third-order calibration methods were investigated for the simultaneous determination of folic acid and methotrexate. The interest in the determination of these compounds is related to the fact that methotrexate inhibits the body's absorption of folic acid and prolonged treatment with methotrexate may lead to folic acid deficiency, and to the use of folic acid to cope with toxic side effects of methotrexate. Both analytes were converted into highly fluorescent compounds by oxidation with potassium permanganate, and the kinetics of the reaction was continuously monitored by recording the kinetics curves of fluorescence emission, the evolution with time of the emission spectra and the excitation-emission matrices (EEMs) of the samples at different reaction times. Direct determination of mixtures of both drugs in urine was accomplished on the basis of the evolution of the kinetics of EEMs by fluorescence measurements and four-way parallel-factor analysis (PARAFAC) or multiway partial least squares (N-PLS) chemometric calibration. The core consistency diagnostic (CORCONDIA) was employed to determine the correct number of factors in PARAFAC and the procedure converged to a choice of three factors, attributed to folic acid, methotrexate and to the sum of fluorescent species present in the urine.

Calibration↗
PubMed1992

Localized deficiencies of folic acid in aerodigestive tissues.

The notion that requirements for folic acid may be higher in some tissues than others, resulting in localized deficiencies in spite of blood levels in the normal range was first suggested by the observation of megaloblastic changes in the cervical epithelium that responded to folate supplementation. Theoretically, such deficiencies may arise from elevated folate turnover in response to rapid tissue proliferation or repair; inactivation or alteration of its function by external agents such as tobacco, alcohol, or drugs; or altered metabolism or tissue uptake caused by an inborn error. Marginal dietary intake could aggravate these effects on cells at risk. Evidence for the possible existence of localized folate deficiencies in the aerodigestive tract includes lower circulating folate levels in smokers as compared with nonsmokers; yet lower circulating levels in smokers with bronchial metaplasia; lower folate levels in scrapings of the buccal mucosa of smokers than non-smokers; apparent improvement in bronchial atypical metaplasia in smokers supplemented with folic acid; lower erythrocyte folate levels and higher prevalence of cellular features compatible with folate deficiency in geographic areas and individuals in South Africa at high risk for esophageal cancer; and a trend toward a lower prevalence of colonic dysplasia in ulcerative colitis patients who use folic acid supplements. These observations, as well as animal and in vitro studies, also suggest that folate deficiency may be co-carcinogenic. Further research in this area will be aided by the development of animal models of localized folate deficiency and of methodologies capable of measuring folate levels in minute quantities of tissues and exfoliated cells.

Colitis, Ulcerative↗
PubMed1965

PRACTICAL EVALUATION OF THE FIGLU TEST IN PREGNANCY WITH SPECIAL REFERENCE TO THE WHITE CELL CHANGES.

Using slight modifications to the method of Kohn, Mollin, and Rosenbach (1961) the histidine loading test has been carried out in 210 pregnant women. Seventy per cent. of the cases showed complete haematological correlation and this rose to 87% when marrow puncture was performed. False positive results occurred in some cases showing active erythropoiesis in response to iron therapy. False negative results were noted when other complications in addition to anaemia were present, and it was felt that these might interfere with the metabolism of histidine. In some cases the histidine test anticipated the haematological change.Seventy-seven per cent. of women with multiple pregnancies showed evidence of folic acid deficiency. Only in a few cases was the test positive before the 25th week of pregnancy. These were either cases of multiple pregnancy, haemolytic anaemia, malabsorption syndrome, or women with a recent history of megaloblastic anaemia of pregnancy. The test appears to confirm the significance of white cell changes as an indication of folic acid deficiency in pregnancy.

Anemia, Macrocytic↗
PubMed1964

ESTIMATION OF SERUM L. CASEI ACTIVITY.

Measurement of the serum Lactobacillus casei (;folic-acid') activity is widely used as an index of folic-acid deficiency. Present methods of assay result in recovery of about half the active material in normal serum. A modified method of assay is described which gives higher L. casei values and a clearer distinction between the sera of normal subjects and of patients with folic-acid deficiency.

Anemia↗
PubMed1977

[Study of folic acid blood levels during estro-progestagen treatments].

When the blood levels of folates were estimated in 100 women following treatment with oestro-progestagens the following facts emerged : 1) There is no significant difference between the folate levels found in women on oestro-progestagens compared with a control population of the same age. 2) We have not found any evidence of frank folic acid deficiency in women on oestro-progestagens, but there have been slight drops in the levels of folates in women who show other reasons for folic acid deficiency than taking oral contraceptives. These are : troubles in absorption, salmonella, an increase in the need for folic acid in pregnancy, and failure of transport. Furthermore the incidence of lower levels in the control population was exactly the same as in the experimental population.

