Folate deficiency in malnutrition, malabsorption, and during phenytoin treatment diagnosed by determination of serine synthesis in lymphocytes.
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Adult↗
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Results for “FOLIC ACID DEFICIENCY”
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A possible negative correlation between the frequency of chromosome lesions induced by folate-deficiency and age in individuals with the fra-Xq27.3 syndrome.
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Adult↗
Morphological changes in relation to haemopoietic nutrient deficiency in nutritional macrocytic anaemia in infancy and childhood.
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Anemia, Hypochromic↗
Role of homocysteine, cystathionine and methylmalonic acid measurement for diagnosis of vitamin deficiency in high-aged subjects.
BACKGROUND: Intracellular B-vitamin and folate deficiency indicated by hyperhomocysteinemia is very frequent in the elderly population. Hyperhomocysteinemia increases the risk of atherothrombotic diseases and neuropsychiatric complications. Our aim was to evaluate the prevalence of increased serum metabolite concentrations in subjects of a higher age, and whether the measurement of metabolite concentrations is more effective in diagnosing B-vitamin deficiency than mere homocysteine. MATERIALS AND METHODS: Homocysteine (HCY), cystathionine (CYS) and methylmalonic acid (MMA) were investigated in serum together with vitamin B-12, B-6 and folate in 90 high-aged subjects (85-102 years), 92 seniors (65-75 years), and in 50 younger subjects (19-50 years). RESULTS: Elderly subjects (high-aged and senior) had elevated serum concentrations of metabolites. High-aged subjects had a higher frequency of pathological increases than seniors: HCY 62% vs. 24%; MMA 62% vs. 23%; CYS 81% vs. 36%. Folate and vitamin B-6 concentrations were significantly decreased in both elderly groups; vitamin B-12 was only decreased in high-aged subjects. Utilising vitamin B-6, B-12 and folate for diagnosis of intracellular vitamin deficiency, the rate was 30% in seniors and 55% in high aged subjects. However, utilising the metabolites (HCY, MMA and CYS) for the diagnosis of intracellular vitamin deficiency, there was a distinctly increased rate of 55% in seniors respective to 90% in high-aged subjects. Backward multiple regression analysis revealed that only folate, MMA, creatinine and age were independent variables influencing the HCY concentration. Furthermore, the MMA concentration was significantly and independently influenced by folate, vitamin B-12, HCY and creatinine, and the serum concentration of CYS by vitamin B-12, creatinine and age. CONCLUSION: The metabolites HCY, MMA and CYS are sensitive indicators diagnosing impaired remethylation of homocysteine to methionine with parallel activation of catabolic pathway. Compared to mere HCY or B-vitamins in serum, the efficiency of diagnosing a disturbed HCY metabolism increases very much in utilising the metabolites HCY, MMA and CYS. For differential diagnosis, parallel measurement of folate and creatinine is recommended. The early and correct diagnosis of B-vitamin deficiency in elderly subjects is of high clinical relevance.
Adult↗
Kearns-Sayre syndrome with reduced plasma and cerebrospinal fluid folate.
A young woman with Kearns-Sayre syndrome and progressive central nervous system deterioration over 15 years had decreased plasma and cerebrospinal fluid folate levels while receiving phenytoin for a seizure disorder. A muscle biopsy showed a "ragged red fiber" myopathy with reduced muscle carnitine and mitochondrial enzymes. Computed tomographic brain scans showed cerebral white matter hypodensities and bilateral calcification of the basal ganglia. The mechanism for the folate deficiency and altered ratio of plasma to cerebrospinal fluid folate is unknown, but the deficiency may be responsive to replacement therapy.
Adolescent↗
Dietary folate deficiency enhances induction of micronuclei by arsenic in mice.
