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PubMed1977

Effect of methionine on the metabolism of formate and histidine by rats fed folate/vitamin B-12-methionine-deficient diet.

The metabolism of formate and histidine were compared in rats and in perfused livers of rats on diets deficient in vitamin B-12, methionine, and folic acid. Excretion of formate and formiminoglutamic acid, and the oxidation of [2-14C]histidine and [14C]formate to 14CO2 were measured. Liver folate levels decreased to 40% of normal on the vitamin B-12- and methionine-deficient diets but the rate of oxidation of histidine to CO2 in the whole animal decreased to 15% of normal. This indicated a reduction in the metabolic activity of the liver folates in vitamin B-12deficiency. Comparison of formate and histidine catabolism in folic acid deficiency showed that the oxidation of histine was decreased to 5% of normal but formate oxidation was decreased to only 30% of normal. This indicates that 25% of formate oxidation normally proceeds by a non-folate-dependent pathway.

Animals↗
PubMed1982

[Immune deficiencies in nutritional anemias].

A transient cellular immunologic defect caused by folic acid deficiency was seen in a goat-milk-fed infant with severe enterocolitis. Data on the immunologic consequences of folic acid, protein and iron deficiencies were reviewed in the medical literature. Investigations are difficult because of the patients' poor general condition. Results are difficult to interpret as many etiologic factors are often combined and mechanisms of immunologic responses are complex. Attention is drawn to the danger of iron therapy in patients with transferrin deficiency.

Anemia, Sideroblastic↗
PubMed1983

[Vitamin B12 as a regulator and methotrexate as an antagonist of folic acid metabolism. Pathophysiologic and clinical aspects].

Biochemical investigations show a decreased bioavailability of 5-methyl-tetrahydrofolic acid in vitamin B12 deficient human cell cultures and bone marrow cells. Tetrahydrofolic acid cannot be liberated from its storage form. This so-called methyl-folate-trap results in a functional folic acid deficiency which is the pathogenetic principle of the defect in the cell proliferation in patients with vitamin B12 deficiency. This knowledge of biochemical mechanisms leads to the identification of rare disorders in the metabolism of vitamin B12 and folic acid. After methotrexate treatment a rescue effect with its antidote Leucovorin can only be achieved, if the ratio antidote: methotrexate is at least 10:1. This ratio is important in cell cultures as well as in bone marrow cells in vivo. The results lead to a formula for the calculation of the optimal dosis to reach a secure rescue for individual patients after high-dose methotrexate treatment. This makes the high-dose methotrexate regimen a treatment modality for malignant tumors without any side effects.

DNA↗
PubMed2006

G1793A polymorphisms in the methylene-tetrahydrofolate gene: effect of folic acid on homocysteine levels.

Mutations or polymorphisms in the gene of the enzyme methylenetetrahydrofolate (MTHFR) are associated with hyperhomocysteinemia and possibly with an elevated risk for vascular diseases. A study was conducted on 83 individuals with type 2 diabetes in order to determine the allelic and genotypic frequencies of the G1793A mutation and to assess the effect of folic acid supplementation on plasma homocysteine concentrations. The patients were attended by the Diabetes and Hypertension Program--Balneario Camboriu/SC and received daily supplements containing 1 mg of folic acid for 3 months. DNA was previously extracted from leukocytes and the G1793A mutation was detected by PCR-RFLP. Blood samples were collected during the basal period and after supplementation for the determination of homocysteine by HPLC, and of folic acid and vitamin B(12) by RIA. The allele frequency for the G1793A mutation was 3.01% and no homozygous individuals with mutant alleles were detected. Hyperhomocysteinemia was diagnosed in 27.71% of the patients, folic acid deficiency in 15.66%, and vitamin B(12) deficiency in 7.23%. Plasma homocysteine concentrations were inversely correlated with folic acid (r = -0.27, p = 0.01) and vitamin B(12) (r = -0.21; p = 0.05) concentrations. The individuals with a heterozygous genotype for the G1793A mutation showed borderlines or deficient values in folic acid and vitamin B(12) concentrations compared to individuals with a normal genotype. Hyperhomocysteinemia and the vitamin deficiencies presented by type 2 diabetic individuals, included with a heterozygous genotype for the G1793A mutation in the MTHFR gene, reached normal values by daily folic acid supplementation.

