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Results for “Serum Folate Level”

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PubMed2004

Heterozygous methylene tetrahydrofolate reductase mutation with mild hyperhomocysteinemia associated with deep vein thrombosis.

Hyperhomocysteinemia is known to be associated with arterial occlusive vascular disease and venous thrombosis. Here, we report a young ethnic Omani patient with recurrent venous thrombosis who was found to be heterozygous for 677C-T mutation in the methyltetrahydrofolate reductase (MTHFR) enzyme. Moderate hyperhomocystenemia was also observed, in the presence of normal red cell folate and serum B12 levels. No other documented marker of hereditary thrombophilia could be demonstrated in this patient, in spite of extensive investigation on multiple occasions.

Adult↗

PubMed1978

Gluten challenge in treated coeliac disease.

Thirty-two children with a past diagnosis of coeliac disease were reinvestigated by means of gluten challenge. They had received a gluten-free diet for a mean period of 6-5 years (range 0-25-11-0) before gluten challenge, and had a mean age of 9-9 years (range 3-0-15-3) at the onset of challenge. Small intestinal biopsies were performed before and after the gluten challenge (at least 10 g natural gluten per day for 3 months in the majority) and, as judged by light microscopy and morphometric techniques, coeliac disease was confirmed in 25 (78%) of the 32 patients; challenge was continued in the remaining 7 for a total period of 2 years when biopsies were repeated in 6 children and all were normal. Serum and RBC folate, serum iron, Hb level, and clinical symptoms were unpredictable variables in identifying children who developed gluten-induced enteropathies. The social and emotional effects of gluten challenge are discussed. The results highlight the importance of gluten challenge and intestinal biopsy in the diagnosis of coeliac disease and strongly suggest that a normal biopsy after a 3-month gluten challenge (as described above) excludes coeliac disease.

Adolescent↗

PubMed1978

Early detection of folic acid deficiency in elderly patients.

Folic acid deficiency is very common in elderly patients who have a mean red cell volume greater than 94 fl. Eighteen out of 40 elderly patients with red cell macrocytosis who initially had normal red cell folate and serum B12 levels subsequently developed folic acid deficiency.

Aged↗

PubMed1992

Congenital dyserythropoiesis and progressive alopecia in Polled Hereford calves: hematologic, biochemical, bone marrow cytologic, electrophoretic, and flow cytometric findings.

Congenital dyserythropoiesis with dyskeratosis is a slow, progressive, and often fatal disease in Polled Hereford calves. Affected calves have a macrocytic normochromic anemia with a mild reticulocytosis. Studies indicate that calves are hyperferremic with increased saturation of serum total iron binding capacity, which rules out iron deficiency as a cause. Other secondary causes of dyserythropoiesis, including cobalamin and folate deficiencies, are unlikely because serum cobalamin and folate levels of affected calves were normal. Virus isolation was negative, and failure to identify bovine retroviral antigens or antibodies from several calves suggested that viral agents were not involved. Bone marrow cytologic findings were similar to those in congenital hereditary dyserythropoiesis in humans and included occasional multinucleate cells, internuclear chromatin bridging between nuclei of partially divided cells, and, more frequently, irregular nuclear shapes and chromatin patterns. DNA content and cell cycle distribution of erythroid cells appeared normal, and no electrophoretic abnormalities were detected in erythrocyte membrane proteins. The Polled Hereford syndrome is similar in many ways to type I congenital dyserythropoiesis in humans and may be an appropriate biomedical model for studying erythroid proliferation during dyserythropoiesis.

Alkaline Phosphatase↗

PubMed2004

A comprehensive evaluation of food fortification with folic acid for the primary prevention of neural tube defects.

BACKGROUND: Periconceptional use of vitamin supplements containing folic acid reduces the risk of a neural tube defect (NTD). In November 1998, food fortification with folic acid was mandated in Canada, as a public health strategy to increase the folic acid intake of all women of childbearing age. We undertook a comprehensive population based study in Newfoundland to assess the benefits and possible adverse effects of this intervention. METHODS: This study was carried out in women aged 19-44 years and in seniors from November 1997 to March 1998, and from November 2000 to March 2001. The evaluation was comprised of four components: I) Determination of rates of NTDs; II) Dietary assessment; III) Blood analysis; IV) Assessment of knowledge and use of folic acid supplements. RESULTS: The annual rates of NTDs in Newfoundland varied greatly between 1976 and 1997, with a mean rate of 3.40 per 1,000 births. There was no significant change in the average rates between 1991-93 and 1994-97 (relative risk [RR] 1.01, 95% confidence interval [CI] 0.76-1.34). The rates of NTDs fell by 78% (95% CI 65%-86%) after the implementation of folic acid fortification, from an average of 4.36 per 1,000 births during 1991-1997 to 0.96 per 1,000 births during 1998-2001 (RR 0.22, 95% CI 0.14-0.35). The average dietary intake of folic acid due to fortification was 70 μg/day in women aged 19-44 years and 74 μg/day in seniors. There were significant increases in serum and RBC folate levels for women and seniors after mandatory fortification. Among seniors, there were no significant changes in indices typical of vitamin B12 deficiencies, and no evidence of improved folate status masking haematological manifestations of vitamin B12 deficiency. The proportion of women aged 19-44 years taking a vitamin supplement containing folic acid increased from 17% to 28%. CONCLUSIONS: Based on these findings, mandatory food fortification in Canada should continue at the current levels. Public education regarding folic acid supplement use by women of childbearing age should also continue.

