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Results for “Serum Folate Level”

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PubMed1988

The total serum homocysteine as an indicator of vitamin B12 and folate status.

Presented is a modification of an assay for total serum homocysteine (Hcy) in which the Hcy plus radioactive adenosine is converted enzymatically to labeled S-adenosylhomocysteine (AdoHcy). The modifications included a commerical source for the AdoHcy hydrolase, adenosine labeled with either 14C or 3H, and separation of the AdoHcy by thin layer chromatography. The assay was sensitive to 25 pmol. Hcy levels in sera from 18 controls ranged from 6.9 to 12.1 mumol/L with a mean of 9.1 and a SD of 1.5 mumol/L. The total serum Hcy was increased in vitamin B12 and folate deficiency. The level was high in congenital defects of vitamin B12 metabolism, blocking the methylation of Hcy regardless of the serum vitamin B12 levels, but was normal in the absence of tissue deficiency even if the serum vitamin B12 levels were low. The procedure has been found practical in two years of use and requires only 0.1 mL of serum.

Adenosine↗

PubMed1993

Lactate dehydrogenase levels during MACOP-B chemotherapy for non-Hodgkin's lymphoma.

Lactate dehydrogenase (LD) levels rose consistently during MACOP-B chemotherapy for intermediate and high-grade non-Hodgkin's lymphoma (NHL). Levels peaked at week nine and fell to normal within six weeks of completion of therapy. Isoenzyme patterns, studied prospectively in seven patients, showed a parallel rise in LD1 and LD2 suggesting a source other than tumour tissue for the rise in total LD. In the absence of evidence of myocardial or renal damage, haematopoietic tissue was the most likely source. With no evidence of haemolysis, normal serum levels of vitamin B12 and folate and normal red cell folate, dyserythropoiesis was considered to be the underlying mechanism. A rising mean corpuscular volume further reinforced this suggestion. Intensive use of methotrexate along with co-trimoxazole as prophylaxis against pneumoycystis carinii is considered the most likely cause of marrow dysfunction. Failure to recognise that rising LD levels during such therapy is treatment-related, rather than of tumour origin, may lead to inappropriate change or abandonment of therapy.

Adult↗

PubMedDate not supplied

Jejunal surface pH measurements in tropical sprue.

The mucosal surface pH of jejunal biopsy samples incubated in vitro in Krebs-phosphate buffer was measured. Biopsies from 7 healthy individuals or tropical sprue subjects in complete remission had a mean surface pH of 5.8 +/- 0.09, similar to values for normal Caucasian subjects living in the UK. The mean surface pH of biopsies from 20 sprue patients, 6.0 +/- 0.08, was significantly higher (P less than 0.05) than that of the control subjects. Sprue patients could be sub-divided into those with 2 or more abnormal results in 3 intestinal function tests, and those with one or no abnormal test. The 9 low scorers showed a mean surface pH of 5.75 +/- 0.06 resembling the control mean, whereas the 11 high scorers had a higher (P less than 0.01) mean surface pH of 6.17 +/- 0.08. Mucosal surface pH correlated directly with 3 d mean faecal fat excretion and inversely with xylose and vitamin B12 absorption values but not with the nutritional indicators serum albumen, folate or blood haemoglobin levels. As in coeliac disease, mucosal surface pH in the jejunum is elevated above normal in tropical sprue and may reflect the extent to which normal ion transport processes are affected.

Feces↗

PubMed2004

Effect of fenofibrate-mediated increase in plasma homocysteine on the progression of coronary artery disease in type 2 diabetes mellitus.

