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In an open study the influence of a pure iron-therapy (Aktiferrin) and a combined iron-folic-therapy (Aktiferrin F) on the blood and the folate levels in the serum of 60 anaemic pregnant women was compared. The prophylactic administration and the therapy of iron and folate acid in pregnancy is demanded because of the results of this examination.
BACKGROUND: Hyperhomocysteinemia, associated with low folate and low B12 levels, is known to be an independent risk factor for atherosclerosis. Only a few available data has been demonstrated in Thai patients. OBJECTIVE: To evaluate serum fasting homocysteine, folate and B12 levels whether to see they are associated with coronary artery disease (CAD). METHOD AND RESULT: Three hundred and one consecutive suspected CAD patients who underwent coronary angiography at the Police General Hospital were studied. The mean age of the patients, 195 males and 106 females, was 63.0 +/- 10.0 year (range 39-85). A total of 218 patients were angiographically demonstrated as having CAD. The mean serum homocysteine level of CAD patients had a non significant higher level than those of 83 non CAD patients: 11.4 +/- 6.2 vs 10.2 +/- 4.2 umol/L, p = 0.06. Means of folate and B12 level in the CAD patients and non CAD patients were 6.6 +/- 4.6 vs 7.0 +/- 4.3 nmol/L, p = 0.49 and 650.9 +/- 415.4 vs 613.3 +/- 443.2 pmol/L, p = 0.56 respectively. No significant correlations were found between homocysteine with folate and B12 levels. Logistic regression analysis showed a significant association between homocysteine and CAD with OR = 1.08 (95%CI, 1.01-1.16), p = 0.03 after being adjusted for age, sex, DM, HT history of hyperlipidemia, smoking, BMI, folate and B12 levels. No significant association between homocysteine level with the number of coronary vessel stenosis, age, BMI, DM, HT smoking and history of hyperlipidemia was observed in the present study. CONCLUSION: Hyperhomocyteinemia, but not folate and B12 levels, may be an independent risk factor for coronary artery disease in Thai patients.
BACKGROUND: Hyperhomocysteinemia is an independent risk factor for cardiovascular events. The aim of this study was to show the results of the reduction of homocysteine in end stage renal failure patients on hemodialysis, as it is known, have higher levels of homocysteine than other groups of subjects. METHODS: Plasma homocysteine concentration was determined before and after the administration of vitamin B6 and folic acid in 12 patients (males: 6) on regular dialysis therapy. Mean monthly fasting serum concentrations of total cholesterol (TCHOL), HDL-chol, LDL-chol and triglycerides (TRG) were determined for a period 68 months (12-120 months) before and 26 months after the administration of vitamin B6 and folic acid. RESULTS: Mean serum concentrations for folic acid and vitamin B12 before and after the administration were: folic acid: 5.03 +/- 4.9 and 18.0 +/- 19.2 ng/mL, (p < 0.0001) and B12: 456 +/- 257 and 514.38 +/- 307 pg/mL respectively). Plasma homocysteine was reduced significantly after the administration of above drugs (from 47 +/- 14 to 29 +/- 9 micromol/mL, p < 0.001). This reduction of homocysteine resulted in a modification of the patients' lipidemic profile: Serum LDL-chol was decreased significantly (119 +/- 38 mg/dL to 110 +/- 35 mg/dL, p<0.005). TCHOL and TRG were also decreased but not significantly (190 +/- 45 mg/dL to 187 +/- 43 mg/dL and 116 +/- 63 mg/dL to 108 +/- 47 mg/dL respectively)). Serum concentrations HDL-chol were increased significantly (from 42 +/- 10 mg/dL to 47 +/- 10 mg/dL, p < 0.001). The atherogenic index for cholesterol, LDL/HDL, was 1.6 times lower after the drugs receiving (before: LDL/HDL = 3.1 and after: LDL/HDL = 2.5, p < 0.001). CONCLUSIONS: These results indicate that the folate and vitamin B6 supplementation resulted in reduction of homocysteine levels and improvement of lipidemic profile in regular dialysis patients.
