Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOLIC ACID DEFICIENCY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed1981

Influence of routine administration of folic acid and iron during pregnancy.

Haematological and folic acid status were assessed in 200 women in the 6th month of pregnancy. Folic acid deficiencies with no or little haematological impairment were found in one third of the cases, and their occurrence increased when the socioeconomic level was low. During the last trimester of pregnancy, the women were given either iron alone or iron and folic acid supplementation. In the mothers, the rise of folate values in serum and red blood cells, in the folic acid-supplemented group, had no obvious haematological consequences, showing that iron therapy alone can, in developed countries, prevent the anaemia in pregnancy. In the infants, there was no difference in the haematological indices, whatever the mothers' treatment had been. However, a significant difference appeared for the gestational age and, therefore, the height and weight. Folic acid supplementation during pregnancy increased its duration by virtually 1 week.

Adult↗
PubMedDate not supplied

[Environment and genetics in the etiology of cleft lip and cleft palate with reference to the role of folic acid].

The combined birth prevalence of cleft palate [CP] and cleft lip with or without cleft palate [CL(P)] in Europe is approximately one in 700 with characteristic regional variations. Orofacial clefting (OC) is therefore now one of the most frequent congenital anomalies, with a higher birth prevalence that Down's Syndrome or Neural Tube defects, but still lower than cardiovascular malformation. Babies with OC require a multidisciplinary medical approach, surgery and rehabilitative treatments over time. This means an important effort in terms of social organization as well as economical costs for the health care system. In Italy, the health care costs for approximately 800 children born with orofacial clefting per year has been estimated at around 150 billion Lire (80 million Euros). The etiology of OC is complex and heterogeneous both for isolated and associated defects; causes linked to environment, genetics and gene-environment interaction are known, although there is still a lot to do, especially in clarifying the role of genetics in producing susceptibility to the environment. Four categories of genes for which there are results suggestive of a genetic susceptibility to OCs are: 1) genes expressed in a particular area of the embryo or in a particular period of the palatine arch development, such as the transforming growth factors alpha and beta (TGF alpha, TGF beta 2, TGF beta 3); 2) genes having biological activities linked to the OC's pathogenesis without direct involvement (e.g. the retinoic acid receptor (RARA), the methylenetetrahydrofolate reductase receptor (MTHFR) and the folic acid receptor (FOLR1); 3) genes or locus identified in experimental animals as the homeotic genes MSX-1 and MSX-2; 4) genes involved in the interaction with the xenobiotics metabolism as those in P-450 cytochrome system. Several environmental factors have been implicated in the OC etiology; among those, the folic acid supplementation during the periconceptional period that was found effective in the prevention of neural tube defects. In fact, folic acid deficiency may be responsible for different malformations through a common mechanism that interferes with the embryonic development, depending on the maternal or embryo genotype. Further investigation is required to study in depth how the genotype would modify the role of environmental factors like folic acid. Well-designed and conducted epidemiological studies seem to be able to give worthwhile information. Studies carried out in Europe on these issues are a few, particularly those on gene-environment interaction. Recent results obtained in molecular biology and the availability of wealth of data can allow to perform ad hoc investigations, being important not only for the basic research but also for their public health implications. For this objective a specific scientific network at the European level has been set by the European Science Foundation (ESF), whose first step will be to establish consistent case ascertainment and data collection across Europe and to develop standardized protocols and methods of analysis. It is hoped that in the longer term such multicentre collaborative research will enable combined analysis and lead to the identification of genetic susceptibility to certain environmental factors, including nutrition. Such studies would inform the current debate about the efficacy of folic acid and other nutritional factors in prevention of disease in the developing embryo. Subsequent public health measures targeted according to risk might reduce the prevalence of disorders such as orofacial clefting.

Adult↗
PubMed1981

Effect of folate deficiency on microsomal drug metabolism and heme content in the intestinal mucosa of guinea pigs.

The relationship between folate deficiency, heme content, and microsomal drug metabolism in the intestinal mucosa of the guinea pig was examined. Weanling male guinea pigs were pair-fed a folate-deficient diet, and intestinal mucosal folate levels were measured. A significant decrease (75%) in these levels was observed at 3 weeks after diet initiation. A significant decrease (78%) in intestinal mucosal drug metabolism (7-ethoxycoumarin O-deethylase activity) and a significant decrease (46%) in intestinal mucosal heme content were also observed at this time. These findings indicate that folic acid deficiency in the guinea pig results in a marked reduction in heme content and microsomal drug metabolism of the intestinal mucosa.

Animals↗
PubMed1995

Anemia in pregnancy.

