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Results for “FOLIC ACID DEFICIENCY”

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At least 523 records · Page 29Linked to original sources
PubMed1996

Vitamin supplementation in the elderly: a critical evaluation.

Routine vitamin supplementation for the elderly has been advocated by many. Specific vitamin deficiencies are rare in free-living elderly, but are not uncommonly encountered in hospitalized and institutionalized patients. Deficiency may result from interactions with medications or overall poor dietary intake. Low blood or plasma vitamin concentration is not necessarily indicative of a deficient state. Specific vitamin supplements are useful in the treatment and prevention of a deficient state. However, there is little, if any benefit from supplementation for reasons other than replacement therapy. The incidence and clinical symptoms of thiamine (vitamin B1), riboflavin (B2), pyridoxine (vitamin B6), vitamin B12, C, D, folate, niacin, vitamin A, E, beta carotene, and K deficiency and their treatment and prevention in the elderly are discussed.

Aged↗
PubMed2005

A comparison of folic acid deficiency-induced genomic instability in lymphocytes of breast cancer patients and normal non-cancer controls from a Chinese population in Yunnan.

We hypothesized that the genomic response to folate deficiency might be different between breast cancer cases and healthy subjects. To test this hypothesis, we performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid (FA) deficiency on primary human lymphocytes from 19 breast cancer patients and 20 age-matched healthy females from Yunnan, China using the cytokinesis-block micronucleus assay. Lymphocytes from the volunteers were cultured in RPMI1640 medium containing 30, 120 or 240 nM FA for 9 days. The results showed that 30 nM FA was associated with increased frequencies of micronucleated binucleated cell (MNed BNC), nucleoplasmic bridges (NPB), nuclear buds (BUD), apoptosis (APO) and necrosis (NEC) relative to 120 and 240 nM FA (P<0.001) in lymphocytes of case and control groups in vitro, however there were no significant differences between the 120 and 240 nM FA within each sampling group. The case group showed significantly higher frequencies of MNed BNC than control at 120 and 240 nM FA (P<0.05-0.001) but not at 30 nM FA (P=0.052). NEC was significantly higher in breast cancer group than control at all concentrations of FA (P<0.005). FA concentration explained 60, 39, 39, 52 and 71% of the variance of MNed BNC, NPB, BUD, APO and NEC, respectively compared with breast cancer status which only explained 6 and 7% of the variance of MNed BNC and NEC(Two way ANOVA, P<0.0001). Difference of difference analysis showed that breast cancer cases were not abnormally sensitive to the genome-damaging effect of folate deficiency. We concluded that (i) increased concentrations of FA abolished the genome-damaging effect of FA deficiency in lymphocytes of both breast cancer patients and controls to a similar extent and (ii) FA concentration is much more important than breast cancer status in determining genomic instability and cell death.

Adult↗
PubMed1985

Nutritional deficiencies in institutionalized mentally retarded and physically disabled individuals.

The folic acid, riboflavin, and vitamin A status of 150 individuals in a hospital for mentally retarded persons was examined. Because many of the subjects were incontinent, it was necessary to use blood samples. Folic acid deficiency was determined from plasma levels and from examination of stained peripheral blood smears for megaloblastic changes in the leucocytes. Riboflavin deficiency was determined from estimation of erythrocyte glutathione reductase and vitamin A in plasma by a colorimetric method. Twenty percent of the subjects had evidence of folic acid deficiency, 17% had evidence of riboflavin deficiency, and none had vitamin A deficiency.

Adolescent↗
PubMed1999

[Extra-intestinal complications of ulcerative colitis: hematologic complication].

Iron deficiency anemia, autoimmune hemolytic anemia, folic acid deficiency megaloblastic anemia, granulocytopenia, acute or chronic leukemia, idiopathic thrombocytopenic purpura have been reported as blood diseases among the extra-intestinal complications with ulcerative colitis until now. Iron deficiency anemia is most frequently seen, and it often derives from apparent or inapparent continuous gastrointestinal bleeding. Autoimmune hemolytic anemia produces antierythrocyte membrane autoantibody while idiopathic thrombocytopenic purpura produces antithrombocyte autoantibody leading to anemia or thrombocytopenia. For folic acid deficiency megaloblastic anemia and granulocytopenia, adverse reaction of sulfasalazine being administered to the patients with ulcerative colitis has been pointed out. While the cases with acute or chronic leukemia are reported increasingly, its cause is still unknown. For treatment of ulcerative colitis, it is considered necessary to find blood complications by carrying out general examinations of peripheral blood and examinations of blood picture, serum iron and folic acid routinely.

Agranulocytosis↗
PubMed1976

Nutrition in cryptogenic cirrhosis and chronic aggressive hepatitis.

The nutritional status of 80 patients with non-alcoholic chronic liver disease was assessed by determination of various nutritional parameters in body fluids. With the exception of vitamin C there was a higher incidence (40%) of fat soluble vitamin deficiency (vitamins A, E, and carotene) than of the water soluble vitamins. Less than 10% of patients showed evidence of vitamin B12, nicotinic acid, thiamin, or riboflavin deficiency, and 17% had evidence of folic acid deficiency. The presence of deficiency was not related to age of the patient or fat absorption, and an inadequate dietary intake was not a major cause of deficiency. The incidence of nutritional deficiency is less frequent in non-alcoholic as compared with alcoholic liver disease.

