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Results for “FOLIC ACID DEFICIENCY”

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PubMed1978

Effects of dietary folate deficiency on developmental increase of myelin lipids in rat brain.

Rats were fed a folic acid deficient purified diet from day 12 of gestation throughout the lactational period. Offsprings were fed the same diet after weaning. Control rats were given 170 microgram of folic acid per day per rat supplemented to the same diet, which was fed ad libitum or by pair-feeding. At 3 and 6 weeks of age, myelin was isolated from rat brains. It was found that in comparison with the controls, myelin yield was significantly decreased as well as the brain weight in the folic acid deficient rats at 6 weeks of age. There were no differences of gross composition of myelin, protein, ratio of cholesterol, glycolipids, phospholipids, and total lipid with or without folate deficiency either at 3 or 6 weeks of age. The hydroxy fatty acid composition of myelin lipids in brain was not changed with folate deficiency at 3 or 6 weeks of age. The developmental increase of the percentages of 22:6, 22:4, and 20:1 in nonhydroxy fatty acids of myelin lipids from the folic acid deficient rats were significantly lower at 6 weeks of age in comparison with the controls. The n-3:n-6 ratio in myelin fatty acids from the folic acid deficient rat brains was abnormally low at 3 weeks of age and was not increased at even 6 weeks of age. The implications of these findings are that folic acid may play an important role in desaturation or chain elongation of polyunsaturated fatty acids in the brain of developing rats.

Animals↗
PubMed1985

Comparison of folic acid coenzyme distribution patterns in patients with methylenetetrahydrofolate reductase and methionine synthetase deficiencies.

Folic acid coenzyme distribution patterns were examined in the liver and kidney of two patients with homocystinuria due to different inborn errors of metabolism affecting the remethylation of homocysteine to methionine. One patient, with severe mental retardation (and death at 3 1/2 yr), had greatly reduced levels of methylenetetrahydrofolic acid (THF) reductase in fibroblasts as well as in liver and kidney. Chromatographic separation of folate coenzymes in liver showed an abnormal pattern with THF as the main component and almost no methyl-THF but total folate was normal. The other patient, who was dystrophic, microcephalic, and had megaloblastic anemia died at age 4 months. He had reduced levels of methionine synthetase in liver and kidney due to a defect of intracellular cobalamin metabolism. Chromatographic analysis of his tissues showed methyl-THF to be the principal folate form and a markedly reduced total folate. These results support the "methyl-THF trap" hypothesis and offer information with respect to the possible therapy of these two disorders.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1965

THE DIRECT ANTIGLOBULIN (COOMBS) TEST IN MEGALOBLASTIC ANAEMIA.

Folic acid deficiency with the picture of a megaloblastic bone marrow may develop in haemolytic anaemia, and, on the other hand, both vitamin B(12) and folic acid deficiency may produce signs of haemolysis. As the correct interpretation of a positive antiglobulin reaction associated with megaloblastic erythropoiesis is particularly important, the effect of deficiency of vitamin B(12) and folic acid on the results of the test was investigated in 32 patients with vitamin B(12) or folic acid deficiency and a positive antiglobulin reaction was obtained in ten. There was no correlation between the result of the test and the degree of anaemia, and there was no significant difference between the incidence of positive results associated with deficiency of vitamin B(12) or folic acid. In determining the significance of a positive result, the time interval before agglutination occurs is sometimes of greater value than the strength of the reaction or the result of the gamma globulin neutralization test.

Anemia, Macrocytic↗
PubMed1961

The significance of Howell-Jolly bodies and giant metamyelocytes in marrow smears.

Howell-Jolly bodies in erythroid precursors can be found in the marrow in a variety of diseases. More than 1% in the later erythroblasts is rarely found except in vitamin B(12) or folic acid deficiency states.Giant metamyelocytes are probably always the result of vitamin B(12) or folic acid deficiency. A distinction is drawn between the deficiency of, and therapeutic need for, vitamin B(12) and folic acid.

Bone Marrow↗
PubMed1987

Modifications of hemato-biological parameters in pregnant women in a migrating population in northern Cameroon: prevalence of anemia, iron and folates deficiencies.

The wholesale displacement of a population can have nutritional consequences for the migrants. With this in mind, the prevalences of anemia and of iron and folic acid deficiencies were studied in a group of 90 pregnant women living in northeast Benoue, an area situated in northern Cameroon where a development project was initiated in 1973. This project aimed at moving a population from the extreme northern highlands to the fertile valley of the Benoue. The following hemato-biological parameters were measured: hemoglobin, hematocrit, mean cell hemoglobin concentration, plasma iron, transferrin saturation, serum concentrations of folates, prealbumin, transferrin, protides and their fractions. The investigation showed that anemia, as well as iron and folic acid deficiencies, were rare when using World Health Organization criteria. The anemia prevalence, judged on a hemoglobin level of less than 11 g per 100 ml, is 8%, iron deficiency prevalence is 10% (plasma iron level below 50 micrograms per 100 ml), and folic acid deficiency prevalence is 3% (serum folic acid level below 3 ng per ml). However, 40% of the pregnant women had a level of transferrin saturation below 15%. In non deficient subjects, we observed a decrease between the first and second trimesters of pregnancy in hemato-biological parameters linked to anemia or to nutritional status (hemoglobin, hematocrit, plasma iron, transferrin saturation, prealbumin). The nutritional conditions in the area appeared sufficient to prevent deficiencies which are frequently observed in pregnant women in Africa.