BACKGROUND: A high prevalence of hyperhomocysteinemia has been reported in type II diabetic patients with documented vascular disease; hence the hypothesis that hyperhomocysteinemia may contribute to overall mortality in diabetic patients. The link between insulin and homocysteine metabolism has not been completely clarified yet; in particular, only few data are available on the effects of insulin in vivo on homocysteine metabolism in the presence of abnormalities of sulphur amino acid metabolism (methionine intolerance). MATERIALS AND METHODS: To establish whether methionine intolerance and which of its determinants could influence total plasma homocysteine in response to insulin infusion in vivo in type II diabetic patients, we submitted 18 patients (Group A) with normal and 18 patients with abnormal (hyperhomocysteinemia) (Group B) response to oral methionine load to a glucose/clamp study. At time 0, and 30, 60 and 120 minutes after hyperinsulinemia, homocysteine and methionine plasma levels were assessed. In order to evaluate the cause of methionine intolerance, all patients were assayed for fasting homocysteine-cysteine ratio (as a marker of suspected heterozygosis for cystathionine-beta-synthase deficit), MTHFR C (677)T status and homocysteine-related vitamin status (serum vitamin B (6) [PLP], vitamin B (12) and folate). RESULTS: After hyperinsulinemia, plasma methionine was reduced (by about - 30 % at 120 minutes vs. basal values) within both groups, whereas tHcy tend to decrease in group A following insulin administration (up to - 6.6 +/- 3.6 % vs. basal values at 120 minutes) with a significantly higher variability, while in patients with "methionine intolerance" (group B) tHcy tended to increase (up to + 29.05 +/- 8.3 % vs. basal values at 120 min from the clamp). Serum folic acid (7.45 +/- 2.8 vs. 4.82 +/- 2.5 nmol/L, p < 0.05), Vit. B (12) (348 +/- 78 vs. 242 +/- 65 pmol/L, p < 0.05) and PLP (84.1 +/- 23.6 vs. 50.6 +/- 32.4 nmol/L; p < 0.01) were significantly higher in group A than in group B; PLP levels significantly correlated with homocysteine after 4 h methionine load (n = 36; r = - 0.327, p < 0.05); group A showed also a significantly lower prevalence of suspected heterozygosis for cystathionine-beta-synthase deficit (1/18 [11.1 %] vs. 5/18 [33.3 %], p < 0.05) and MTHFR T allele presence (4/18 [22.2 %] vs. 11/18 [61.1 %], p < 0.01). A stepwise regression analysis with tHcy plasma level variations (event A = reduction; event B = increase) as the dependent variable showed that low serum folate and PLP levels and presence of MTHFR T allele were the variables associated with insulin-induced tHcy increase. CONCLUSIONS: Methionine intolerance may influence the effect of insulin administration on plasma homocysteine in patients affected by type 2 diabetes. To prevent a possible acute (and repeated) hyperhomocysteinemia due to insulin administration in cases of methionine intolerance, it may be useful to assess the presence of methionine intolerance (tHcy after oral methionine loading) and Hcy-related vitamin status in all patients due to be subjected to insulin therapy.