Contraceptives, Oral↗
PubMed1982

Drug-nutrient interaction.

The effect of certain drugs on nutrient metabolism is discussed. Antituberculotic drugs such as INH and cycloserine interfere with vitamin B6 metabolism and may produce a secondary niacin deficiency. Oral contraceptives interfere with the metabolism of folic acid and ascorbic acid, and in cases of deficient nutrition, they also seem to interfere with riboflavin. Anticonvulsants can act as folate antagonists and precipitate folic acid deficiency. Therefore, in some cases, supplementation with folate has been recommended simultaneously with anticonvulsant therapy. Cholestyramine therapy has been associated with malabsorption of vitamins; several reports suggest that cholestyramine affects absorption of the fat-soluble vitamins K and D and, in addition, may alter water-soluble vitamins, including folic acid. The study of the interaction of drugs and nutrients is an area that deserves a greater attention in the future, especially in groups where nutrient deficiencies may be prevalent.

Anticonvulsants↗
PubMed1987

Liver folylpolyglutamate synthetase activity in folic acid-deficient rats.

To investigate the influence of folate deficiency on the addition process of glutamyl unit to folylpolyglutamates, liver folylpolyglutamate synthetase was studied. The enzyme activity appears slightly decreased in deficient liver as compared with control. This decline might be more evident in the hepatic cell owing to the lesser availability of reduced forms, preferred substrates of the enzyme.

Animals↗
PubMed1991

Folate Status Following Gastric Bypass Surgery (The Great Folate Mystery).

Several previous investigators have reported an incidence of folic acid deficiency following gastric bypass surgery of up to 38%. Failure to encounter any folic acid deficiencies in our postoperative patients led us to discontinue follow-up folate studies for several years. However, due to repeated references to this deficiency in the literature, we re-instituted folate studies as part of the routine follow-up of our patients. Preoperative serum folate levels were obtained in 1,067 patients and preexisting deficiencies found in 63, an incidence of 6%. Of the 588 folate levels determined 1 to 10 years following gastric bypass, only six were less than 3.0 ng/di, an incidence of 1%. All patients were instructed preoperatively and postoperatively to take multivitamin/mineral supplements after gastric restrictive surgery, and were continually educated on their importance. In a bariatric surgery practice in which patients are instructed, reminded, encouraged and even badgered into taking postoperative vitamin/mineral supplements, folate deficiency should be a rarity. In such circumstances, folate deficiency may well act as a sensitive marker of non-compliance.

Journal Article↗
PubMed1997

Acute methionine load-induced hyperhomocysteinemia enhances platelet aggregation, thromboxane biosynthesis, and macrophage-derived tissue factor activity in rats.

A moderate elevation of plasma homocysteine is a risk factor for atherosclerosis and arterial and veinous thrombosis. However, the mechanisms leading to vascular disorders are poorly understood because studies that have investigated the potential atherothrombogenicity of hyperhomocysteinemia in vivo are scarce. Using a rat model, we were the first to show that dietary folic acid deficiency, a major cause of basal hyperhomocysteinemia, is associated with enhanced macrophage-derived tissue factor and platelet activities. We proposed that an homocysteine-induced oxidative stress may account for this hypercoagulable state. To determine the true thrombogenicity of moderate hyperhomocysteinemia and better understand its etiology, we have carried out an acute methionine load in control and folate-deficient animals. When rats were fed the control diet, a transient fourfold increase in plasma homocysteine levels was observed 2 h after the methionine administration. As with prolonged dietary folic acid deficiency, this methionine load potentiated the platelet aggregation in response to thrombin and ADP as well as the thrombin-induced thromboxane synthesis. It also stimulated the basal and lipopolysaccharide-induced tissue factor activity of peritoneal macrophages. These prothrombotic effects were associated with an increased lipid peroxidation characterized by an elevation of plasma conjugated dienes, lipid hydroperoxides, and thiobarbituric acid-reactive substances. When rats were fed a folic acid-deficient diet, the methionine load did not cause any further increase in plasma homocysteine concentration, platelet activation, macrophage tissue factor-dependent coagulation, or lipoperoxidation. Altogether, our data showed that the prethrombotic state due to both the altered remethylation and transsulfuration pathways resulted from the moderate elevation of circulating homocysteine. We conclude that moderate hyperhomocysteinemia plays a role in the development of a thrombogenic state that might be mediated by the occurrence of oxidative stress.

Adenosine Diphosphate↗