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Results for “FOLIC ACID DEFICIENCY”

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PubMed2002

Neutrophil hypersegmentation in children with iron deficiency anemia.

Neutrophil hypersegmentation (NH) is usually associated with vitamin B12 or folic acid deficiency. NH is seen in iron deficiency anemia but there are very few case studies about this. Neutrophil hypersegmentation was evaluated in 94 children with iron deficiency anemia; 23 healthy children comprised the control group with similar ages. NH was found in 76/94 (81%) in the study group and 2/23 (9%) of the control group. The difference was statistically significant (p < .01).

Anemia, Iron-Deficiency↗
PubMed1984

Effect of phenobarbitone on folic acid metabolism in the rat.

Anticonvulsant drugs have well-known relationships with folic acid, often leading, in epileptic patients on long term treatment to signs of folic acid deficiency and to haematological complications. The findings of this work, carried out on rats, show strong interference of phenobarbitone with folic acid metabolism, particularly with pteroylpolyglutamate synthesis in liver. This is proved by lower polyglutamate content, lower 3H folate incorporation in polyglutamate forms and in protein-bound folates, and also by lower blood radioactivity, higher urinary excretion of 3H folate metabolites and by higher 3H folate concentration in kidneys.

Animals↗
PubMedDate not supplied

Phenytoin-folic acid interaction: a lesson to be learned.

A case of a patient who developed symptomatic phenytoin-induced folic acid deficiency is reported. Folate supplementation of 5 mg/d was followed by a decrease of serum phenytoin concentration to a subtherapeutic level with a breakthrough seizure. Estimation of phenytoin's Km-Vmax Michaelis-Menten pharmacokinetic parameters in this patient demonstrated that folate supplements indeed caused a significant decrease in the Km value. This decrease correlates with a greater affinity of the metabolizing hepatic enzymes for the drug, and hence, with the resultant increase in phenytoin's metabolism and decrease of its serum concentration and anticonvulsive effect. In an era of increasing knowledge of folate's pivotal role in various diseases, we call attention to this drug-vitamin interaction, and to the previously suggested recommendation that folate supplementation should be initiated whenever phenytoin therapy commences. Because folic acid dosages as low as 1 mg/d may perturbate phenytoin's metabolism, smaller deficiency preventive doses may be the advisable allowance for phenytointreated patients with normal pretreatment folate levels. This suggestion must be confirmed by a prospective study in a large cohort of patients.

Drug Interactions↗
PubMed1987

[Can zinc deficiency in the mother be responsible for the occurrence of spina bifida aperta in the fetus?].

The occurrence in the fetus of closure defects of the neural tube and especially spina bifida aperta (SBA) has been related, by some authors, to nutritional deficiencies of the mother, in addition to well-known genetic factors: a folic acid deficiency and more recently a zinc deficiency have been evoked. The retrospective study of 23 couples mother/newborn selected from the presence of a SBA in the child, and 14 reference couples, shows that the mothers of children with SBA have a zinc blood level lower than that of the reference group; this result is confirmed by the alkaline phosphatases and zinc enzymes which are markedly decreased. Measurement of the incorporation of radioactive zinc in the skin fibroblasts shows, in case of SBA, in the mother, an increased incorporation rate, and in the newborn a decrease of that rate in relation to the reference group. We believe that the results of our study which confirm those from other authors, demonstrate that the administration of zinc during pregnancy is at least as important as the administration of folic acid to prevent recurrence of neurulation abnormalities.

Alkaline Phosphatase↗
PubMed2005

[Vitamins C, B12 and folic acid in latent iron deficiency].

The aim of the work was to study the level of vitamins C, B12 and folic acid in latent iron deficiency of different etiology (hipo- and anacid gastritis and menorrhagia). 81 patients with latent iron deficiency were investigated. Vitamin C levels were measured by refractometry, folic acid and vitamin B12 by radioimmune assay. The obtained results showed significant decrease of ascorbic acid and less apparent decrease of folic acid in the blood plasma. The content of vitamin B12 was unchanged. Decrease of vitamin C level is related to the changes of initial stages of iron metabolism and its further absorption. Less apparent changes of folic acid and vitamin B12 indicates, that such important stages of erithropoesis as DNA replication and cell proliferation are intact. Our results indicate to the development of metabolic disorders prior to revelation of iron deficiency anaemia, which need timely correction.