OBJECTIVES: To determine the frequency of serum cobalamin (Cbl) deficiency and to clarify the biologic importance of low screening Cbl levels in patients with multiple sclerosis (MS) and idiopathic myelopathy (MYL). BACKGROUND: A significant association between Cbl metabolism and MS has been postulated based on the observations that patients with MS have lower serum Cbl levels, higher unsaturated Cbl binding capacities, and a higher prevalence of macrocytosis than do normal controls. Whether such observations have biologic importance as documented by abnormal accumulation of metabolites that would result from Cbl deficiency has not yet been determined. METHODS: Serum Cbl and folate levels were determined in 208 consecutively evaluated patients seen in an outpatient MS clinic setting during a 7-month period. Necessary blood samples were obtained for 165 of these patients. One hundred twenty-five patients had clinically definite MS, 31 had clinically probable MS, and nine had MYL. Serum methylmalonic acid (MMA) and homocysteine (HCY) concentrations, which rise in biologically severe Cbl deficiency, were subsequently determined in all patients whose Cbl levels were lower than 301 pg/mL. RESULTS: A Cbl level lower than 301 was found in 32 of 156 patients with either clinically definite MS or clinically probable MS but in none of the patients with MYL. Elevated MMA or HCY levels were found in seven of 32 patients with either clinically definite MS or clinically probable MS, six of whom had an elevated HCY level and one of whom had elevated HCY and MMA levels. CONCLUSIONS: Despite the observation that 32 (19.4%) of 165 of these patients with MS and MYL had screening Cbl levels less than 301 pg/mL, only seven (4.2%) of 165 had elevated MMA or HCY levels. The frequency of biologically severe Cbl deficiency in these patients with MS and MYL was very low.
In a group of haemodialysis patients who were iron loaded secondary to parenteral iron administration a slight but significant increase in red cell size was noted when compared to a normal population. This macrocytosis was not related to serum B12 or folate levels, or to the reticulocyte count. On stopping iron therapy both mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH) values declined significantly as did serum ferritin and iron levels. Bone marrow smears were of normal or increased cellularity. When iron therapy was discontinued there was a steady fall in serum ferritin levels without a drop in haemoglobin values suggesting that the excess iron was available for haemopoiesis. These findings suggest that the increase in red cell size in this group of patients may have been induced directly by iron overload.
Neutrophil hypersegmentation is an expected peripheral blood smear finding in megaloblastic anemias. But some clinical reports suggest that neutrophil hypersegmentation may also occur in patients with iron deficiency anemia. In this study we searched the presence of neutrophil hypersegmentation and thrombocytosis in patients with iron deficiency anemia but who had normal serum vitamin B12 and folic acid levels. The study comprised 102 patients with iron deficiency anemia and 21 age-matched healthy controls. All routine tests for iron deficiency anemia were done, serum folate and cobalamin levels were measured, and platelets were counted in all patients and controls. Peripheral blood smears were examined for neutrophil hypersegmentation. Hypersegmentation was found in 30.4% of anemic patients and in 9.5% of controls (p < 0.05). The number of platelets was also significantly higher in anemic children (p < 0.05). These results show that neutrophil hypersegmentation may also be seen in patients with iron deficiency anemia, and thrombocytosis is a common laboratory finding in this disorder.
A serum cobalamin level lower than 250 pmol/l combined with high values of plasma homocysteine and serum methylmalonic acid confirms the diagnosis of vitamin B12 deficiency. A low serum and erythrocyte folate level and high plasma homocysteine confirm folate deficiency. If the cobalamin level is higher than 250 pmol/l no further tests are needed. In patients with neurologic or psychiatric disorders combined with elevated levels of homocysteine and methylmalonic acid, cobalamin deficiency is likely if these levels decrease during vitamin B12 therapy. The causes of elevated homocysteine levels are often obscure, and homocysteine should therefore not be used as a screening test.