Folate deficiency increases background levels of DNA damage and can enhance the genotoxicity of chemical agents. Arsenic, a known human carcinogen present in drinking water supplies around the world, induces chromosomal and DNA damage. The effect of dietary folate deficiency on arsenic genotoxicity was evaluated using a mouse peripheral blood micronucleus (MN) assay. In duplicate experiments, male C57Bl/6J mice were fed folate-deficient or folate-sufficient diets for 7 weeks. During week 7, mice on each diet were given four consecutive daily doses of sodium arsenite (0, 2.5, 5, or 10 mg/kg) via oral gavage. Over the course of the study the folate-deficient diet produced an approximate 60% depletion of red blood cell folate. Folate deficiency by itself was associated with small but significant increases in MN in normochromatic erythrocytes (NCEs) and polychromatic erythrocytes (PCEs). Arsenic exposure was associated with significant increases in MN-PCEs in both folate-deficient and folate-sufficient mice. MN-PCE frequencies at the 10 mg/kg dose of arsenic were increased 4.5-fold over vehicle control in folate-deficient mice and 2.1-fold over control in folate-sufficient mice. At the 5 and 10 mg/kg doses of arsenic, MN-PCE levels were significantly higher (1.3-fold and 2.4-fold, respectively) in folate-deficient mice compared to folate-sufficient mice. Very few MN from either control or treated animals in either experiment exhibited kinetochore immunostaining, suggesting that the MN were derived from chromosome breakage rather than from whole chromosome loss. These results indicate that folate deficiency enhances arsenic-induced clastogenesis at doses of 5 mg/kg and higher.
Animals↗
Effects of nutritional folate deficiency on the adhesive properties of murine melanoma cells.
Folate deficient murine B16 melanoma cells adhered more rapidly and in higher percentages to plastic plates or dishes coated with laminin or fibronectin than folate replete cells. These changes in the adhesive properties of murine melanoma cells induced by nutritional folate deficiency were not mediated by changes in cell size, proliferative capacity or cell cycle distribution. While melanoma cells served as a suitable surface for prothrombinase complex formation, folate deficiency did not alter this membrane function, suggesting that the membrane changes associated with folate deficiency are relatively specific.
Animals↗
Uracil in human DNA from subjects with normal and impaired folate status as determined by high-performance liquid chromatography-tandem mass spectrometry.
A sensitive and selective method for determination of the uracil content in human DNA was first developed on the basis of high-performance liquid chromatography-tandem mass spectrometry. Uracil was excised from DNA using uracil DNA glycosylase. The released uracil was derivatized with 4-bromomethyl-7-methoxycoumarin, thereby forming bis-N,N'-(4-methylene-7-methoxycoumaryl)-uracil (uracil-MMC). 15N2-Uracil was used as an internal standard. The analytes were separated on an Adsorbsphere XL ODS column. A SCIEX API III tandem mass spectrometer equipped with a turbo ion-spray interface was used as the detector. Multiple reaction monitoring using the parent --> product ion combinations of m/z 489 --> 232 and 491 --> 233 were used to detect uracil-MMC and the internal standard, respectively. The detection limit for this assay is <1.0 x 10(-10) mol/L uracil, and the linearity is from 1.0 x 10(-10) to 2.5 x 10(-6) mol/L. The method was used for determination of uracil in human DNA. Our data show that the uracil levels in human DNA isolated from peripheral white blood cells did not differ between subjects with folate deficiency and subjects with normal red cell folate levels.
Base Composition↗
Folate affects apoptosis in human trophoblastic cells.
Effects of folate deficiency on the rate of apoptosis in human cytotrophoblastic cells has been investigated. Apoptosis was determined in cytotrophoblastic cells after culture in 1. control medium, 2. folate-free medium and 3. folate-free medium plus 10% fetal calf serum. Apoptosis rates in cells cultured in mediums 2 and 3 were significantly higher than those cultured in the control medium (P<0.02 and P<0.03, respectively). In conclusion, human cytotrophoblastic cells show a significantly increased rate of apoptosis in vitro after culture in a folate-free medium. Possible explanations for the association between folate deficiency and pregnancy complications are suggested.
Apoptosis↗
Deoxyuridine-suppression test and bone marrow culture for the diagnosis of macrocytic refractory anaemias.
Deoxyuridine (dU) suppression test and granulocyte macrophage colony forming unit (CFU-GM) assay were performed, along with morphological analysis, vitamin B12 and folate assays, in 22 cases of macrocytic anaemia corresponding to various types of idiopathic dysmyelopoietic syndromes. The dU suppressive effect was found to be normal in 19 cases, and slightly subnormal in 3 cases. The parallel study of the in vitro bone marrow growth showed, except in cases of primary acquired sideroblastic anaemia, a reduced number of colonies associated with a relative increase of the cluster formation. Consequently, these two parallel functional studies can support a formal diagnosis of potentially preleukaemic myelodysplasia, whatever may be the morphological pattern and even in cases of marked macrocytic anaemias and secondary epiphenomenal folate or vitamin B12 deficiency.