Journal Article↗

PubMed1991

Screening for dementia and investigating its causes.

OBJECTIVE: To examine, from the perspective of primary care physicians, the value of mental status findings and ancillary tests in diagnosing dementia or its causes. DATA SOURCES: Studies identified using MEDLINE and bibliographies of pertinent articles. STUDY SELECTION: Selection based on availability of information on specific findings or tests, the criterion standard used to confirm diagnoses, the disease spectrum, and the richness of the reported data. DATA EXTRACTION: Data collected on sensitivity and specificity. In many cases, the originally reported data are re-analyzed to illustrate the usefulness of alternative cut-off values or to answer specific clinical questions. Likelihood ratios estimated to summarize test results. DATA SYNTHESIS: Probability of dementia is greatly reduced (likelihood ratio, 0.06 to 0.2) when either normal serial 7s, 7-digit span, 3-item recall, or clock drawing test results are obtained; abnormal results only moderately increase the odds of disease. Low (less than or equal to 20), intermediate (21 to 25), or high (greater than or equal to 26) scores on the Mini-Mental State Examination (MMSE) increase (likelihood ratio greater than or equal to 8.2), have little effect (likelihood ratio, 1.3 to 2.4), or decrease (likelihood ratio, 0.06 to 0.1) the odds of disease. The usefulness of tests to investigate the cause of dementia varies depending on the pretest probability of the specific condition. CONCLUSIONS: Several useful methods exist to screen for cognitive impairment, and clinicians need to be familiar with the strengths and limitations of their preferred screening methods. In investigating the cause of dementia, routinely obtaining a VDRL test, cerebral imaging studies, serum cobalamin level, or folate level is unwarranted.

Aged↗

PubMed2003

Homocysteine plasma concentration is related to severity of lung impairment in scleroderma.

OBJECTIVE: To investigate the correlation between plasma concentration of total homocysteine and pulmonary involvement in patients with limited or diffuse scleroderma (systemic sclerosis, SSc). METHODS: Seventy-one patients with scleroderma were divided into 3 groups based on pulmonary involvement: Group A comprised patients without lung involvement (9 cases); Group B patients with lung involvement of mild and moderate stages (44 cases); and Group C patients with lung involvement of severe stage and endstage (18 cases). At the time of evaluation of lung involvement all patients underwent determination of plasma homocysteine concentration. Homocysteine concentration was also measured in 30 healthy controls homogeneous for sex and age. RESULTS: In patients with scleroderma the homocysteine concentration was significantly higher than in controls (11.1 and 6.9 micromol/l, respectively; p < 0.001). We found a significant association between plasma homocysteine concentration and severity of lung involvement that was not modified by correction for age, time from the diagnosis, type of scleroderma pattern, and serum creatinine and folate levels. Homocysteine concentration progressively increases in scleroderma patients with more severe pulmonary involvement. Subjects with high homocysteine concentration (i.e., > or = 75th percentile of homocysteine concentration in patients with scleroderma without lung involvement) were mostly present in the group with the greatest lung involvement. CONCLUSION: High level of homocysteinemia is associated with an increased risk of pulmonary disease in patients with scleroderma. We hypothesize that hyperhomocysteinemia may worsen injury of the endothelium, a key lesion in scleroderma disease, favoring the development of lung involvement. Our data support the hypothesis that homocysteine could be involved in the pathogenetic process of scleroderma pulmonary involvement.

Adult↗

PubMed2002

Heterozygous methylene tetrahydrofolate reductase mutation with mild hyperhomocysteinemia associated with deep vein thrombosis.