The Diabetes Atherosclerosis Intervention Study (DAIS) examined the effects of fenofibrate or placebo on the progression of coronary artery disease (CAD) in 418 type 2 diabetic subjects with dyslipidemia. Fenofibrate use was associated with a 6% increase in high-density lipoprotein cholesterol, a 28% decrease in triglycerides, a 5% decrease in low-density lipoprotein cholesterol, and a 55% increase in plasma homocysteine (tHcy). The purpose of the present study was to determine whether this increase in tHcy in the fenofibrate group was associated with CAD progression or with clinical events. The increase in tHcy with fenofibrate (n = 207) was not related to changes in factors known to modulate tHcy levels (serum levels of Vitamin B(12), folate, or renal function). CAD was quantified by angiography at baseline and after a minimum of 3 years of therapy with fenofibrate or placebo. The primary end point was change in mean segment diameter (MSD), minimal lumen diameter, and percent stenosis. Baseline tHcy level was correlated with percent diameter stenosis (r = 0.111, p = 0.028). Baseline, but not end-of-study elevated tHcy levels, decreased the beneficial effect of fenofibrate. Unexpectedly, the final tHcy levels correlated negatively with CAD progression (r = -0.111, p = 0.031) in the overall group. In the fenofibrate group, there was no significant correlation between tHcy and minimal lumen diameter (r = -0.135, p = 0.069), or percent stenosis. An increase in tHcy levels was not correlated with adverse clinical events in the fenofibrate group. This analysis of the the DAIS reveals that the fenofibrate-mediated increase in tHcy levels does not attenuate the beneficial effects of fenofibrate on CAD progression or clinical events.

Aged↗

PubMed1997

Homocysteine in sickle cell disease: relationship to stroke.

PURPOSE: The risk factors and pathophysiology of stroke and other serious complications of sickle cell disease (SCD) are poorly defined. Hyperhomocysteinemia has recently been identified as a risk factor for stroke and other vascular diseases in the general population, however its role in SCD has not been investigated. PATIENTS AND METHODS: We measured serum homocysteine and red cell folate levels in 100 patients with SCD, including 16 patients with stroke. A disease severity score was determined for all patients and those without stroke were classified into mild (44 patients) or severe (40 patients) disease groups. RESULTS: Homocysteine levels for the stroke group (median 13.3 mumol/L, mean 13.1 +/- 4.3 mumol/L) were significantly higher than those in patients without stroke (median 9.7 mumol/L, mean 10.7 mumol/L) (P < 0.02), and on multiple regression analysis homocysteine level was independently correlated with stroke (P < 0.026). Homocysteine and folate levels were inversely correlated (r = -0.41, P < 0.00005). Using logistic regression, the odds ratio for stroke in patients with homocysteine levels above the median (10.1 mumol/L) was 3.5 in this group of patients (95% confidence interval 1.1 to 11.9). CONCLUSION: High homocysteine levels may be a risk factor for development of stroke in SCD patients. The role of homocysteine in the pathogenesis of stroke in SCD needs to be examined in a longitudinal, prospective study.

Adolescent↗

PubMed1998

High third-trimester ferritin concentration: associations with very preterm delivery, infection, and maternal nutritional status.

OBJECTIVE: To determine whether a high concentration of serum ferritin during the third trimester is a marker of subclinical maternal infection and very preterm delivery and is associated with maternal nutritional status. METHODS: A total of 1162 gravidas was followed prospectively from entry to prenatal care (15.0 +/- 4.9 completed weeks' gestation) in Camden, New Jersey, between 1985 and 1995. Multiple logistic regression and analysis of covariance were used to examine the influence of serum ferritin on the outcomes of interest. RESULTS: High concentrations of serum ferritin (at or above the 90th percentile) at week 28, but not at entry to prenatal care, increased risk of preterm and very preterm delivery, but the risk changed if the concentration of ferritin declined from entry. If the concentration declined as expected, high ferritin concentration had no influence on outcome. If the concentration increased, then high ferritin concentration at week 28 was associated with very preterm delivery (adjusted odds ratio [AOR] 8.77; 95% confidence interval [CI] 3.90, 19.72), preterm delivery (AOR 3.81; 95% CI 1.93, 7.52), low birth weight (AOR 5.15; 95% CI 2.47, 10.72), clinical chorioamnionitis (AOR 2.56; 95% CI 1.01, 6.52), and symptoms of "flu" as an index of unmeasured infection (AOR 6.02; 95% CI 1.16, 31.17). Factors associated with failure of the ferritin concentration to decline included iron deficiency anemia earlier in pregnancy (AOR 3.98; 95% CI 1.17, 8.98) and lower levels of serum and red cell folate. CONCLUSION: High serum ferritin concentration in the third trimester, resulting from a failure of ferritin to decline, is associated with very preterm delivery and markers of maternal infection. Iron deficiency anemia and other indicators reflecting poor maternal nutritional status earlier in pregnancy underlie this relationship.