Anemia↗
PubMed2005

[Differential diagnosis of a macrocytic, hyperchromic anemia following alcohol abuse and simultaneous therapy with triamterene and cotrimoxazole].

HISTORY AND ADMISSION FINDINGS: A 50-year-old woman was admitted to our emergency room because of progressive weakness. She collapsed the night before admission. Skin and mucosa were pale, she denied major infections or bleedings. An alcohol abuse was known for many years. Because of edema she received a therapy with triamteren, an infection of the urinary tract was treated with cotrimoxacol. INVESTIGATIONS: In addition to thrombocytopenia (50 Gpt/l) and leukocytopenia (1,51 10 (9)/l) we diagnosed a hyperchromic and macrocytic anemia (Hb 3,6 mmol/l [5,8 g/dl], Hk 0,17, MCH 2.52 fmol, 116,8 fl). Folic acid was decreased to 0.677 ng/ml, whereas levels of cobalamin, ferritin and iron were normal. Examination of bone marrow showed a hypercellular marrow with typical megaloblastic features of erythropoiesis and granulopoiesis. A systemic hematological disorder could be ruled out. The folic acid deficiency in our patient was the result of a long time alcohol abuse and a simultaneous therapy with mild folate antagonists (triamteren and cotrimoxacol). CLINICAL COURSE: The patient received folic acid (5 mg/d orally). Within one week the peripheral blood counts increased to normal, the follow up bone marrow examination showed a hyperplastic marrow with normal hematopoietic maturation. CONCLUSIONS: Folic acid deficiency can be aggravated because of simultaneous therapy with mild folate antagonists. In addition to megaloblastic anemia this can lead to thrombocytopenia and/or leukocytopenia. Therefore in patients with pancytopenia a deficiency of folic acid should be ruled out.

Alcoholism↗
PubMed1982

Interactions between folate and ascorbic acid in the guinea pig.

Possible interactions between folic acid (folate) and ascorbic acid (AA) have been suspected because megaloblastic anemia is occasionally observed in scorbutic patients, and it may or may not respond to folate treatment. Male weanling guinea pigs were fed diets containing high levels of folate and AA or diets deficient in one or both vitamins. A total of 36 animals, including 9 controls, were studied. When anorexia began to appear in the deficient groups, all animals were killed by exsanguination, and tissue samples (blood, liver, adrenal, kidney, spleen, and intestinal mucosa) were removed for AA and folate analyses. Folate and AA deficiency lowered tissue folate and AA levels, respectively. AA deficiency, either alone or in combination with folate restriction, did not affect tissue folate levels, nor did AA deficiency significantly exacerbate the anemia and leukopenia caused by folate deficiency. However, there was an unexpected decrease in AA levels in the liver and adrenal glands with folate deficiency. Although AA does not appear to be needed for normal folate metabolism, the lower AA levels associated with a folate deficiency are indicative of an interaction between the two vitamins.

Anemia, Megaloblastic↗
PubMed1991

Folate deficiency in chicks fed diets containing practical ingredients.

Development of folate deficiency was evaluated in young chicks fed diets containing corn and soybean meal as major constituents. Folic acid deficiency, as indicated by retarded growth and feed efficiency, could be produced in 18-day-old chicks. Chicks fed the basal diet had increased growth when given supplements of either folic acid, choline Cl, or DL-methionine, but not vitamin B12. Relative liver size (grams per 100 g of body weight) was reduced by a methionine or methionine plus choline supplement in two experiments but by folic acid in only one of two experiments. Plasma hemoglobin was reduced by folic acid or a methionine and choline supplement after 42 days on the diets. Folic acid deficiency can be produced in young chicks with a diet based on practical ingredients. Purified diets or very high levels of antibiotic feeding are not necessary to produce folic acid deficiency as long as low levels of methionine and choline are present in the basal diet.

Animal Feed↗
PubMed2005

Decreased TGF-beta1 and IGF-1 protein expression in rat embryo skull bone in folic acid-restricted diet.