BACKGROUND: Fortification of cereal-grain products was introduced in 1941 when iron and three vitamins were added to flour and bread. Ready-to-eat cereals were fortified at about the same time. These fortifications have contributed to increased dietary iron intake and reductions in iron deficiency anemia in the US. In 1996, FDA finalized rules for fortification of specific enriched cereal-grain products with folic acid. This measure was instituted to increase the folate intakes of women of child-bearing age and thereby reduce the risk of having a pregnancy affected with a neural tube birth defect. However, with recent increases in fortification, public health officials in the US are concemed that excess intake of specific nutrients such as iron and folic acid may result in toxic manifestations. OBJECTIVE: Our objective was to measure iron and total folate content in breakfast cereals and compare assay to label values for % Daily Value. We also determined by weight the amount of a ready-to-eat breakfast cereal adults would eat and compared this to the labeled serving size, for which the reference amount for this cereal per eating occasion was 1 cup or 30 g. DESIGN: Twenty-nine breakfast cereals were analyzed for iron content using the bathophenanthroline reaction. Twenty-eight cereals were analyzed for total folate, utilizing a microbiological assay with tri-enzyme digestion. Serving size quantities were estimated in seventy-two adults who regularly ate breakfast cereal and were asked to fill a 16 or 22 cm round bowl with the amount of cereal that they would consume for breakfast. RESULTS: When the labeled value was compared to the assayed value for iron content 21 of the 29 breakfast cereals were 120% or more of the label value and 8 cereals were 150% or more of the label value. Overall, analyzed values for iron ranged from 80% to 190% of label values. Analyzed values for folate ranged from 98% to 320% of label values. For 14 of 28 cereals, analyzed values exceeded label declarations by more than 150%. Bran-containing cereals contained the highest amounts of folate relative to their label declarations. The median analyzed serving size for the breakfast cereal was 47 g for females, 61 g for males with a combined median of 56 g as compared to the label value of 30 g. CONCLUSIONS: Analyzed values of iron and folic acid in breakfast cereals were considerably higher than labeled values. For adults, the amount of cereal actually consumed was approximately 200% of the labeled serving size. When the quantity of cereal consumed is more than the labeled serving size and when the levels of iron and folate are higher than declared, the intake of both will be significantly greater than the labeled values. It will be important to continue monitoring serum ferritin and folate levels in NHANES IV, since daily consumption of breakfast cereals may contribute to excessive intakes of iron and folate.
Haemoglobin, serum vitamin B(12), and serum and red cell folate levels have been measured in 322 pregnant immigrant women in London at their first booking and in a proportion at 34 weeks of gestation and postnatally. The Indian, East-African Indian, and Pakistani and Bangladeshi patients showed significantly lower initial mean serum vitamin B(12) levels than the European group, the levels being lower in Hindu and Sikh patients than in Moslems. The patients of West Indian, Indian, and East-African Indian origin showed significantly lower initial mean haemoglobin levels than the immigrants from European countries. Though there was no overall correlation between haemoglobin and serum vitamin B(12) level the incidence of hypersegmented polymorphs and macrocytosis in the peripheral blood was highest in the Indian and East-African Indian patients, and both these features were particularly frequent in patients with subnormal serum vitamin B(12) levels. Only one patient, however, had overt megaloblastic anaemia due to vitamin B(12) deficiency. The Indian patients whose red cell folate levels were less than 200 ng/ml also had a lower mean serum vitamin B(12) level than those with red cell folate levels greater than 200 ng/ml. The Indian patients had smaller babies than the Europeans but this was not related to the differences in vitamin B(12) status between the two groups. However, out of 39 babies of the Indian group 5 (13%) showed subnormal serum vitamin B(12) levels in the first 10 days of life, the lowest level being 120 pg/ml.Though there was an overall statistically significant fall in serum vitamin B(12) between first booking and 34 weeks of pregnancy there was no significant fall in serum vitamin B(12) in those who initially had subnormal levels. Thus many Indian women are vitamin B(12) deficient in pregnancy, and this is associated with morphological blood abnormalities in many cases, but megaloblastic anaemia due to this deficiency is relatively infrequent.