Adolescent↗
PubMed2001

The effect of folate deficiency on the cytotoxic and mutagenic responses to ethyl methanesulfonate in human lymphoblastoid cell lines that differ in p53 status.

Folic acid deficiency acts synergistically with alkylating agents to increase genetic damage at the HPRT locus in Chinese hamster ovary cells in vitro and in rat splenocytes in vivo. The present studies extend these observations to human cells and, in addition, investigate the role of p53 activity on mutation induction. The human lymphoblastoid cell lines TK6 and WTK1 are derived from the same parental cell line (WI-L2), but WTK1 expresses mutant p53. Treatment of folate-replete or deficient WTK1 and TK6 cells with increasing concentrations (0-50microg/ml) of ethyl methanesulfonate (EMS) resulted in significantly different HPRT mutation dose-response relationships (P<0.01), indicating that folate deficiency increased the EMS-induced mutant frequency in both cell lines, but with a greater effect in TK6 cells. Molecular analyses of 152 mutations showed that the predominant mutation (65%) in both cell types grown in the presence or absence of folic acid was a G>A transition on the non-transcribed strand. These transitions were mainly at non-CpG sites, particularly when these bases were flanked 3' by a purine or on both sides by G:C base pairs. A smaller number of G>A transitions occurred on the transcribed strand (C>T=14%), resulting in 79% total G:C>A:T transitions. There were more genomic deletions in folate-deficient (15%) as compared to replete cells (4%) of both cell types. Mutations that altered RNA splicing were common in both cell types and under both folate conditions, representing 33% of the total mutations. These studies indicate that cells expressing p53 activity exhibit a higher rate of mutation induction but are more sensitive to the toxic effects of alkylating agents than those lacking p53 activity. Folate deficiency tends to reduce toxicity but increase mutation induction after EMS treatment. The p53 gene product did not have a major influence on the molecular spectrum after treatment with EMS, while folate deficiency increased the frequency of deletions in both cell types.

Antineoplastic Agents, Alkylating↗
PubMed1975

Folic acid dosage for chronic hemodialysis patients.

The doses of folic acid, necessary to avoid folic acid deficiency in patients being maintained on hemodialysis, have been estimated to be between 1 and 5 mg daily. To more precisely define an adequate dose of folic acid, 6 anephric patients were studied. The patients were maintained on hemodialysis and received, in a crossover fashion, 1 mg and 5 mg of folic acid for 3 wk. In a second crossover study, 3 anephric patients were first maintained on 0 and then on 1 mg of folic acid after each dialysis for 3 wk periods. Pre- and postdialysis folic acid blood levels were measured and dialyzer clearances of folic acid were determined. The results of this study support the conclusion of the Food and Drug Administration report suggesting that daily doses of 1 mg of folic acid are adequate to sustain therapeutic folate levels. The data further indicate that the administration of 1 mg of folic acid after each dialysis, rather than 1 mg of folic acid daily, can provide adequate folate.

Administration, Oral↗
PubMed2003

Addition of essential micronutrients to foods--implication for public health policy in Israel.

Micronutrient deficiencies have reoccupied the center stage of public health policy with the realization that folic acid deficiency results in neural tube defects and possibly other birth defects as well as ischemic heart disease. These, in turn, have raised an older debate on food fortification policy for the elimination of iodine, iron and vitamin D deficiencies. Data from the First Israeli National Health and Nutrition Survey (MABAT 2000) provided an impetus to develop an active national nutrition policy aimed to improve the nutritional status of iodine, iron, vitamins A and D and B-vitamins, including folate. In this paper we examine some of the micronutrient deficiency issues in Israel and their implications for public health, and suggest options for the formulation of policy.

Food, Fortified↗
PubMed1979

Biochemical evidence of thiamin deficiency in young Ghanian children.

Detailed biochemical studies for nutritional status were carried out on 146 Ghanaian children ages 6 months to 6 years over a 2-year period. Study children comprised three main groups: severe protein-calorie malnutrition; mild to moderate protein-calorie malnutrition and apparently healthy children. Erythrocyte transketolase activity and the percentage of erythrocyte transketolase pyrophosphate effect were also determined. In the first year of the study elevated percentage of transketolase pyrophosphate effect indicative of thiamin deficiency was found in all three of the above-mentioned groups, with the most widespread deficiency in the normal groups. In year 2, repeat studies of the severely malnourished group after 2 weeks of nutritional therapy with the administration of vitamin capsules, which included thiamin, resulted in the normalization of transketolase pyrophosphate effect. Apoenzyme activity was comparable in all groups studied. There were no obvious clinical signs of thiamin deficiency, although sensory testing was not performed. A relatively large number of children with high percentage of transketolase pyrosphosphate effect also had serum folic acid deficiency. This evidence of widespread biochemical thiamin deficiency is indicative of an at-risk population among young children for clinical thiamin deficiency. Further studies are needed to identify whether the problem is inadequate thiamin intake, destruction of thiamin by thiaminases or food preparation methods, or malabsorption of thiamin.