Adult↗
PubMed1969

Aetiology of extrahepatic epithelial iron deposits in siderosis in Bantu.

Twenty-seven specimens of human tissue, obtained by operation, were tested to evaluate the theory that iron uptake by tissues from serum is greater when transferrin is nearly completely saturated than when the degree of saturation is normal. Samples of each tissue were incubated in autologous serum so prepared that in one instance the transferrin was 50% saturated and in the second 90% saturated with iron containing (59)Fe. In all samples the uptake of iron was greater from the transferrin which was 90% saturated. The uptake by tissues of epithelial origin was significantly greater than that by non-epithelial tissues. Considerable variation in uptake was noted between samples of the same tissue from different individuals. The role of iron stores in the tissue and folic acid deficiency are discussed. It is concluded that the degree of transferrin saturation is important in determining iron uptake by tissues, especially in those of epithelial origin, and that such uptake may be modified by tissue stores and folic acid deficiency. It is felt that these factors are probably responsible for the extrahepatic parenchymal deposits of iron sometimes found in Bantu subjects with siderosis.

Epithelium↗
PubMed2000

Anemia and deficiencies of folate and vitamin B-6 are common and vary with season in Chinese women of childbearing age.

Little is known about the micronutrient status of Chinese women of childbearing age. We assessed nonfasting plasma concentrations of folic acid, vitamin B-12, vitamin B-6 (as pyridoxal-5'-phosphate), hemoglobin (Hb), ferritin and transferrin receptor (TfR) in 563 nonpregnant textile workers aged 21-34 y from Anqing, China. All women had obtained permission to become pregnant and were participating in a prospective study of pregnancy outcomes. Mean (SD) plasma concentrations were 9.7 (4.1) nmol/L folic acid, 367 (128) pmol/L vitamin B-12, 40.2 (15.8) nmol/L vitamin B-6, 108 (12. 9) g/L Hb, 42.6 (34.2) microgram/L ferritin and 5.2 (2.7) mg/L TfR. Twenty-three percent of women had biochemical evidence of folic acid deficiency, 26% were deficient in vitamin B-6 and 10% had low vitamin B-12. Overall, 44% of women were deficient in at least one B vitamin. Although anemia (Hb < 120 g/L) was detected in 80% of women, only 17% had depleted iron stores (ferritin < 12 microgram/L); 11% had elevated TfR concentrations. Distinct seasonal trends were observed in the prevalence of moderate anemia (Hb < 100 g/L) and deficiencies of folic acid and vitamin B-6, with significantly lower concentrations of folate and Hb occurring in summer and lower concentrations of vitamin B-6 occurring in winter and spring than in other seasons. We conclude that deficiencies of folic acid, vitamin B-6 and iron were relatively common in this sample of Chinese women of childbearing age and were contributing to the high prevalence of anemia. Without appropriate supplementation, these deficiencies could jeopardize the women's health and increase their risk of adverse pregnancy outcomes.

Adult↗
PubMed1989

Diet-induced DNA damage and altered nucleotide metabolism in lymphocytes from methyl-donor-deficient rats.

Tumor induction with chronic feeding of methyl-donor-deficient diets has been well established; however, the biochemical and molecular mechanisms which predipose to tumorigenesis in this model are still not well understood. The purpose of the present investigation was to assess DNA damage and altered nucleotide metabolism in lymphocytes from Fischer 344 rats fed one of four semi-purified diets: (i) deficient in methionine and choline; (ii) deficient in folic acid; (iii) deficient in methionine, choline and folic acid; or (iv) a supplemented control diet. The accumulation of DNA-strand breaks, as assessed by DNA unwinding in alkali, was increased in lymphocytes from both the methionine/choline-deficient and folate-deficient groups, but was most severe in the group deficient in all three methyl donors. Lymphocyte DNA damage was consistently associated with alterations in folate-dependent thymidylate synthesis, and a decrease in intracellular levels of the DNA-repair-associated pyridine nucleotide, nicotinamide adenine dinucleotide. In the liver, a synergistic lipotropic interaction between folate deficiency and methionine/choline deficiency was observed, confirming the metabolic inter-relationship between these nutrients. Taken together, the results suggest that folate deficiency interacts with methionine/choline deficiency to potentiate symptoms of methyl-donor deficiency and that alterations in folate-dependent thymidylate synthesis are related to DNA damage in lymphocytes. These metabolic aberrations may contribute to immune dysfunction with chronic feeding of methyl-donor-deficient diets.