Folic acid deficiency during conception up to the end of the third month of gestation is believed to play the most important factor in neural tube defects (NTDs). However, the exact molecular mechanism remains to be elucidated. It has been suggested that transforming growth factor-beta (TGF-beta1) and insulin-like growth factor-1 (IGF-1) play a critical role in supporting bone formation. Therefore, folic acid deficiency may contribute to NTD occurrence via decreased TGF-beta1 and IGF-1 expression. This study aimed to determine the correlation between folic acid deficiency and the expression of TGF-beta1 and IGF-1 in rat skull bone. Thirty female Sprague-Dawley rats were divided into three groups. Purified diet containing 5 (restricted), 15 (low) and 30 microg (normal) of folic acid was given to the first, second and third groups, respectively. At 16 weeks of a given diet, blood samples were taken to examine folic acid (folate immunoassay method), TGF-beta1 and IGF-1 (enzyme-linked immunosorbent assay method) levels. After forced mating, on the 18th-19th day of gestation (E18-19), the pregnant rats were subjected to hysterectomy. The skull bone samples of E18-19 rats were taken to examine the TGF-beta1 and IGF-1 protein expression by immunohistochemistry. The folic acid-restricted diet (5 microg) resulted in decreased serum TGF-beta1 and IGF-1 levels. Furthermore, protein expression of TGF-beta1 and IGF-1 in E18-19 rat skull bones was also significantly lower in the folic acid-restricted diet than in the normal diet. Folic acid deficiency could result in reduction of TGF-beta1 and IGF-1 protein levels and might contribute to formation of defects in the skull bone as observed in mengingocele patients.

Animals↗
PubMed2006

[Hereditary enzyme defects of erythrocytes: glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency].

Possible causes for a normocytic hyperregeneratory anemia are beside an incomplete treatment of iron deficiency, vitamin B12 deficiency or folic acid deficiency notably a hemolysis. After exclusion of other causes of hemolysis like immune hemolytic anemias, microangiopathic hemolytic anemias and hemoglobinopathies, an enzyme deficiency of erythrocytes should be considered. By far the most common form worldwide is the Glucose-6-phosphate deficiency. In the most frequent variants of this disease hemolysis occurs only during stress, imposed for example by infection, "oxidative" drugs or after ingestion of fava beans. The most serious clinical complication of the Glucose-6-phosphate deficiency is the rarely observed neonatal icterus. Some enzyme variants can cause chronic hemolysis which is described as chronic nonsperocytic hemolytic anemia. This form of chronic anemia can also be caused by other enzyme deficiencies, most frequently by the Pyruvate kinase deficiency. All other deficiencies of glycolytic enzymes are even rarer. It should be noted that in some of these very rare forms neurological rather than hematological symptoms predominate the clinical syndrome. If there is suspicion, on the basis of clinical symptoms and/or familial history, diagnosis of an enzyme deficiency can be achieved relatively easy by measurement of the enzyme activity. Accurate diagnosis might be helpful in therapeutic decisions (e.g. splenectomy in certain forms) and it is essential for genetic counseling, since certain deficiencies are transmitted as autosomal recessive disorders (e.g. pyruvate kinase deficiency), while the most common form, the glucose-6-phosphate dehydrogenase deficiency is linked to the X-chromosome.

Anemia, Hemolytic, Congenital↗
PubMedDate not supplied

Vitamins and endurance training. Food for running or faddish claims?

The inter-relationship of food and physical performance, food is considered as a conglomerate of nutrients and man is depicted as a kind of organic pudding. This 'machine' concept of human performance in combination with the mysticism surrounding vitamins, has led to the faddish belief that additional vitamins are necessary to improve physical performance by means of supercharging the metabolic processes in the body. Various vitamins and their dietary recommendations as well as the indicators for vitamin status are discussed. It is concluded that a marginal or subclinical deficiency state can be defined as an intermediate between optimal vitamin status and frank clinical deficiency. Marginal deficiency is characterised by biochemical values deviating from statistically derived reference limits as well as the absence of clinical signs and symptoms of vitamin deficiency. Besides the static, mostly biochemical, indicators of vitamin status, more functional indicators are considered, among them work capacity. An extensive historical review on depletion studies, epidemiological surveys and supplementation studies is presented. It is concluded that a restricted intake of some B-complex vitamins-individually and in combination-of approximately less than 35 to 45% of the recommended dietary allowance may lead to decreased endurance capacity within a few weeks. Studies on ascorbic acid (vitamin C) depletion and fat-soluble vitamin A deficiency have noted no decrease of endurance capacity. However, in a few recent epidemiological surveys, biochemical vitamin C deficiency was actually shown to decrease aerobic power. Although the general conclusion is that a reduced water-soluble vitamin intake decreases endurance capacity, it is believed that further controlled experimentation is needed with B-complex vitamins and vitamin C individually. Furthermore, usually employed reference limits for vitamins need reappraisal translating them into impairment limits. With respect to the available evidence, it can be concluded that supplementation of diet with either single or multivitamin preparations containing B-complex vitamins, vitamin C or E does not improve physical performance in athletes with a normal biochemical vitamin balance resulting from a well-balanced diet. Although vitamin supplementation does not seem to produce any effect when the diet is adequate, it is possible that vitamin B-complex supplementation is useful in sports with a high energy expenditure, because of the unavoidable consumption of 'empty calories' i.e. food products with a low nutrient density. The side effects of megavitamin supplementation are discussed briefly.

Animals↗