Child↗
PubMedDate not supplied

Enhanced incidence of leg abnormalities in reovirus WVU 2937-infected chickens fed various dietary levels of selected vitamins.

Five experiments were conducted to evaluate the incidence of leg abnormalities of 4-, 6-, and 8-week-old reovirus WVU 2937-infected and uninfected chickens fed diets containing 20%, 100%, or 200% of the 1977 National Research Council nutrient requirements (NRC-77) of poultry for manganese, biotin, niacin, choline, or folic acid. Reovirus infection significantly elevated the incidence of leg abnormalities in the biotin-, niacin-, and folic-acid-deficient chickens and decreased the incidence of leg abnormalities in choline-deficient chickens. Reovirus-infected male chickens had a significantly greater incidence of leg abnormalities than reovirus-infected female chickens in the biotin, niacin, and folic acid studies. No sex differences in the incidence of leg abnormalities were observed in uninfected chickens. The incidence of leg abnormalities decreased with increasing dietary levels of biotin, niacin, choline, or folic acid in all chickens except reovirus-infected male chickens in the biotin study. In the manganese study, neither reovirus infection nor dietary level had any effect on the incidence of leg abnormalities in male or female chickens.

Age Factors↗
PubMed1980

Effect of folic acid supplementation on pregnancy in the squirrel monkey (Saimiri sciureus).

Supplementation of squirrel monkeys with folic acid improved hematologic and folate status, maternal weight gain during pregnancy, and infant birth weight. Thus the folate content in the stock diet (1.4 microgram/g) did not meet the requirement for pregnancy. Low plasma vitamin B12 values suggest that vitamin B12 in the stock diet (22 ng/g) also was not adequate. Changes with folic acid supplementation are similar to those for human subjects, indicating that the squirrel monkey is an appropriate model for folic acid deficiency in pregnancy in man.

Animals↗
PubMed2003

Gene-diet interactions in brain aging and neurodegenerative disorders.

While there are many examples of people who live for 100 years or more with little evidence of a decline in brain function, many others are not so fortunate and experience a neurodegenerative disorder, such as Alzheimer disease or Parkinson disease. Although an increasing number of genetic factors that may affect the risk for neurodegenerative disorders are being identified, emerging findings suggest that dietary factors play major roles in determining whether the brain ages successfully or experiences a neurodegenerative disorder. Dietary factors may interact with disease-causing or predisposing genes in molecular cascades that either promote or prevent the degeneration of neurons. Epidemiologic findings suggest that high-calorie diets and folic acid deficiency increase the risk for Alzheimer disease and Parkinson disease; studies of animal models of these disorders have shown that dietary restriction (reduced calorie intake or intermittent fasting) and dietary supplementation with folic acid can reduce neuronal damage and improve behavioral outcome. Animal studies have shown that the beneficial effects of dietary restriction on the brain result in part from increased production of neurotrophic factors and cytoprotective protein chaperones in neurons. By keeping homocysteine levels low, folic acid can protect cerebral vessels and prevent the accumulation of DNA damage in neurons caused by oxidative stress and facilitated by homocysteine. Although additional studies are required in humans, the emerging data suggest that high-calorie diets and elevated homocysteine levels may render the brain vulnerable to age-related neurodegenerative disorders, particularly in persons with a genetic predisposition to such disorders.

Aging↗
PubMed1976

Folic acid absorption in regional enteritis.

The authors have investigated intestinal absorption of folic acid by jejunal perfusion with a triple lumen tube in five subjects with regional enteritis. The subjects' intestinal disabilities ranged from terminal ileitis to short bowel syndrome. Two had steatorrhea and two had low serum folate levels. Absorption of pteroylglutamic acid was normal in all five. This suggests that folic acid deficiency, common in this disorder, is largely caused by malnutrition, not malabsorption.

Adult↗