Animals↗
PubMed1999

Vitamins and brain development.

Effects of deficiency of vitamins on early development of brain have been reviewed. Unusual developmental problems in neurogenesis specific for the brain and impairment of its functional capacities due to vitamin deficiency have been discussed. The species-specific "critical periods" in development of various systems have been mentioned. Indices such as reflex activity, locomotion, special senses, cognition and adaptive behavior were used for assessing brain maturation in experimental models and humans. Significant examples include brain anomalies in humans and other mammals caused by retinoid excess or deficit; increase in calbindin D28K, a vitamin D dependent calcium-binding protein during postnatal period in rat; hydrocephalus and exencephaly in prenatal rats and subarachnoidal or intracerebral hemorrhage in infants caused by vitamin E deficiency. Peripheral neuropathic lesions leading to infantile beriberi is caused by thiamine deficiency. Impaired growth in retinal layers leading to delay in maturation of electroretinogram and depth-perception in postnatal rats occur due to pyridoxine deficiency. Infants of severely vitamin B12 deficient mothers show abnormalities in behavior involving basal ganglia and pyramidal tract. Folic acid deficiency results in delayed maturation of the basic electroencepalographic patterns. In addition, vitamin-interactions leading to developmental errors have been pointed out. Vitamin B6 deficiency impairs vitamin B12 absorption and biotin deficiency may be aggravated by pantothenic acid deficiency. Vitamin C deficiency resulting in impaired metabolism may produce symptoms of deficiency of folic acid. Another characteristic examples is that iron absorption from dietary sources is dependent on ascorbic acid.

Animals↗
PubMed2004

[8 out of 10 midwives informed about folic acid. Most of them considered their knowledge about folic acid not sufficient].

UNLABELLED: Deficiency of folic acid increases the risk for neural tube defects among newborn children and megaloblastic anaemia in the mother. The aim of this study was to make a survey of how midwives working in maternity health care, family planning guidance, and specialist prenatal care in a Swedish county inform women of childbearing age about folic acid. The questionnaire study showed that 79% of the midwives informed the women about folic acid. Usually, the women received information first when they asked for it and midwifes were less prone to inform young women about folic acid. 87% of the midwives felt that they did not know enough about folic acid. CONCLUSIONS: Midwives play an important role in information about the need of folic acid intake for women in childbearing age. Changes in local routines, guidelines and further education of midwifes would subsequently provide information about the importance of folic acid to women in childbearing age.

Education, Nursing, Continuing↗
PubMed1995

Does folic acid harm people with vitamin B12 deficiency?

Oral folic acid given before and during pregnancy can prevent about 75% of fetal neural tube defects. Even in large dose (20 mg daily) folic acid has never been shown to harm normal people, but it has acquired a bad reputation in pernicious anaemia. Before 1930, if untreated patients survived the anaemia, they succumbed to peripheral neuritis, subacute combined degeneration of the spinal cord, and death. The speed of this progression was extremely variable. From 1947 onwards, there were many reports of rapid neurological deterioration during administration of folic acid as sole therapy to people with pernicious anaemia. However, a review of clinical studies published before the introduction of liver and vitamin B12 therapy shows that neurological deterioration was often quite as rapid and severe in untreated patients. Oral folic acid can usually correct or prevent the anaemia of pernicious anaemia. Thus it could mask the underlying disease, and allow the development or progression of neurological deterioration, if diagnosis depended on the presence of anaemic symptoms. This possibility can readily be overcome by adequate education of doctors, so that a macrocytic anaemia is not regarded as a necessary accompanying sign of the neurological disorder. The hypothetical and avoidable side-effects of food fortification with folic acid have to be balanced against the certain benefit of preventing neural tube defects in unplanned pregnancies, and also against the probability that adults may be spared the neuropsychiatric and other ill-effects which result from inadequate dietary folic acid.