Anemia is the most common hematologic complication of pregnancy and is associated with increased rates of premature birth, low birth weight and perinatal mortality. Iron deficiency is the most common cause of anemia, and most pregnant women benefit from daily supplementation of 30 to 60 mg of elemental iron. Folic acid deficiency, the most common cause of megaloblastic anemia in pregnancy, is associated with open neural tube defects and other complications. It is recommended that daily supplementation with 4 mg of folic acid be started at least one month before conception and continued through the first trimester. Other less common causes of anemia include glucose-6-phosphate dehydrogenase deficiency, sickle cell trait and disease, and the thalassemias. The primary care provider should emphasize risk evaluation, dietary and preconceptual counseling, testing and appropriate treatment.

Anemia↗
PubMed1968

Malabsorption syndrome in Paget's disease of bone.

Of eight patients with Paget's disease one had diarrhoea, steatorrhoea, impaired xylose absorption, and macrocytic anaemia due to folic acid deficiency, while another had diarrhoea and very low xylose absorption. In both patients jejunal biopsy was normal, and they responded to folic acid therapy with considerable increase in xylose absorption. Low xylose excretion was seen in three more patients, one of whom also had steatorrhoea. Thus malabsorption may be a systemic complication of Paget's disease of bone, possibly due either to secondary folate deficiency or to relative ischaemia of the bowel.

Aged↗
PubMed2004

Is there a role for folate determinations in current clinical practice in the USA?

Our objectives were to determine the likelihood of true folate deficiency among patients tested for this disorder, to identify whether there were differences between the clinical indications for folate testing in folate-normal and folate-deficient patients and to assess the impact of a diagnosis of folate deficiency on patient management. The results of all blood samples analyzed for serum and erythrocyte folate levels during the year 2001 at the Cleveland Clinic Foundation were retrieved. Folate deficient patients were identified and their medical charts were reviewed to determine the indications, patient characteristics, and impact of this diagnosis on patient management. For comparison, medical chart review was also conducted on a control group composed of an equal number of randomly selected patients with normal serum folate values. A total of 6024 (4689 serum and 1335 erythrocyte) samples from 4985 patients were collected. In the study, 77 (1.6%) of the serum folate levels, from 74 patients, were identified as low. When compared with the control group, patients with low serum folate levels had lower hemoglobin and a greater red cell distribution width. Mean corpuscular volume, however, did not differ between the two groups. No significant differences in the clinical indications for serum folate level determinations could be identified. Only 39 of the 74 patients with low serum folate levels were given folate replacement, representing only 0.9% of the clinically suspected and tested patients. We conclude that determination of serum folate level infrequently led to appropriate folate replacement therapy. Moreover, even when suspected, true folic acid deficiency is rare and clinical indications are not helpful in diagnosis.

Adult↗
PubMed2005

[Iron, folic acid and vitamin B12 deficiencies related to anemia in adolescents from a region with a high incidence of congenital malformations in Venezuela].

Since in recent years for certain age groups, the main cause of anemia is not iron deficiency, we intended to study the effect of iron, folic acid and vitamin B12 deficiencies on anemia prevalence in adolescents from Venezuela. One hundred adolescents aged between 12 and 19 years participated in the study. Each subject was interviewed about antecedents and habits and a physical examination and a 24-hour food recall questionnaire were performed. From a blood sample, hemoglobin and hematocrit concentrations were determined and serum was separated for quantification of ferritin, folic acid and vitamin B12 concentrations. Prevalence of anemia was 78% and for iron, folic acid and vitamin B12 deficiencies were 34.66, 90.9 and 18.18%, respectively. From anemic cases, 35.89% presented iron deficiency, while 91.02% presented folic acid deficiency. Only 19.23% of adolescents with anemia presented also vitamin B12 deficiency, but all the cases with vitamin B12 deficiency, were anemic. Simultaneous iron and folic acid deficiencies affected 30.76% of anemic cases. The high prevalence of deficiencies found in this work could be explained by insufficient intake and inadequate food habits. The prevalence of anemia was associated to folic acid deficiency rather than to iron deficiency, due to the high prevalence of folic acid deficiency. The high prevalence of nutritional deficiencies found in this work, especially regarding folic acid deficiency, require immediate interventions.

Adolescent↗
PubMed1986

Iron deficiency anaemia and pica.

Pica was a surprise finding in 8 cases of severe iron deficiency anaemia of unknown cause and 2 patients with pregnancy-related anaemia who had a mixed picture of iron deficiency and megaloblastic features owing to folic acid deficiency. The pica cases demonstrated an apparently consistent pattern: severe anaemia, young age, normal psychiatric assessment, good nutrition and lack of an overtly disadvantaged background. Pica was significantly absent in other forms of anaemia in a series of 53 subjects. The literature is briefly reviewed to highlight the unanswered questions about this disorder. The cases reported do not furnish any clues to the enigma of pica, but reveal an obscure form of idiopathic iron deficiency anaemia. Pica may be commoner than is thought.