Hyperhomocysteinemia is known to be associated with arterial occlusive vascular disease and venous thrombosis. Here we report a young ethnic Omani patient with recurrent venous thrombosis who was found to be heterozygous for the C677T mutation in the enzyme methyltetrahydrofolate reductase (MTHFR). Moderate hyperhomocysteinemia was also documented in the presence of normal red cell folate and serum B12 levels. No other marker usually associated with hereditary thrombophilia could be demonstrated in the patient, despite extensive investigations on multiple occasions.

Adult↗

PubMed1987

Hydroxyurea treatment of myeloproliferative disorders. Macro-megaloblastic blood and bone marrow changes.

Blood and bone marrow changes induced by continuous low-dose hydroxyurea treatment are described. A linear increase in mean red cell volume was observed after onset of therapy. The entire normocyte population was replaced by abnormally large erythrocytes within 150 days. The bone marrow morphology changed in megaloblastic direction. Bone marrow iron stores and number of sideroblasts increased, findings compatible with ineffective erythropoiesis. Serum folate and cobalamin levels remained normal. These morphologic changes might cause confusion when examining blood or bone marrow samples from patients treated with hydroxyurea.

Bone Marrow↗

PubMed1986

Recognition of deficiency of vitamin B12 using measurement of serum concentration.

Of 504 patients with low concentrations of vitamin B12 in serum by microbiologic assay (less than 120 pg/ml) in whom clinical information was available to evaluate vitamin B12 status, 109 (22%) were found to have clinically important deficiency of vitamin B12, and another 10 had pernicious anemia with deficient serum levels of both vitamin B12 and folate. Serum from patients deficient in vitamin B12 was assayed by several commercially available assay techniques. These used either purified or impure preparations of gastric intrinsic factor as binder, extracted cobalamins with either heat or alkali ("no boil") and separated bound from free vitamin B12 either with activated charcoal or by binding the intrinsic factor to glass beads ("solid state"). These kits were purchased commercially from Becton-Dickinson Co. (SimulTrac), BioRad Corp. (Quantaphase), Amersham Corp. (Vitamin B12/folate radioassay) and Corning Medical and Scientific (Immophase). Serum vitamin B12 concentrations assayed in sera from patients deficient in vitamin B12 overlapped the normal range in 6% of all samples assayed by techniques using purified intrinsic factor assays (BioRad, Amersham, and the "blocked" SimulTrac assay), but no such overlap was found between deficient and nondeficient sera assayed with the solid-state pure intrinsic factor assay (Corning), the "unblocked" SimulTrac, or Euglena gracilis. It would appear that (1) radiodilution assays extracting serum by boiling and binding vitamin to binder fixed on a solid matrix may be the most reliable available at this time. These may be as reliable as microbiologic assay for separation of patients with deficiency from those without deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia, Pernicious↗

PubMed1979

Small intestinal biopsy in a patient with Crohn's disease of the duodenum. The spectrum of abnormal findings in the absence of granulomas.

The case is reported of a patient who presented with an occult anemia that was due to Crohn's disease of the duodenum. The initial evaluation revealed low serum levels of iron, folate, and carotene, and a small bowel series was abnormal but not diagnostic of Crohn's disease. Numerous small intestinal biopsy specimens were obtained from the duodenum and proximal jejunum in an unsuccessful attempt to make a diagnosis. It was shown by radiography and laparotomy 2 yr later that the patient had Crohn's disease of the proximal small intestine. This report provides a detailed analysis of the spectrum of abnormalities found by peroral mucosal biopsy in this patient. These abnormalities were patchy and included flattened mucosa, an abnormal surface epithelium which was infiltrated by large numbers of polymorphonuclear leukoyctes, increased plasma cells and polymorphonuclear leuckocytes within the lamina propria, crypt abscesses, erosions, granulation tissue, and pyloric gland metaplasia, all in the absence of granulomas. Crohn's disease should always be considered in the differential diagnosis of a proximal small bowel mucosal disease, especially when a constellation of acute inflammatory changes is present.

Adolescent↗

PubMed1988

Folic acid lowers elevated plasma homocysteine in chronic renal insufficiency: possible implications for prevention of vascular disease.