Aged↗
PubMed1991

[Vitamin B12 and folic acid in chronic kidney failure and after kidney transplantation].

Vitamin B12 in plasma, folic acid in plasma and erythrocytes were examined in 11 patients in the polyuric stage of chronic renal failure without dialyzation treatment, in 38 patients included in a long-term dialyzation programme before and after 3 months' oral administration of folic acid--(2 X 5 mg week)--and in 23 patients after transplantation of the kidneys. In none of the examined groups vitamin B12) and folic acid deficiency in plasma was detected. A reduced folic acid level in erythrocytes, but still in the reference range, was found in patients in the long-term dialyzation programme without supplementation. Supplementation with folic acid increased its concentration in plasma 4.5 times and in red cells 5.5 times. Haemodialysis did not influence the concentration of the examined indicators in plasma and red cells. According to the recorded results it is not necessary to supplement patients in long-term dialyzation programme and after renal transplantation with vitamin B12 and folic acid, if their dietary protein intake is not restricted.

Female↗
PubMedDate not supplied

Drug therapy and nutritional management of patients with gastrointestinal fistulas.

The drug therapy and nutritional management of patients with gastrointestinal fistulas are reviewed. The goal of therapy is to compensate for loss of electrolytes, nutrients, and water in the fistula drainage and to monitor the acid-base status of the patient. Positive nitrogen balance is essential for anabolism and closure of the fistula. Usually it is not feasible to analyze the fistula drainage for nitrogen content, and nitrogen requirements must be estimated. To prevent folic acid deficiencies, patients should receive daily doses of folic acid 1 mg orally or 0.5 mg in parenteral nutrient solutions. Positive zinc balance usually can be established with the addition to parenteral nutrient solutions of zinc 3-12 mg/day. It is not clear whether the parenteral or enteral route of nutrient administration is preferable. Drug therapy may be needed to treat diarrhea, infection, and any underlying disease. Reductions in the acidity and the volume of fluid lost may allow spontaneous closure and healing; antacids and anticholinergic drugs are not recommended for these purposes. The use of cimetidine has been effective in decreasing the acid content and volume of output from fistulas in the upper gastrointestinal tract and has allowed spontaneous healing to occur. Drainage of any intra-abdominal abscesses is essential; this should be combined with systemic antibiotic therapy. The management of patients with gastrointestinal fistulas is complex because of disturbances in fluid, electrolyte, and acid-base balance and because of difficulties in determining nutritional requirements.

Acid-Base Equilibrium↗
PubMed1978

Bone marrow studies in myelomatosis.

The percentage of fat-cell areas in bone marrow particles from 22 patients with untreated myelomatosis was estimated. In only 1 patient was the mean fat cell area below 25% of the bone marrow area measured. A negative correlation was found between the area of fat cells and plasma cells, indicating a displacement of the fat cell area by the plasma cells. 28% of the patients had empty bone marrow deposits of iron. However, based on a normal iron saturation of S-transferrin and a normal sideroblast count in the bone marrow, the supply of iron to the erythropoiesis was considered sufficient. All patients but one had normoblastic bone marrows. Using a deoxyuridine suppression test in 10 patients, no biochemical defect could be demonstrated. To judge from the correlation coefficient a minor degree (9-14%) of the variation in Hb values could be predicted from the cellularity in the bone marrow while a major degree (70%) could be predicted from the renal glomerular filtration rate. The results do not support a displacement of blood-forming elements, iron deficiency, vitamin B12 or folic acid deficiency to be of general significance in the pathogenesis of anaemia, but agrees with a causal relationship between anaemia and renal failure.

Adult↗
PubMed1977

[Folic acid levels in patients with compensated renal failure and during long-term haemodialysis (author's transl)].

