PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “FOLIC ACID DEFICIENCY”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,711 records · Page 95Linked to original sources
PubMed1975

Oral contraceptives, serum folate, and hematologic status.

Previous reports have suggested deleterious effects on folate balance in users of contraceptives. A study of folate in 526 women attending a family-planning clinic demonstrated, both with the Lactobacillus casei assay and with a new radioassay, that the mean serum folate level for women taking oral contraceptives was not significantly lower than that for women in a control group. There was no correlation between serum folate level and length of time oral contraceptives were taken. Also, there was no macrocytosis or hypersegmentation of polymorphonuclear leukocytes and no case of macrocytic anemia in the 280 users of oral contraceptive agents. Probably, oral contraceptive agents do not cause folate deficiency anemia in otherwise normal subjects.

Analysis of Variance↗
PubMed1978

[Anaemia induced by vitamin B12 or folate deficiency: diagnostic value of the "dU suppression" test (author's transl)].

The "dU suppression" test, studying thymine-DNA synthesis from deoxyuridine is abnormal in folate and vitamin B12 deficiency, these two vitamins being involved in this reaction. We have done it in 7 cases of anaemia by folate deficiency, 12 cases of anaemia by vitamin B12 deficiency, in 3 cases of combined deficiency, in 3 cases of acute myeloïd leukaemia, 2 cases of sideroblastic anaemia and 2 cases of intoxication by antifolate. This test is very sensitive: it is abnormal even when there is an anaemia related to a vitamin deficiency with only very light morphologic abnormalities and can discriminate the cases, mainly in myelodysplastic syndromes, where folate deficiency is only an epiphenomen in the genesis of anaemia. The abnormalities of the "dU suppression" are quite corrected by added folate derivatives in folate deficiency. However, cobalamin derivatives did not correct completely the test in vitamin B12 deficiency except when a folate compound is also added. The "dU suppression" test becomes normal about one week after starting vitaminotherapy in vitamin B12 deficiency.

Anemia↗
PubMed2006

Cerebral folate deficiency and leukoencephalopathy caused by a mitochondrial DNA deletion.

OBJECTIVE: Our aim was to describe a child with an incomplete form of Kearns-Sayre syndrome who presented profound cerebrospinal fluid (CSF) folate deficiency and his response to folinic acid supplementation METHODS: CSF 5-methyltetrahydrofolate was analyzed by HPLC with fluorescence detection and mitochondrial DNA deletions by southern blot hybridization. RESULTS: Cranial magnetic resonance imaging showed a leukoencephalopathy. Profound CSF 5-methyltetrahydrofolate deficiency was observed with normal blood folate values and decreased CSF/serum folate ratio, suggesting a transport defect across the blood-brain barrier. Folinic acid treatment was established, and after 1 year clinical response to folinic supplementation was remarkable, with almost normal white matter image. INTERPRETATION: The clinical response after folinic therapy highlights the need for the study of cerebral folate deficiency in patients with mitochondrial disorders and white matter lesions.

Brain Chemistry↗
PubMed1997

Is metabolic evidence for vitamin B-12 and folate deficiency more frequent in elderly patients with Alzheimer's disease?

BACKGROUND: It is still unclear whether there is an association between Alzheimer's disease and vitamin B-12 or folate deficiency. This study was designed to investigate whether patients with Alzheimer's disease are particularly prone to metabolically significant cobalamin or folate deficiency as compared to nondemented hospitalized controls and healthy elderly controls living at home. METHODS: Evaluation for the diagnosis of Alzheimer's disease, routine laboratory tests, serum folate and vitamin B-12, serum methylmalonic acid (MMA), total homocysteine (tHcy), and radiological tests was performed in 52 patients with Alzheimer's disease (AD), 50 nondemented hospitalized controls, and 49 healthy elderly subjects living at home. RESULTS: Serum vitamin B-12 and folate levels are comparable between patients with AD, hospitalized control patients, and subjects living at home. Patients with AD have the highest serum MMA and tHcy levels. The MMA levels of patients with AD and hospitalized controls are not different, but the mean tHcy level is significantly higher in patients with AD as compared to nondemented patients or subjects living at home. CONCLUSION: The interpretation of the vitamin B-12 and folate status in patients with AD depends largely on the methodology (i.e., serum vitamin vs metabolite levels) and the selection of the control group. Although patients with AD have the highest tHcy and MMA levels, metabolically significant vitamin B-12 and folate deficiency is also a substantial problem in nondemented elderly patients.

Aged↗
PubMed1982

Incidence and pathogenesis of acute megaloblastic bone-marrow change in patients receiving intensive care.