Adolescent↗

PubMed1997

Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid.

Elevated plasma homocysteine, an independent risk factor for cardiovascular disease (CVD) can be lowered by administration of pharmacological doses of folic acid. The effect of lower doses in apparently normal subjects is currently unknown but is highly relevant to the question of food fortification. Healthy male volunteers (n = 30) participated in a chronic intervention study (26 weeks). Folic acid supplements were administered daily at doses increasing from 100 micrograms (6 weeks), to 200 micrograms (6 weeks), to 400 micrograms (14 weeks). Fasting blood samples collected before, during and 10 weeks post intervention were analysed for plasma homocysteine, serum and red-cell folate levels. Results, expressed as tertiles of baseline plasma homocysteine concentration, showed significant (p < or = 0.001) homocysteine lowering in the top (10.90 +/- 0.83 mumol/l) and middle (9.11 +/- 0.49 mumol/l) tertiles only. In the low tertile, where the mean baseline homocysteine level was 7.07 +/- 0.84 mumol/l, no significant response was observed. Of the three folic acid doses, 200 micrograms appeared to be as effective as 400 micrograms, while 100 micrograms was clearly not optimal. There is thus a minimal level of plasma homocysteine below which folic acid has no further lowering effect, probably because an optimal folate status has been reached. A dose as low as 200 micrograms/day of folic acid is effective in lowering plasma homocysteine concentrations in apparently normal subjects. Any public health programme for lowering homocysteine levels, with the goal of diminishing CVD risk, should not be based on unnecessarily high doses of folic acid.

Adult↗

PubMed1989

Hematologic complications of gastric bypass for morbid obesity.

Of 530 patients who have had a gastric bypass operation for morbid obesity at Allegheny General Hospital, 41 had decreases in serum iron, vitamin B12, and/or folate levels. These abnormalities were detected eight months to eight years (median, two years) after the operation. The hemoglobin level ranged from 7.4 to 14.1 gm/dl at the time of detection, and mean corpuscular volume (MCV) ranged from 58 to 119 cu microns. The most common problem was combined iron and vitamin B12 deficiencies. Physicians should be aware that folate, vitamin B12, and iron deficiencies occur after gastric bypass, though the time to development is variable. Hemoglobin level and MCV are not predictive of these deficiencies.

Anemia, Hypochromic↗

PubMed1983

Studies on the haemopoietic toxicity of nitrous oxide in man.

Nitrous oxide inactivates vitamin B12 and in man can produce a megaloblastic anaemia. Haematological and biochemical changes were studied in nine surgical patients ventilated with 70% N2O for up to 24 h and in three control patients. There was a rise in the numbers of hypersegmented neutrophils in peripheral blood following N2O. Serial bone marrow aspirates showed gross megaloblastic change after 24 h of N2O which had reverted to normoblastic but dyserythropoietic haemopoiesis by 1 week. Giant forms of early myeloid precursors were also seen after 24 h ventilation with N2O but by 1 week abnormalities were evident in more mature cells, metamyelocytes and segmented neutrophils. Megaloblastosis was associated with abnormal dU suppression which showed a correction pattern similar to that seen in vitamin B12 deficiency. Administration of N2O was also associated with a progressive rise in serum folate and fall in serum methionine levels. No similar patterns were seen in the three control patients.

Anesthesia, General↗

PubMed1994

Teratogenic effects of antiepileptic drugs: implications for the management of epilepsy in women of childbearing age.