To explore interrelations between folic acid and methionine metabolism in chronic renal insufficiency, we measured plasma amino acids in 21 patients with mean serum creatinine +/- SD of 560 +/- 240 mumol/L, after a ten-hour overnight fast, before and after administration of 5 mg of oral folic acid daily for 15 +/- 6 days. Mean plasma homocysteine was 12.9 +/- 6.8 mumol/L in the patients and 4.2 +/- 0.8 mumol/L in 24 normal controls (P less than .001), and after folic acid administration it declined in the patients to 6.8 +/- 2.8 mumol/L (P less than .0001) in linear proportion (r = .92) to the prefolate homocysteine level. Methionine concentrations were normal in the patients and did not change after folate administration, nor did elevated cysteine and creatinine. Plasma serine was lower (88.3 +/- 17.2 v 121 +/- 25 mumol/L, P less than .41) and declined further to 67.8 +/- 16.4 (P less than .0001) after folate, while prefolate glycine levels increased from 273.3 +/- 61.2 to 313.2 +/- 97.5 mumol/L (P less than .01). Serum and red-cell folate levels were normal in the patients before treatment. The results show that homocysteine levels are increased in chronic renal insufficiency, but may be lowered by folate enhancement of remethylation of homocysteine to methionine. Since elevated plasma homocysteine is associated with premature vascular disease, folic acid may reduce cardiovascular risk in chronic renal insufficiency.

Adult↗

PubMed1987

Haematological and immunological features of patients with fissured tongue syndrome.

Blood samples from 40 patients with fissured tongue syndrome (FTS) were examined, and the results were compared with those of 20 healthy control subjects. FTS was diagnosed when a) the patient had a fissured tongue with smooth-surfaced papillae (n = 25) or b) the patient had geographic tongue and some relatives had fissured tongue (n = 15). These tongue forms were verified also histologically. To evaluate the possibility of systemic disorders in patients with FTS we determined the whole blood picture and levels of vitamin B12, serum folate, serum ferritin, and immunoglobulins (IgA, IgG, IgM, IgE). None of the patients with FTS nor any of the controls were found to be anaemic. The mean levels of serum vitamin B12, ferritin and folate were, however, slightly lower in the patient group than in the controls. These findings suggest that anaemia does not play a primary role in the aetiology of fissured tongue syndrome. The most striking haematological findings were the decreased thrombocyte and leucocyte counts in patients with fissured tongue syndrome compared with the control subjects. Furthermore, the lymphocyte count and serum IgG were low in the patient group. When the two patient groups were compared no differences were found. These observations are discussed from the standpoint of deficiency in the immunological defence mechanism of patients with fissured tongue syndrome.

Adult↗

PubMed1983

Folate deficiency in rats fed amino acid diets.

Growth rate, hematological changes, serum, erythrocyte and liver folate levels, and urinary excretion of formiminoglutamic acid (FIGLU) were measured in rats fed p-aminobenzoic acid (PABA)-free, sulfonamide-supplemented purified amino acid diets with and without folic acid and fiber, individually and in combination. Fiber had no effect on growth but was necessary to prevent mortality in the absence of folic acid. Folic acid did not affect growth during the first 40 days, but after this period rats failed to gain weight in the absence of folic acid. Although blood hematocrit was lower when the diet was devoid of fiber and folic acid and leucocyte counts were lower when the diets were devoid of folic acid, the hematological values remained within normal physiological limits for healthy rats of comparable age. FIGLU excretion was increased and serum, erythrocyte and liver folate levels were depressed when rats were fed folic acid-free diets for 28 days. Neutrophil hypersegmentation was clearly evident after 28 days of feeding the folic acid-free diets. The use of an amino acid diet without PABA but containing 5% fiber and 1% succinylsulfathiazole is a useful system to study chronic folic acid deficiency in the rat.

Amino Acids↗

PubMed2004

Homocysteine in Alzheimer disease and vascular dementia.

Hyperhomocysteinemia is an important risk factor for atherosclerosis and it has recently been suggested as a diagnostic marker for Alzheimer disease (AD). The present studies compared homocysteinemia in patients with AD and with vascular dementia (VD),as well as in controls. Homocysteinemia was measured in 137 probable AD patients,diagnosed by the NINCDS-ADRDA criteria, in 40 probably VD patients diagnosed by the NINDS-AIREN criteria, and in 42 control subjects. Homocysteine levels were significantly higher in AD and VD groups, than in controls, however, VD patients were significantly older than the controls. The proportion of females was higher in the AD group, while serum folate and B12 vitamin levels tended to be lower in both the AD and VD groups, compared to the controls. In order to adjust the results for these potentially interfering factors, a multivariate ANCOVA calculation was performed, where homocysteine levels were analyzed considering 2 grouping factors (gender and neurological type) and 4 covariates (age, albumin,serum folate and vitamin B12 ). This analysis confirmed that even after adjusting for the covariates, the difference between AD and VD groups and controls remain highly significant,while neither the gender itself, nor the interaction of gender and the neurological type had any significant influence on the homocysteine levels. The main finding, therefore, is a significant increase of homocysteine levels in the 2 disease groups, compared to controls.

Aged↗

PubMed1999

Serum cystatin C as a determinant of fasting total homocysteine levels in renal transplant recipients with a normal serum creatinine.