The incidence and pathogenesis of acute megaloblastic bone-marrow change and of abnormalities in DNA synthesis, as assessed with the deoxyuridine(dU) suppression test, have been investigated in a prospective study of 70 seriously ill patients admitted to an intensive-care unit. On admission megaloblastic bone-marrow change was present in 22 patients, 18 of whom had been anaesthetised with nitrous oxide for 2-6 h during surgical procedures before admission. 16 of these 18 patients died, compared with 7 of 22 patients in whom haemopoiesis remained normoblastic despite receiving equivalent amounts of nitrous oxide. An abnormal dU-suppression test developed only in patients who had received nitrous oxide; on admission an abnormal dU-suppression test was found in 39 of the 42 patients tested who had been exposed to the anaesthetic. The abnormality produced in the dU-suppression test by nitrous oxide in patients admitted to the intensive-care unit was more severe and recovery was slower than the abnormality seen in patients undergoing cardiac-bypass surgery. During the recovery period from the effects of nitrous oxide the pattern of correction of the dU-suppression test changed from that of vitamin-B12 deficiency to folate deficiency.

Adolescent↗
PubMed2003

Antinutritional effects of fumonisin B1 and pathophysiological consequences.

Due to its structural similarity with sphingosine, fumonisin B(1) (FB(1)) inhibits ceramide synthase (a key enzyme of sphingolipid biosynthesis) leading to an intracellular accumulation of sphingoid bases with a consequent increase of sphinganine/sphingosine (SA/SO) ratio. In adult male rats, dietary exposure to fumonisin induces a significant increase in both SA concentrations and SA/SO ratio in kidney, but not in liver and brain, as well as a significant reduction of body weight gain. Regarding the brain, the developing rat is more sensitive to FB(1) than the adult rat. FB(1) treatment produces in the forebrain and brainstem: (i) an increase in SA levels and SA/SO ratio, (ii) a reduction in myelin deposition, and (iii) an impairment of 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) activity. FB(1) effects on myelin are similar to those produced by starvation (temporary removal of pups from dam during postnatal period), thus suggesting that hypomyelination could be due, at least partly, to a nutritional deficiency. Finally, FB(1) reduces the uptake of folate in different cell lines. The resulting folate deficiency could explain the association of FB(1) exposure with neural tube defects.

Animals↗
PubMed1983

Impaired chemiluminescence and bactericidal killing by neutrophils from patients with severe cobalamin deficiency.

Neutrophil function was examined in 24 patients with megaloblastic haemopoiesis due to vitamin B12-or folate deficiency. Defective bactericidal activity was demonstrated in the B12-deficient group only and was associated with normal phagocytic activity but impaired intracellular killing. Luminol amplified luminescence was consistently low in B12-deficient subjects with RBC counts of less than 2 X 10(12)/l. These defects were not seen in the folate-deficient cases although isolated abnormalities were present in those who were also alcoholic.

Adult↗
PubMed1992

Effects of ethanol on tissue folate incorporation and recovery from folate deficiency in rats.

Studies in folate-deficient alcoholics suggest that ethanol interferes with the recovery of folate status and the hematopoietic response to folate. Previous animal studies have suggested diverse effects of ethanol on intestinal absorption, hepatic metabolism, and urinary excretion of folate. In order to examine the effects of ethanol on folate distribution during folate deficiency, tissue incorporation of a tracer dose of folate was studied in rats chronically fed ethanol-containing and/or folate-deficient diets. Rats fed these diets were also used to study the effect of chronic ethanol consumption on the dietary reversal of folate deficiency by changing the diets (adding folate or replacing ethanol) from 12 to 16 weeks. After 16 weeks, tissue folate depletion was severe in rats fed folate-deficient diets. Plasma and whole body retention of the tracer dose of folate was decreased in folate-deficient rats consuming ethanol. In folate-deficient rats, ethanol consumption increased the incorporation of folate by the kidney and brain, but had no effect in other tissues (liver, lung, spleen, intestine, testis). In ethanol-fed folate-deficient rats that continued to consume ethanol, but with added folate in their diets, urine, plasma, liver, and kidney folate levels returned to control levels in 4 weeks. In the rats that stopped ethanol, but continued low folate diet consumption, no recovery of tissue folate levels was seen in 4 weeks. These results suggest that chronic ethanol consumption can exacerbate folate requirements by inhibiting body retention of small doses of folate. However, these effects are minor because ethanol consumption does not block recovery from folate deficiency when rats are fed sufficient amounts of folate.

Alcohol Drinking↗
PubMed1997

Poor metabolic control, early age at onset, and marginal folate deficiency are associated with increasing levels of plasma homocysteine in insulin-dependent diabetes mellitus. A five-year follow-up study.