Adult↗
PubMed2006

Cytokinesis-block micronucleus assay evolves into a "cytome" assay of chromosomal instability, mitotic dysfunction and cell death.

The cytokinesis-block micronucleus (CBMN) assay was originally developed as an ideal system for measuring micronuclei (MNi) however it can also be used to measure nucleoplasmic bridges (NPBs), nuclear buds (NBUDs), cell death (necrosis or apoptosis) and nuclear division rate. Current evidence suggests that (a) NPBs originate from dicentric chromosomes in which the centromeres have been pulled to the opposite poles of the cell at anaphase and are therefore indicative of DNA mis-repair, chromosome rearrangement or telomere end-fusions, (b) NPBs may break to form MNi, (c) the nuclear budding process is the mechanism by which cells remove amplified and/or excess DNA and is therefore a marker of gene amplification and/or altered gene dosage, (d) cell cycle checkpoint defects result in micronucleus formation and (e) hypomethylation of DNA, induced nutritionally or by inhibition of DNA methyl transferase can lead to micronucleus formation either via chromosome loss or chromosome breakage. The strong correlation between micronucleus formation, nuclear budding and NPBs (r=0.75-0.77, P<0.001) induced by either folic acid deficiency or exposure to ionising radiation is supportive of the hypothesis that folic acid deficiency and/or ionising radiation cause genomic instability and gene amplification by the initiation of breakage-fusion-bridge cycles. In its comprehensive mode, the CBMN assay measures all cells including necrotic and apoptotic cells as well as number of nuclei per cell to provide a measure of cytotoxicity and mitotic activity. The CBMN assay has in fact evolved into a "cytome" method for measuring comprehensively chromosomal instability phenotype and altered cellular viability caused by genetic defects and/or nutrional deficiencies and/or exogenous genotoxins thus opening up an exciting future for the use of this methodology in the emerging fields of nutrigenomics and toxicogenomics and their combinations.

Animals↗
PubMed2005

Initial findings on teratological and developmental relationships and differences between neural tube defects and facial clefting. First experimental results.

Unless genetically caused, the occurrence of neural tube defects and clefts of the lip, alveolus and palate are not associated. These malformations do, however, share some common causes, one of which is folic acid deficiency. Nevertheless, it is not known why a neural tube defect resulting from folic acid deficiency does not occur in combination with facial clefts. Based on animal experiments and a review of the literature, it is assumed that other factors--such as vitamin B6 deficiency--though clinically not diagnosed, can more often cause malformations.

Alveolar Process↗
PubMedDate not supplied

Association of esophageal cytological abnormalities with vitamin and lipotrope deficiencies in populations at risk for esophageal cancer.

Esophageal brush cytological screening was undertaken and blood concentrations of micronutrients (vitamin A, E, B12, folic acid and methionine) determined from adults at risk for esophageal carcinoma (EC) in Transkei and Ciskei, Southern Africa. Age-standardised EC rates per 100,000 per annum for both sexes in high, intermediate and low risk districts in Transkei were 74, 51 and 34, respectively. Corresponding rates in high and low EC risk districts in Ciskei were 129 and 9, respectively. Esophageal cytological changes including esophagitis, signs of folic acid deficiency, cellular atypia, dysplasia and cancer, were more prevalent in patients from high than from low EC risk areas. Dietary questionnaires revealed that corn was the main dietary staple in all populations, but that lower intakes of green vegetables, fruits and animal protein occurred in the high risk areas. Significantly lower concentrations of vitamins A, E, B12 and folic acid were present in the blood of patients presenting with cellular dysplasia or malignancy than in cytologically normal patients and in patients from low risk areas. Concentrations of red cell and plasma folate were significantly lower in patients presenting with cytological signs of folic acid deficiency or cellular atypia. The association of vitamin A, vitamin E and folic acid deficiencies with specific esophageal cytological abnormalities in populations at risk for EC is reported for the first time.

Adult↗
PubMedDate not supplied

The aetiology of severe anaemia among antenatal patients of the Port Moresby General Hospital.

Between October 1998 and September 2000, 111 consecutive pregnant patients admitted to the Port Moresby General Hospital antenatal ward with a haemoglobin level of 6 g/dl or less were studied. The main causes of the severe anaemia were as follows: iron deficiency on its own or in combination with another factor 66%--iron deficiency on its own 43% and combined folate and iron deficiency 23%--and folate deficiency 18%. Malaria was a contributory factor in 13 patients (12%). A combination of blood film, bone marrow study, serum assays of ferritin, folate and vitamin B12, and mean corpuscular volume (MCV) was used to determine the cause of the anaemia. Ferritin levels on their own poorly correlated with the presence of iron in the bone marrow. A low MCV correlated well with iron deficiency anaemia while a high MCV was associated with folic acid deficiency. It would seem therefore that while a bone marrow study is mandatory to reach a definitive diagnosis of severe anaemia, MCV, in conjunction with the red cell morphology on blood film, would be a good marker for iron and folic acid deficiency anaemia, especially as we do not have serum assays readily available for folate, ferritin and vitamin B12 in Papua New Guinea.

Adult↗