BACKGROUND: Homozygosity for MTHFR C677T polymorphism can lead to significantly high homocysteine levels and hyperhomocysteinemia is an important risk factor for thrombotic events. AIMS: The aim was to determine role of MTHFR C677T polymorphism in North Indians with ischemic stroke. SETTINGS AND DESIGN: In a prospective study, the subjects of stroke were recruited from the neurology clinic of the hospital. Controls were healthy individuals from the Hematology clinic without any history of stroke. MATERIALS AND METHODS: Plasma homocysteine levels were measured by enzyme immuno assay method after 3 months of acute episode. Serum folate and Vitamin B12 levels were estimated by competitive inhibition radioassay. MTHFR polymorphism was detected by PCR-RFLP using Hinf I enzyme. STATISTICAL ANALYSIS: The analysis of significance of results was done using SPSS software package. A p-value. RESULTS: Thirty-two acute ischemic stroke patients (aged 1-44 years) were studied. Fourteen (43.8%) had recurrent stroke. Nine (28%) had multiple infarcts. Four of 32 patients (12.5%) had high homocysteine levels. Three out of these 4 hyper-homocysteinemia patients were homozygous ( TT ) for MTHFR polymorphism (2 with recurrent stroke). Two of three homozygous cases with TT genotype had low serum folate. Five of 32 stroke cases (18.8%) were heterozygous ( CT ) genotype. CONCLUSIONS: Primary hyper-homocysteinemia appears to be an important risk factor for ischemic stroke in North Indians, most due to MTHFR C677T homozygosity. Folate levels may modify the presentation of the MTHFR TT genotype.
This study was designed to identify the factors affecting folate status in pregnant women and to explore the relationship between folate status and alcohol consumption during pregnancy. For this purpose, 347 French women were recruited during 1985-1986 on their first visit to the antenatal clinic at Roubaix Hospital (northern France). Alcohol consumption was ascertained by a standardized interview. Folate status assessment was available for 246 pregnant women who were not given folate supplementation. Average folate levels during pregnancy were lower among young women and smokers. Serum folate values diminished with the educational level, and red cell folate values increased with high parity. Unexpectedly, high red cell folate values were strongly related with high alcohol consumption after adjustment for the maternal risk factors associated with alcohol consumption and folate status. This was probably because in the Roubaix region where the study was conducted women consume mostly beer, which contains folates. Pregnancy outcome was not related to folate levels; birthweight was negatively associated with alcohol consumption during the first trimester of pregnancy.
The Dietary Intervention Study in Children (DISC) is a multicenter prospective study designed to assess the efficacy and safety of a lipid-lowering diet in 8- to 10-year-old children with moderately elevated low-density-lipoprotein cholesterol (LDL-C) levels. Six-hundred sixty-three children were randomized to a dietary intervention group (n = 334) and a usual-care group (n = 329). At baseline, mean LDL-C levels, nutrient intakes, anthropometric measures, and blood pressures were similar in the two groups. The intervention consists of a series of group and individual sessions to teach children and their families to follow a diet containing 28% of calories as total fat (< 8% as saturated fat, up to 9% as polyunsaturated fat, 11% as monounsaturated fat) and dietary cholesterol intake less than 75 mg/1000 kcal (< 150 mg/d) and designed to meet nutritional requirements of growing children. The usual-care group was provided with a packet of general dietary information only. Efficacy of the intervention will be assessed by comparing changes in LDL-C levels between the two groups at 36 months. Primary safety outcome assessments will involve comparisons of linear growth and serum ferritin levels. Secondary safety outcomes include serum zinc, folate, retinol, and albumin levels; ratio of LDL-C to high-density-lipoprotein cholesterol; sexual maturation; cognitive development; and child behavior. Thus, DISC aims to address long-term efficacy and concerns about the overall safety of dietary modifications in growing children.