Adolescent↗
PubMed1978

[Complex genesis of anemia in chronic liver diseases].

36% of a total of chronic liver patients suffered from anaemia and 50.5% of patients affected with liver cirrhosis. In most cases the anaemias were normochrome and hypochrome or hyperchrome only in some cases. In analyzing possible single factors the reductions of vitamin B12 absorption could be made probable by means of the Schilling test and sometimes a folic acid deficiency in macrocyte anaemia with normal vitamin B12 absorption by determining the folic acid content in the serum and by successes of test treatment 82% of patients with liver cirrhosis showed a latent or manifest haemolysis. However, it was only in 1/3 of the patients with liver cirrhosis that the spleen turned out to be the place of an increased degradation of erythrocytes. In some cases an increased erythrocytoclasia into the liver could be identified. Predominantly, however, an increased degradation of erythrocytes in the total RHS had to be assumed. Twice an ineffective erythropoiesis could be found by ferrokinetic examinations. As a whole ferrokinetic examinations cannot be interpreted easily, because their static and dynamic values of iron transport in the plasma volume of liver patients will undergo considerable changes. Patients with disturbances of haematopoiesis and with haemolysis remaining in the latent stage may develop a manifest anaemia because of the influence of additional factors, such as increase of the plasma volume at lowered haematocrit value or microbleedings. The cause of anaemia cannot be concluded with sufficient probability from the type of anaemia; in a single case all pathogenetic factors will rather have to be analyzed. Therapeutic possibilities for hepatogenous anaemia of complex genesis are discussed.

Adult↗
PubMed2003

In vitro effect of methanol on folate-deficient rat hepatocytes.

Methanol is primarily metabolized by oxidation to formaldehyde and then to formic acid. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports the in vitro antioxidant effect of vitamin E on isolated hepatocytes of folic acid deficient rats rendered so as to emulate a human hepatocyte model. These hepatocytes were treated with 320 microM of methanol per million cells and incubated for 30 min. The microsomal fraction of these hepatocytes showed a decreased level of superoxide dismutase (SOD), with increase in lipid peroxidation (LPO) shown by increase in recorded levels of malondialdehyde (MDA). Catalase activity was shown to be increased. Levels of reduced glutathione (GSH) were decreased and the activity of glutathione peroxidase (GSH-Px) and of glutathione reductase (GSSG-R) were not altered. The hepatocytes of folate deficient rats pretreated with vitamin E, when subjected to methanol treatment, showed no significant change in SOD levels and a significant decrease in MDA levels. The catalase activity in this group of animals showed a highly significant decrease. These animals had normal levels of GSH, while a significant fall in GSH-Px and GSSG-R levels were observed. These results suggest that Vitamin E exerts a protective effect on hepatocytes by acting as a free radical scavenger, proving its usefulness in treating methanol toxicity.

Animals↗
PubMed1989

[Nutritional intake of folic acid in breast-fed infants].

The relationship of natural and artificial feeding to serum and red cell folate levels, as a means of evaluating nutritional intake of this vitamin, was studied. First a cross-sectional study was undertaken in which a group of 112 infants still being breast-fed at 4, 6, and 9 months of age had significantly higher folate concentrations than another group of 102 infants who had been weaned before 2 months. At 6 months of age the prevalence of folic acid deficiency (red cell folate less than 160 micrograms/l of erythrocytes) was 0% in the first group and 15.4% in the second (P less than 0.02), and at 9 months the respective proportions were 3.6 and 28.9% (P less than 0.01). In a second study, 50 nursing infants were followed longitudinally during their first 15 months of life, and up to 9 months of age a direct correlation was observed between the folate concentrations and the duration of breast-feeding. In order to prevent a deficiency of this vitamin, it is recommended that infants be exclusively breast-fed at least through the age of 6 months or, failing this, that they be fed infant formula enriched with folic acid.

Breast Feeding↗
PubMed1984

Mean corpuscular hemoglobin is increased in Martin-Bell syndrome.

Studying the blood picture of 11 patients with Martin-Bell syndrome, we found the erythrocytes relatively hyperchromic when compared to the data from 171 matched controls living in the same institution. Because mean corpuscular hemoglobin is increased also in patients with folic acid deficiency states, we feel that our data provide further evidence that Martin-Bell syndrome is an inherited disease of folate metabolism.

Adult↗
PubMed1998

Effect of maternal folate levels on somatic mutation frequency in the developing colon.

Folic acid deficiency is associated with an increase in chromosomal aberrations in adult rodents and humans. Somatic mutations have a critical role in carcinogenesis. Since most mutations arise during early development, the effect of maternal folic acid levels on the spontaneous mutant frequency in the developing colon was examined using lacZ transgenic mice. No significant difference in mutant frequencies at both 3 and 8 weeks of age were found between offspring whose mothers were fed low folate and those on high folate diets during pregnancy. Our results suggest that the correlation between folic acid intake and cancer risk may only be effective at extreme folate deficiencies or in combination with other dietary deficiencies or an underlying predisposition.