Folic acid concentration in plasma and erythrocytes and vitamin B12 concentration in plasma were determined by radioassay in 56 patients with chronic renal failure. Compensated retention was present in 31, while 25 were haemodialysed at regular intervals, 14 at home, and 11 in hospital. One patient had megaloblastic anaemia. Mean folic acid concentration in plasma for the whole group was 4.60 microgram/l (normal 8.30 +/- 2.57 microgram/l), in RBC 385 microgram/l (normal 459 +/- 143 microgram/l. Vitamin B12 levels were normal. These was no significant difference in folic acid levels betwwen patients on home or on hospital dialysis. During dialysis there was a fall in folic acid concentration in plasma which was proportional to the intial levels. After a four-week replacement pause folic acid concentration in RBC had not decreased in those patients on long-term dialysis who had previously received folic acid. The decreased folic-acid concentration in plasma of patients in compensated chronic renal failure is not due to the renal failure. Folic acid concentration in RBC is decisive in the assessment of folic acid deficiency.

Adult↗
PubMed2001

Red blood cell status in alcoholic and non-alcoholic liver disease.

Macrocytosis is most commonly associated with vitamin B(12) and folic acid deficiency, followed by alcoholism, liver disease, and other pathologic conditions. We studied the red cell and vitamin status in 423 consecutive patients with various liver diseases, including 31 with acute viral hepatitis (AVH), 105 with chronic hepatitis (CH), and 134 with alcoholic liver disease (ALD), who consisted of 84 with non-cirrhotic alcoholic liver disease (NCALD) and 50 with alcoholic liver cirrhosis (ALC), 60 with non-alcoholic liver cirrhosis (NALC), and 93 with hepatocellular carcinoma (HCC). The mean corpuscular volume (MCV) and red cell distribution width (RDW) were significantly higher in patients with ALD and NALC, and among them macrocytosis occurred more frequently in patients with ALC. Macrocytic anemia was mostly found in cirrhotic patients, in which the Child-Pugh score was closely related to the development of macrocytic anemia. In ALD, the MCV was significantly correlated with the estimated alcohol consumption and inversely correlated with the serum folic acid level, which, however, was often maintained within the normal range in patients with macrocytic ALC. After abstinence from alcohol, the MCV and RDW were reduced significantly and were associated with an increasing serum folic acid level. This suggests that macrocytic anemia was a common feature of alcoholic and non-alcoholic liver cirrhosis and that alcohol abuse and folic acid deficiency play a secondary role in macrocytosis.

Adult↗
PubMed1978

Megaloblastic anemia.

Most, but not all, megaloblastic anemia is produced by "ineffective erythropoiesis" in the bone marrow due to either folic acid or vitamin B12 deficiency. In folic acid deficiency the cause frequently is inadequate dietary intake, whereas vitamin B12 deficiency is almost always conditioned by some specific type of malabsorption. Anemia with oval macrocytes, few reticulocytes, moderate leukopenia, and thrombocytopenia is typical of both. Aplastic anemia, refractory anemias with cellular marrow, preleukemia, aleukemia, and erythroleukemia may have somewhat similar blood findings but are usually recognizable from bone marrow biopsy. Decreased levels of folate or vitamin B12 are the most reliable criteria of megaloblastic anemia. With these available in advance, therapy with the appropriate vitamin can be begun at once. If serum levels are unavailable or available only in retrospect, initial treatment, especially of severe anemia, should be with both vitamins. Differentiation between folate and vitamin B12 deficiency is important but impossible by blood and bone marrow morphology alone. Thus, if serum levels are unavailable, the distinction must be made, sometimes retrospectively, on the basis of other laboratory examinations, such as gastric analysis, small-bowel x-ray films, and the Schilling test.

Anemia, Macrocytic↗
PubMed1983

[Thalassemia major manifested by megaloblastic anemia caused by folate deficiency].

In a 11 month-old child, a deep anemia with reticulocytopenia and megaloblastosis on bone marrow aspiration revealed a thalassemia major. The low folate intake and the increased needs probably account for initial findings. Folic acid deficiency has already been described in patients with dyserythropoiesis or chronic hemolysis. Daily folic acid treatment is necessary in these patients.

Anemia, Macrocytic↗