Exposure to antiepileptic drug (AED) treatment in utero occurs in 1 of every 250 newborns. The absolute risk of major malformations in these infants is about 7-10%, approximately 3-5% higher than in the general population. Specific risk factors include high maternal daily dosage or serum concentrations of AED, low folate levels, polytherapy, and generalized seizures during pregnancy. Adverse pregnancy outcomes, including congenital heart malformations, facial clefts, spina bifida aperta, hypospadias, growth retardation, and psychomotor and mental retardation, are associated with, although not necessarily caused by, AED exposure. Specific cognitive defects, hypertelorism, and nail hypoplasia can be causally related to specific AED exposures. To prevent teratogenic side effects, the prospective mother should be treated with AEDs only when absolutely necessary. Monotherapy with the AED that is most effective in the lowest possible daily dose (divided into at least two or three administrations) should be prescribed. High-dose folate supplementation (4-5 mg/day) reduces the risk of a neural tube defect in a child whose sibling had such a defect, but its impact on the specific teratogenic risks of AEDs is unknown. A substantial proportion of fetal malformations may be secondarily prevented by prenatal diagnosis, consisting of a fetal structural ultrasound examination at weeks 18 and 20 of gestation and, with VPA or CBZ administration, an alpha 1-fetoprotein analysis of amniotic fluid at week 16. Determination of a specific defect prevention strategy depends largely on parental attitudes toward prenatal diagnosis and termination of pregnancy, which should be discussed before conception.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗

PubMed1979

Acquired stomatocytosis in alcoholic liver disease.

The occurrence of transient stomatocytosis observed on peripheral blood smears and by scanning electron microscopy, was studied in 100 alcoholic patients admitted to a general medical ward. 15% of the patients manifested marked stomatocytosis, i.e. 10% or more of the cells being stomatocytes and a further 29% had slight stomatocytosis (3--9%). All patients with marked stomatocytosis had a daily average ethanol ingestion of 100 g or more, and had also more pronounced histological and biochemical evidence of alcoholic liver disease than those lacking stomatocytosis. MCV was significantly higher in these patients, but there were no differences in Hb, serum B12, folate, cholesterol or triglyceride levels. The stomatocytosis subsided gradually during 4--6 weeks of abstinence. Triconcave cells (knizocytes) were observed in 2 patients with terminal alcoholic liver disease. Along with an increased MCV, the presence of stomatocytosis may be a useful erythrocyte indicator of alcoholic liver disease.

Adult↗

PubMed1975

Motor nerve conduction study in patients on diphenylhydantoin therapy.

Mean motor conduction velocity of posterior tibial nerves was significantly reduced in epileptic patients treated with diphenylhydantoin formore than 10 years or in patients with serum diphenylhydantoin level above 20 mug/ml. Subnormal serum folate was not responsible for this reduction and clinical peripheral neuropathy was infrequent.

Adolescent↗

PubMed2004

Serum vitamin B12 and folic Acid levels in acute cerebral atherothrombotic infarction.

Hyperhomocysteinemia is an independent risk factor for atherothrombotic cerebral stroke. Vitamin B12 and folic acid are important determinants of homocysteine metabolism. We aimed to evaluate the relationship, if present, between vitamin B12 and folic acid levels and acute cerebral stroke in this study. Blood aliquots drawn within 24 hours after the stroke from hospitalized patients (n=66) with the diagnosis of acute ischemic cerebrovascular episode and also blood samples from 38 healthy controls without any vascular risk factor were analyzed. With a competitive, chemoluminescence assay, serum levels of vitamin B12 and folic acid were measured in blood samples taken within 24 hours after the stroke. The differences and correlations were tested using frequency test, student-t test and multivariate analysis. Mean serum vitamin B12 levels were significantly lower in the patients than in the control subjects, 245.40 (S.D.: 72.9) and 343.2 (S.D.: 113.0) pg/ml respectively (p=0.0001). This difference was independent from other risk factors. Likewise, mean serum folic acid levels were lower in the patients than in the control subjects, 4.62 (S.D.: 1.94) and 5.97 (S.D.: 1.19) ng/ml, respectively (p=0.003). Mean serum levels of vitamin B12 and folate at the convalescence phase were 253.05 (S.D.: 68.78) pg/ml and 4.48 (S.D.: 2.08) ng/ml, respectively; the values obtained at the acute phase were not significantly different from the values obtained at the convalescence phase. We conclude that low vitamin B12 and folic acid concentrations are associated with an increased risk of stroke, and the relationship for vitamin B12 is independent from the other known modifiable stroke risk factors. For understanding the effects of B12 and folate in stroke patients, more detailed follow-up studies with long period are needed.

Acute Disease↗

PubMed1989

Dietary folate as a risk factor for neural-tube defects: evidence from a case-control study in Western Australia.