Anemia, Macrocytic↗
Significance of tests of iron nutrition in pregnancy.
Tests of iron and folate nutrition have been carried out in early pregnancy and at delivery in 63 Bantu females. Accepted normal values for serum iron, and percentage saturation of transferrin, but not for unsaturated iron-binding capacity, for non-pregnant subjects were found to apply equally well in pregnancy. Concomitant folate deficiency in early pregnancy did not render tests of iron deficiency less valid. The unsaturated iron-binding capacity, percentage saturation, and marrow iron stores in early pregnancy all showed a significant correlation with the haemoglobin value at term. Patients with normal marrow iron stores and a percentage saturation of transferrin of 20 or more at or before the 24th week are unlikely to become anaemic from iron deficiency during pregnancy.
Adult↗
Folate deficiency reduces the GPI-anchored folate-binding protein in rat renal tubules.
A folate-binding protein (FBP) anchored to cell membranes by a glycosyl phosphatidylinositol (GPI) adduct is constitutively expressed in some transformed and cultured cell lines. Its expression is upregulated when these cells are grown in medium containing low folate, but whether this occurs in vivo with nutritional folate deficiency is unknown. To address this question, the GPI-FBP in the liver, kidney, and brain of rats on control and folate-deficient (FD) diets was measured. The GPI-FBP in the kidney of FD rats decreased significantly in contrast to the upregulation of this protein in cultured cells. Northern blot analysis and nuclear run-on assays indicated that transcription of the GPI-FBP gene in the kidney was not reduced by folate deficiency. This decrease of the GPI-FBP appears to result from its proteolysis, similar to the enzymatic degradation of the apoprotein that occurs in vitro. Because the GPI-FBP is on the brush borders of the proximal renal tubules and provides for the reabsorption of folate, this function diminishes when the protein decreases in folate deficiency.
Animals↗
[Comparative study of the detection of plasma folate with microbial assay and radioimmunoassay].
OBJECTIVE: To compare two methods (microbial assay and radioimmunoassay) for measuring plasma folate concentrations, and to examine the relationship between plasma folate levels, and alcohol consumption, tobacco use and body mass index, and the risk of hyperhomocysteinemia in China. METHODS: We used a microtiter plate microbial assay and a radioimmunoassay to measure the folate concentration in 88 plasma samples. After comparing the results of these two methods and fitting a regression line, we examined the geographical, seasonal, and gender differences in folate concentration of plasma collected from 2,422 adults in south and north areas in China, and evaluated the association of plasma folate concentration, with alcohol consumption, cigarette smoking, and body mass index, and with the risk of hyperhomocysteinemia, using the data from the two assays. RESULTS: The data from the two assays had a linear relationship (r=0.879, P=0.000); the regression was Y=0.683X+0.308 (where X and Y were nature logarithmic transformations of plasma folate by microbial assay and radioimmunoassay, respectively); however, the mean plasma folate levels by microbial assay were much higher than those obtained by radioimmunoassay. Both data sets showed similar plasma folate distributions among Chinese adults, associations with other risk factors, and the risk of hyperhomocysteinemia. We estimated that 19.9% of the Southerners and 67.1% of the Northerners had plasma folate concentrations by radioimmunoassay lower than the 6.8 nmol/L used to define plasma folate deficiency. CONCLUSION: There is a linear relationship between plasma folate levels determined by microbial assay and radioimmunoassay, but because of the different levels obtained in the two assays, it is difficult to use the microbial assay results to evaluate folate status at this time. The use of 10.5 nmol/L as a cut-off for plasma folate deficiency by microbial assay needs further study.
Adult↗
Multivitamin prophylaxis in prevention of post-gastric bypass vitamin and mineral deficiencies.