BACKGROUND: Endothelial dysfunction, a precursor of vascular disease, begins early in type 1 diabetes mellitus and is associated with folate status. METHODS: A randomized, double-blind, placebo-controlled study of folate (5 mg daily) and vitamin B6 (100 mg daily) in 124 children with type 1 diabetes determined the immediate and 8-week effects of these vitamins, alone and in combination, on endothelial function. Endothelial function, assessed as flow-mediated dilation and glyceryltrinitrate-induced dilation with high-resolution ultrasound of the brachial artery, was measured at baseline, at 2 and 4 hours after the first dose (n = 35), and at 4 and 8 weeks of treatment (n = 122). RESULTS: Flow-mediated dilation normalized in all treatment groups. From baseline to 8 weeks, flow-mediated dilation improved with folate from 2.6% +/- 4.3% (mean +/- SD) to 9.7% +/- 6.0%, with vitamin B6 from 3.5% +/- 4.0% to 8.3% +/- 4.2%, and with folate/vitamin B6 from 2.8% +/- 3.5% to 10.5% +/- 4.4%. This improvement in flow-mediated dilation occurred within 2 hours and was maintained at 8 weeks for each treatment. Flow-mediated dilation in the placebo group, and glyceryltrinitrate-induced dilation in all groups, did not change. Increases in serum folate, red cell folate, and serum vitamin B6 levels related to increases in flow-mediated dilation. Improvement in flow-mediated dilation was independent of changes in total plasma homocyst(e)ine, glucose, hemoglobin A1c, and high-sensitivity C-reactive protein levels. Baseline red cell folate levels and baseline diastolic blood pressure were related inversely to improvement in flow-mediated dilation. Serum triglyceride and low-density lipoprotein cholesterol inversely related to baseline flow-mediated dilation. CONCLUSIONS: High-dose folate and vitamin B6 normalized endothelial dysfunction in children with type 1 diabetes. This effect was maintained over 8 weeks, with no additional benefit from combination treatment.
Megaloblastic anaemia due to bacterial overgrowth of the small intestine is due to vitamin B12 malabsorption. This report describes a patient with bacterial overgrowth of the small intestine who had megaloblastic anaemia and malabsorption of vitamin B12, but persistently normal levels of serum vitamin B12 and normal serum and red cell folate levels. However, there was evidence of vitamin B12 deficiency as shown by an abnormal deoxyuridine suppression test and by the response to treatment with physiological doses of vitamin B12. A relative increase in biologically inactive vitamin B12 analogues may be the explanation for the normal vitamin B12 level in this patient.
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.
Serum pyridoxal and folate concentrations were measured in 518 diabetics. There were 185 males and 333 females. The level of pyridoxal was significantly lower in the diabetics when compared with 371 'healthy' controls and 25% had levels below the lower limit of the normal range. No significant difference was observed between diabetics being treated by diet alone, oral hypoglycaemics or insulin. Only 20 patients had a reduced serum folate level and in 6 this was accompanied by a low pyridoxal concentration. The results suggest that diabetics may have an increased demand for pyridoxal.
BACKGROUND: Elevated plasma total homocysteine (tHcy) is associated with a higher risk of thrombosis. Crohn's disease (CD) is associated with hypercoagulability of undefined etiology. We investigated tHcy in patients with CD and its relationship with vitamin status, disease activity, location, duration, and history of terminal ileum (TI) resection. STUDY: We examined fasting plasma tHcy, folate, serum vitamin B12 levels, and sedimentation rate in consecutive adult patients with CD. Harvey-Bradshaw index of CD activity and history of TI resection and thromboembolism were recorded. RESULTS: Median plasma tHcy was 10.2 micromol/L in 125 patients with CD. Men (n = 60) had higher plasma tHcy than women (n = 65) (11.2 vs. 9.1 micromol/L; p = 0.004). Patients with a history of TI resection showed lower serum B12 levels (293 vs. 503 pg/mL; p < 0.001) and higher plasma tHcy levels (11.0 vs. 9.35 micromol/L; p = 0.027) than patients without such history. Multivariate analysis showed history of TI resection, serum B12, and creatinine levels to be significant predictors of elevated plasma tHcy. Fourteen patients with CD with a history of thrombosis had an elevated median plasma tHcy of 11.6 micromol/L. CONCLUSIONS: Terminal ileum resection contributes to elevated plasma tHcy levels in CD cases. We recommend tHcy screening in patients with CD, especially in those with prior history of TI resection, and the initiation of vitamin supplementation when appropriate.