A population-based case-control study was conducted to test the hypothesis that the risk of the occurrence of neural-tube defects in infants with no other birth defects (isolated neural-tube defects) is associated inversely with the maternal dietary intake of free and/or total folate in early pregnancy. Information was collected from the mothers of 77 case subjects with isolated neural-tube defects who were born in Western Australia from 1982 to 1984, from the mothers of 77 control subjects with birth defects other than neural-tube defects (control group 1) and from the mothers of 154 control subjects with no birth defects (control group 2). The case and control subjects were matched individually by the date of the mother's last menstrual period. Odds ratios were adjusted for a number of potentially-confounding variables, such as the country of birth of the parents, paternal social class, previous pregnancy outcome, interval between index and previous pregnancy and pregnancy order. Crude and adjusted odds ratios showed a protective effect of an increasing intake of free folate in the first six weeks of pregnancy. Adjusted odds ratios, with reference to the lowest quartile of intake, (and their 95% confidence intervals) were 0.72 (0.25-2.08), 0.37 (0.11-1.23) and 0.31 (0.10-0.97) for quartiles 2-4 when control group 1 was used, and 0.44 (0.17-1.13), 0.34 (0.13-0.90) and 0.16 (0.06-0.49) when control group 2 was used. Similar, but weaker, trends were seen when total folate intake was the exposure variable. These findings support the hypothesis that the dietary intake of folate in early pregnancy protects against the occurrence of isolated neural-tube defects in infants. Measures of postpartum dietary folate and of postpartum serum and red-cell folate levels showed no association with the occurrence of neural-tube defects in infants.

Diet↗

PubMed2000

Chemopreventive effects of dietary folate on intestinal polyps in Apc+/-Msh2-/- mice.

Epidemiological and animal studies (reviewed in Y. I. Kim, J. Nutr. Biochemistry, 10: 66-88, 1999; J. B. Mason and T. Levesque, Oncology, 10: 1727-1743, 1996) suggest that dietary folate intake is inversely related to the risk of colorectal cancer. However, the optimal timing of folate intervention and mechanisms by which folate modulates colorectal carcinogenesis have not been clearly established. A recently developed murine model of intestinal tumorigenesis, which carries a heterozygous mutation in the Apc gene and a null mutation in the Msh2 gene (Apc+/-Msh2-/-), was used to determine the effect of dietary folate on intestinal tumorigenesis. Apc+/- Msh2-/- mice were randomized to receive either 0 or 8 mg of folate/kg diet starting at either 3 or 6 weeks of age. The 3- and 6-week diet starts represent intervention before and after the establishment of neoplastic foci, respectively. At 11 weeks of age, mice were killed, and the small intestines and colons were analyzed for adenomas and aberrant crypt foci (ACF). Serum folate concentrations were determined by a standard microbiological assay. Genomic DNA methylation was assessed by in vitro [3H]methyl incorporation into hepatic DNA and by a methyl-sensitive restriction digestion method. Microsatellite instability was determined in matched normal and polyp DNA from the small intestine and colon at 5 loci. Serum folate concentrations accurately reflected dietary folate levels (P < 0.005). Folate supplementation, started before the establishment of neoplastic foci, significantly decreased the number of small intestinal adenomas (by 2.7-fold; P = 0.004) and colonic ACF (by 2.8-fold; P = 0.028) and colonic adenomas (by 2.8-fold; P = 0.1) compared with a moderate degree of folate deficiency. In contrast, a moderately folate-deficient diet, started after the establishment of neoplastic foci, significantly reduced the number of small intestinal adenomas (by 4.2-fold; P = 0.001) but had no effect on colonic ACF and adenomas compared with folate supplementation. Genomic DNA methylation and microsatellite instability do not seem to play a major role in folate-modulated intestinal and colonic tumorigenesis in this model. In conclusion, in this murine model, dietary folate supplementation significantly protects against small intestinal and colorectal tumorigenesis if it is provided before the establishment of neoplastic foci However, if it is provided after the establishment of neoplastic foci, dietary folate seems to have an opposite effect. These data suggest that the timing of folate intervention is critical in providing an effective and safe chemopreventive effect on intestinal tumorigenesis. Notwithstanding the limitations associated with this model, our data suggest that the optimal timing of folate intervention must be established before folate supplementation can be used as a safe chemopreventive agent against colorectal cancer.