Age Factors↗
PubMed2003

Vitamins A, and C and folate status in Mexican children under 12 years and women 12-49 years: a probabilistic national survey.

OBJECTIVE: To describe the epidemiology of Vitamin A and C and folic acid deficiencies and their association with sociodemographic and dietary factors in a national probabilistic sample of Mexican women and children. MATERIAL AND METHODS: This is a probabilistic sample from the National Nutrition Survey 1999 (ENN-99) including 1,966 children and 920 women. Vitamins A and C were measured in serum by high-performance liquid chromatography, and folic acid in total blood by a microbiological method. Determinants for such deficiencies were explored by multiple regression models. RESULTS: Vitamin A deficiency (retinol < 10 micrograms/dl) was rare in both children and women. But subclinical deficiency (retinol > 10 and < 20 micrograms/dl) was present in 25% of children. The likelihood of subclinical deficiency of vitamin A was less in older children (OR = 0.98, p = 0.01) and in women with higher body mass index (OR = 0.93, p = 0.01). About 30% of children < 2 years of age and 40% of women were vitamin C deficient. The likelihood of vitamin C deficiency was less in children and women as socioeconomic level increased (OR = 0.69, p = 0.03, and OR = 0.80, p = 0.04), and higher in older women (OR = 1.02, p = 0.05). The prevalence of folate deficiency varied in children (2.3 to 11.2), in women it was 5%. Folate deficiency was less in children of higher socioeconomic level (OR = 0.62, p = 0.01), and in those eating more vegetables (OR = 0.22, p = 0.01). CONCLUSIONS: The high prevalence of subclinical deficiency of vitamin A in children is indicative of risk of further deterioration under adverse circumstances. Vitamin C deficiency in both children and women implies in addition diminished ability for iron absorption. The English version of this paper is available too at: http://www.insp.mx/salud/index.html.

Adolescent↗
PubMedDate not supplied

Phenytoin-folic acid interaction.

OBJECTIVE: To review information regarding the dual and interdependent drug-nutrient interaction between phenytoin and folic acid and other literature involving phenytoin and folic acid. DATA SOURCES: Information was retrieved from a MEDLINE search of English-language literature conducted from 1983 (time of the last review) to March 1995. Search terms included folic acid, phenytoin, and folic acid deficiency. Additional references were obtained from Current Contents and from the bibliographies of the retrieved references. STUDY SELECTION: All human studies examining the effects of phenytoin on serum folate concentrations and folic acid supplementation on serum phenytoin concentrations were selected. These included studies of patients with epilepsy and healthy volunteers as well as case reports. Case reports were included because of the extensive length of time needed to study this drug interaction. DATA EXTRACTION: Data extracted included gender, dosing, serum folate concentrations if available, pharmacokinetics, and adverse events. DATA SYNTHESIS: Serum folate decreases when phenytoin therapy is initiated alone with no folate supplementation. Folic acid supplementation in folate-deficient patients with epilepsy changes the pharmacokinetics of phenytoin, usually leading to lower serum phenytoin concentrations and possible seizure breakthrough. Folate is hypothesized to be a cofactor in phenytoin metabolism and may be responsible for the "pseudo-steady-state," which is a concentration where phenytoin appears to be at steady-state, but in reality, is not. Phenytoin and folic acid therapy initiated concomitantly prevents decreased folate and phenytoin obtains steady-state concentrations sooner. CONCLUSIONS: Folic acid supplementation should be initiated each time phenytoin therapy commences because of the hypothesized cofactor mechanism, decreased adverse effects associated with folate deficiency, and better seizure control with no perturbation of phenytoin pharmacokinetics.

Anticonvulsants↗
PubMed1997

Effect of folate deficiency on mutations at the hprt locus in Chinese hamster ovary cells exposed to monofunctional alkylating agents.

Multiplex PCR amplification of hprt exons from 113 Chinese hamster ovary cell clones selected for resistance to 6-thioguanine was performed to investigate the molecular basis for the synergistic mutagenic effects of nutritional folic acid deficiency and alkylating agents. In cells treated with ethyl methanesulfonate, intragenic deletions were detected in 9 of 46 (19.6%) clones derived from folate-deficient cells, but in none of 16 mutants grown in folate-replete medium. The number of deletions found in mutants generated by N-nitroso-N-ethylurea was low in both folate-deficient (1 of 25; 4%) and folate-replete (1 of 26; 3.8%) cells. Correction of folate deficiency may decrease the frequency of intragenic deletions caused by some alkylating agents.

Alkylating Agents↗