One hundred forty patients were followed for a mean 24.2 months after gastric bypass. Postop multivitamin (MV) prophylaxis was recommended for all patients and 90 of 140 patients (64 percent) were regularly compliant. Deficiencies in iron, vitamin B-12 or folate were recognized in 88 of 140 patients (63 percent). Thirty of 45 patients (67 percent) with iron deficiency developed anemia. Forty-three of the 52 patients who did not have deficiencies were regularly taking MV vs 47 of 88 patients who developed deficiencies (P less than 0.001). MV prophylaxis was successful in preventing folate (P less than or equal to 0.05) and vitamin B-12 deficiencies (P less than or equal to 0.02) but did not prevent development of iron deficiency or subsequent anemia. There was no correlation between taking prescribed supplements and resolution of either iron deficiency of anemia. B-12 and folate supplements corrected deficiencies in 73 percent of cases. We conclude that oral MV prophylaxis is useful in preventing folate and B-12 deficiency after gastric bypass. Additional prophylactic iron supplements should be provided for women to prevent iron deficiency and associated anemia.
Anastomosis, Roux-en-Y↗
Bone marrow iron in nutritional anaemias.
Bone marrow smears of 168 patients with nutritional anaemias attending the Dr. J.C. Patel, Department of Hematology, K.E.M. Hospital were stained by Prussian blue method for iron (haemosiderin). Iron in the bone marrow was classified as absent, decreased, normal or increased. Amongst 93 cases with transferrin saturation (TS) of less than 16% and normoblastic erythropoiesis, bone marrow iron was absent in 48 (51.6%) and decreased in 45 (48.4%). In 50 cases with TS of less than 16% and marrow showing megaloblasts and/or giant myelocytes and metamyelocytes, bone marrow iron was absent in 15 (30%), decreased in 22 (44%), normal in 7 (14%) and increased in 6 (12%). In 25 cases with TS over 16% and megaloblastic erythropoiesis, bone marrow iron was absent in 4 (16%), decreased in 1 (4%), normal in 7 (28%) and increased in 13 (52%). In 150 (89.3%) patients out of 168, bone marrow iron and TS gave concordant results whereas in 18 (10.7%), the results were discordant; former was encountered in cases of uncomplicated iron deficiency while latter was found with megaloblastic morphology of the marrow. It is concluded that there is a good correlation between TS and bone marrow iron and hence, either of the criteria can be used for the diagnosis of iron deficiency especially when it is not complicated by megaloblastosis.
Anemia, Hypochromic↗
B12 and folate deficiency dementia.
Both B12 and folate deficiency have been linked to a dementia syndrome. In the case of B12, the neurologic sequelae may precede the hematologic by months to years. Treating a B12 deficient patient with folate or conversely a folate deficient patient with B12 may exacerbate the neurologic consequences of either deficiency. Iron deficiency is a frequent concomitant of both B12 and folate deficiency, often developing during replacement therapy. Patients with borderline B12 deficiency states have shown biochemical evidence of megaloblastosis and B12 replacement is recommended for those patients.
Aged↗
Folate status in the aged.
Folate deficiency has become a popular topic in geriatric literature recently. There are two main reasons for this interest: folate deficiency is prevalent among the elderly population, and many chronically ill elderly patients suffer from hematologic or neuropsychiatric disorders of which folate deficiency may be one of the causal factors. This article discusses serum, erythrocyte, and liver folate levels, the neurologic and psychiatric symptoms associated with folate deficiency, folate nutrition and absorption in the elderly, and the interrelationships of folate with vitamins, iron, and zinc.
Aged↗
Vitamin B12 deficiency is the primary cause of megaloblastic anaemia in Zimbabwe.
In a study of the pathogenesis and clinical features of megaloblastic anaemia in southern Africa, we evaluated 144 consecutive Zimbabwean patients with megaloblastic haemopoiesis. Vitamin B12 deficiency was diagnosed in 86.1% of patients and was usually due to pernicious anaemia; isolated folate deficiency accounted for only 5.5% of cases. Anaemia was present in 95.8% of patients; the haemoglobin (Hb) was < or = 6 g/dl in 63.9%. Neurological dysfunction was noted in 70.2% of vitamin B12-deficient patients and was most striking in those with Hb values > 6 g/dl. Serum levels of methylmalonic acid, homocysteine, or both, were increased in 98.5% of patients. Vitamin B12 deficiency is the primary cause of megaloblastic anaemia in Zimbabwe and, contrary to textbook statements, is often due to pernicious anaemia. Isolated folate deficiency is less common. As reported in industrialized countries 75 years ago, anaemia is almost always present and often severe. Neurological dysfunction due to vitamin B12 deficiency is most prominent in patients with mild to moderate anaemia.
Anemia, Megaloblastic↗