Serum creatinine, a surrogate for both renal function and homocysteine generation, is an important determinant of fasting plasma total homocysteine levels in stable renal transplant recipients. In this study, it is hypothesized that among stable renal transplant recipients with normal creatinine levels (i.e., < or = 1.5 mg/dl), serum cystatin C, a more sensitive indicator of GFR, would better predict fasting total homocysteine levels compared with serum creatinine. Fasting plasma total homocysteine, folate, vitamin B12, and pyridoxal 5'-phosphate levels, along with serum cystatin C, creatinine, and albumin levels, were determined in 28 consecutive renal transplant recipients (mean age 47 +/- 14 yr; 60.7% men) with stable allograft function, whose serum creatinine was < or = 1.5 mg/dl. General linear modeling with analysis of covariance revealed that serum cystatin C was independently predictive (partial R = 0.494; P = 0.023) of fasting total homocysteine levels after adjustment for age, gender, vitamin status, albumin, and creatinine levels. In contrast, creatinine levels were not predictive of fasting total homocysteine levels in this model (P = 0.110) or an identical model that excluded cystatin C (P = 0.131). Serum cystatin C levels may reflect subtle decreases in renal function that independently predict fasting total homocysteine levels among stable renal transplant recipients with a normal serum creatinine.

Adult↗

PubMed2003

Increased plasma homocysteine levels without signs of vitamin B12 deficiency in patients with multiple sclerosis assessed by blood and cerebrospinal fluid homocysteine and methylmalonic acid.

OBJECTIVE: The aim of this study was to evaluate if multiple sclerosis (MS) is associated with vitamin B12 (cobalamin) deficiency. METHODS: We measured serum vitamin B12, plasma folate, serum methylmalonic acid (MMA), plasma homocysteine (tHcy) and also cerebrospinal fluid (CSF) MMA and tHcy in 72 patients with MS and 23 controls. RESULTS: The mean plasma tHcy level was significantly increased in MS patients (11.6 micromol/L) compared with controls (7.4 micromol/L) (P = 0.002). Seven patients showed low serum vitamin B12 levels but only one of them had concomitant high plasma tHcy. None of them showed high serum MMA. Plasma or blood folate levels did not differ between MS patients and controls. We found no significant differences in mean values or frequency of pathological tests of serum B12, serum MMA, mean corpuscular volume (MCV), haemoglobin concentration, CSF tHcy or CSF MMA between patients and healthy subjects. There were no correlations between CSF and serum/plasma levels of MMA or tHcy. Serum vitamin B12, serum MMA, plasma tHcy, CSF Hcy or CSF MMA were not correlated to disability status, activity of disease, duration of disease or age. CONCLUSIONS: The relevance of the increased mean value of plasma tHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. We can not, however, exclude the possibility of a genetically induced dysfunction of the homocysteine metabolism relevant for the development of neuroinflammation/degeneration. Our findings indicate that, regardless of a significant increase in plasma tHcy in MS patients, the MS disease is not generally associated with vitamin B12 deficiency since we did not find any other factors indicating vitamin B12 deficiency. Analysis of CSF MMA and CSF tHcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. We conclude that B12 deficiency, in general, is not associated with MS.

Adult↗

PubMed1994

Vitamins, folic acid and the cause and prevention of neural tube defects.

Primary prevention of neural tube defects has been demonstrated in humans by maternal therapy with multivitamins and folic acid or folic acid alone. It has also been shown in several animal models of neural tube defects. One of these, the curly tail mouse, has been used extensively to study which agents will prevent neural tube defects in embryos when administered to the mother in early pregnancy. Prevention is achieved with retinoic acid, inositol and the DNA inhibitors hydroxyurea, mitomycin C, 5-fluorouracil and cytosine arabinoside. In no case were neural tube defects prevented in every embryo. A possible preventive effect was seen with riboflavin, vitamin C and vitamin D2. Despite the use of a variety of dose levels, no prevention was achieved with folic acid, folinic acid, Pregnavite Forte F tablets, pyridoxine or vitamin B12, or triamcinolone and cycloheximide (inhibitors of mRNA and protein synthesis, respectively), zinc, homocysteine, methionine and thymidine. Various studies have investigated whether there is a biochemical lesion in folate metabolism in women who have had children with neural tube defects. While there is no difference in their dietary intake of folate compared with control patients, the correlation between their dietary folate and the level of folate in both serum and red blood cells is distorted. Also they are less efficient at raising their folate levels after a folate load. The effects are minor but may hint at a lesion which, if identified, could act as a marker for 'at risk' women.

Animals↗