Adenoma↗

PubMed1976

Thrombocytosis in patients with celiac sprue.

In 57% of the patients (12 of 25) seen with celiac sprue, as shown by clinical course and small bowel biopsy, peripheral blood thrombocytosis was present (range: 350,000 to 815,000 platelets per mm(3); mean: 546,000 +/- 44,060 SE). After clinical and histological remission, the platelet counts in these patients fell significantly (range: 188,000 to 300,0000 platelets per mm(3); mean 252,750 +/- 13,211 SE). There was no correlation between thrombocytosis and serum iron, folate, or vitamin B12 levels. Celiac sprue joins inflammatory bowel disease among gastrointestinal disorders as a consideration in the differential diagnosis of thrombocytosis. In these patients, thrombocytosis reflected active disease and was not present during remission. Evaluation of peripheral blood platelets may be useful in the assessment of patients with celiac sprue.

Adult↗

PubMed1998

The nutritional health of New Zealand vegetarian and non-vegetarian Seventh-day Adventists: selected vitamin, mineral and lipid levels.

AIM: To determine whether adult non-vegetarian Seventh-day Adventists differ in selected nutrition related health aspects from adult vegetarian Seventh-day Adventists. METHODS: One hundred and forty-one Seventh-day Adventist church members responded to a general health questionnaire. Forty-seven sex and age matched subjects (23 non-vegetarians and 24 vegetarians) were selected for further investigation. Blood lipids, serum vitamin B12, folate, haemoglobin and ferritin levels were measured along with stature, weight and blood pressure. A quantitative 7-day diet record was also completed. RESULTS: Body mass index was similar between the non-vegetarian and vegetarian groups but diastolic blood pressure was higher for non-vegetarian than vegetarian males. Even though the dietary vitamin B12 intake was significantly lower (p < 0.01) in the vegetarian group both vegetarians and non-vegetarians recorded similar serum vitamin B12 levels. The vegetarian and non-vegetarian groups had similar haemoglobin concentrations. While dietary iron intake was higher in the female vegetarian group, though predominantly in the non-haem form, the difference was not significant. Low serum ferritin levels were found in both female dietary groups even though the vegetarian group had a significantly (p < 0.05) higher vitamin C intake. Blood lipid levels were similar in the two diet groups even though the vegetarian group had a lower percentage energy contribution from total and saturated fat (p < 0.01) and consumed significantly less cholesterol. CONCLUSION: Both non-vegetarian and vegetarian Seventh-day Adventists appear likely to enjoy a lower risk of nutrition related chronic degenerative disease than the average New Zealander and have a satisfactory iron and vitamin B12 status.

Adult↗

PubMed1999

Whole blood folate, homocysteine in serum, and risk of first acute myocardial infarction.

High level of total homocysteine (tHcy) is a risk factor for coronary artery disease (CAD), but the mechanism is not known. The serum concentration of tHcy, total cholesterol, high density lipoprotein cholesterol (HDL-C), and apolipoprotein A-I (apo A-I) and the concentration of folate in whole blood were measured in 107 patients with first acute myocardial infarction (MI) and 103 controls. The level of whole blood folate was lower and that of tHcy higher in cases than in controls. An increase of 50 nmol/l whole blood folate was associated with an OR for MI of 0.75, and an increase of 5 micromol/l tHcy with an OR for MI of 1.57. Correlations were observed between the levels of whole blood folate and tHcy and between whole blood folate and alcohol intake, and in MI cases, between tHcy, HDL-C, and apo A-I as well as between HDL-C and alcohol intake. The number of cigarette smokers was higher among cases than controls. In smokers, the level of tHcy was higher and that of whole blood folate lower than in non-smokers. After adjustment for smoking, the whole blood folate and tHcy-associated risks of MI became non-significant. We conclude that smoking may affect folate status and tHcy level adversely. The risk of MI in smokers may at least partly be attributed to hyperhomocysteinemia or low folate.

Age Distribution↗