In a previous study, we showed that diabetic patients exhibited significantly increased concentrations of total plasma homocysteine (tHcy), but not until the onset of nephropathy. It was suggested that the hyperhomocysteinaemia might contribute to the accelerated atherosclerotic process in diabetic patients. In the present study, we have analysed the main determinants of plasma homocysteine (i.e. serum cobalamin, blood folate and serum creatinine), and also some other parameters related to diabetes mellitus, such as medical history, metabolic and renal quantities, on two occasions with a 5-year interval in 50 patients with insulin-dependent diabetes mellitus, in order to further elucidate the relation between plasma tHcy and diabetes mellitus. The result of the present study shows that diabetic patients with the lowest age at onset and with the poorest metabolic control are those most prone to a rapid increase in plasma tHcy concentration. The increment in plasma tHcy concentration in this group of patients may at least partly be explained by a marginal deficiency of blood folate concentrations.

Adult↗
PubMed1981

Blood thiamine and blood folate levels. A comparative study in control, alcoholic and folate-deficient subjects.

A group of 85 patients underwent serum, red blood cell (RBC) folate and whole blood thiamine determinations. The group was divided into three subgroups: 1) a control group (41 patients who had no neurological or mental disorders which could be attributable to a vitamin deficiency); 2) a subgroup of folate-deficient patients (29 Ss) who had folate-responsive neuropsychiatric symptoms and 3) 15 alcoholic patients. There was no significant correlation between blood thiamine levels on one hand and serum and RBC folate on the other in the entire group. Alcoholic patients showed significant lower whole blood thiamine levels (p less than .001) and lower RBC folate (p less than .025) as compared with controls. We conclude that in the great majority of folate-deficient patients there is no correlation between folate and thiamine blood levels.

Adolescent↗
PubMed1976

Protein calorie malnutrition and nutritional anaemia in Black pre-school children in a South African semirural community.

The incidence of nutritional anaemia and of protein calorie malnutrition in 119 randomly selected Black children living in the Muldersdrift area was studied. The ecology of nutritional problems in the community was also investigated. Major problems in the area were poor educational and medical facilities, a high childhood mortality rate and poor cash incomes. An important factor which influenced nutrition was large family size. The incidence of protein calorie malnutrition was 27,6% and of nutritional anaemia 13,3%. In the second year of life the incidence of anaemia was 27,3%. The main cause of anaemia was iron deficiency.

Black or African American↗
PubMed1993

Metabolic abnormalities in cobalamin (vitamin B12) and folate deficiency.

Mammalian cells contain two Cbl-dependent enzymes, L-methylmalonyl-CoA mutase and methionine synthase. The former requires adenosyl-Cbl and catalyzes the conversion of L-methylmalonyl-CoA to succinyl-CoA. The latter requires CH3-Cbl and catalyzes the conversion of 5-CH3-tetrahydrofolate and homocysteine to tetrahydrofolate and methionine, respectively. Biochemical abnormalities related to a decrease in the activity of methionine synthase are thought to be responsible for the indistinguishable hematologic abnormalities seen in both Cbl and folate deficiency. The biochemical basis for the neuropsychiatric abnormalities seen in Cbl deficiency, but not in folate deficiency, is not known although hypotheses have been proposed that implicate one or the other of the two Cbl-dependent enzymes. Recent studies have shown that levels of serum methylmalonic acid, 2-methylcitric acids I and II, total homocysteine, and cystathionine are elevated in most patients with Cbl deficiency and that total homocysteine, cystathionine, N,N-dimethylglycine, and N-methylglycine are elevated in most patients with folate deficiency. Analysis of these metabolic abnormalities in various patient groups fails to support hypotheses that either L-methylmalonyl-CoA mutase or methionine synthase alone are responsible for the neuropsychiatric abnormalities. We suggest that they may result from a third, unknown mammalian Cbl-dependent enzyme or from a combined deficiency of both Cbl-dependent enzymes together with an unknown genetic or environmental factor.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1987

Depressed folate incorporation into milk secondary to iron deficiency in the rat.

The present study was designed to determine whether reduced folate incorporation into milk can account for folate depletion of iron-deficient suckling rats. Dams were fed diets containing 2 mg/kg folate and either 8, 12 or 250 mg/kg iron throughout gestation and lactation to produce severely iron-deficient, moderately iron-depleted and iron-sufficient states in 17-d-old pups (n = 15 litters/group). On d 17 of lactation, dams were separated from litters and given intraperitoneal injections of [3',5',7,9-3H]pteroylmonoglutamic acid ([3H]PteGlu) or physiological saline. Mean [3H]PteGlu incorporation into milk of severely iron-deficient dams was 67% of that in iron-sufficient controls, while "total" and "free" milk folate activities were 54 and 61%, respectively. Values for milk [3H]PteGlu incorporation and folate activities were intermediate in moderately iron-depleted dams. Pup red blood cell folate activity was positively correlated with both free (r = 0.43, P = 0.004) and total (r = 0.37, P = 0.015) milk folate activities. Mean plasma folate activities of severely and moderately iron-deficient pups were 68 and 86% of control values, respectively. Results show that in both mild and severe iron deficiency, reduced folate secretion into milk is at least partially responsible for impaired folate status of suckling pups.

Animals↗