[Prevalence and pathogenesis of folate deficiency in patients with quiescent or clinically mildly active Crohn disease].
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Adolescent↗
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Results for “FOLIC ACID DEFICIENCY”
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Anemia in adolescence. 2. Hemoglobinopathies and other causes.
Many complex forces are at work during adolescence which can contribute to the occurrence of anemia. Careful consideration of the entire patient should enable a physician to identify the unusual as well as the more common causes of anemia in this age group. Anemia in teenage girls is primarily due to menstrual iron loss. In boys, borderline diets and the demands of rapid growth predominate as causative factors. Hemoglobinopathies (thalassemia, sickle cell disease), G6PD deficiency, infectious mononucleosis, and illicit drug use account for small proportions of cases.
Adolescent↗
Variation in plasma folate levels among groups of healthy persons.
Levels of plasma folate, erythrocyte folate and serum vitamin B12 were measured in 106 essentially healthy persons grouped both as to race and economic--educational status. Whereas the mean values of the three assays did not differ significantly among groups, values of plasma folate below the usual limits of normal were more prevalent in the migrant worker and urban clinic groups. Persons with low plasma folate levels did not have symptomatic deficiency as evaluated by hematocrit, peripheral blood smears and erythrocyte folate levels. The interpretation of the plasma folate requires reference values from a healthy population selected to be comparable to the study group. The diagnosis of deficiency, or at least the degree of deficiency, requires clinical and laboratory evaluations beyond the plasma folate.
Adult↗
Evaluation of the frequency of anaemia and iron-deficiency anaemia in a group of Algerian menstruating women by a mixed distribution analysis: contribution of folate deficiency and inflammatory processes in the determination of anaemia.
Frequency of anaemia was estimated by two methods for 254 menstruating women living in South-eastern Algeria. One method defines the frequency of anaemia as the percentage of women with haemoglobin concentrations below the cut-off point defined by WHO (12 g/dl). The second method defines the frequency of anaemia as the percentage of women whose haemoglobin values are shifted downwards relative to a Gaussian distribution of haemoglobin of nonanaemic women. The conventional cut-off point probably tends to overestimate the true frequency of anaemia: 7% of women with haemoglobin concentration less than 12 g/dl were not found as anaemic using the cumulative frequency method. The contribution of iron deficiency folate deficiency and inflammatory process was estimated using the cumulative frequency distribution after excluding respectively women with biological evidence of iron deficiency (serum ferritin of 12 micrograms/l or less, transferrin saturation less than 15% and/or MCV less than 80 fl), of folate deficiency (red blood cell folates less than 100 micrograms/l) and of inflammatory process (C. Reactive Protein more than 12 mg/l, orosomucoid more than 1.4 g/l or white cell counts of more than 10,000/mm3). According to this method iron deficiency represented the most important cause of anaemia in the context of our sample: iron deficiency contributed to 77% of anaemia. Folate deficiency and inflammatory processes do not in themselves appear to contribute to anaemia.
Adult↗
Acquired and inherited disorders of cobalamin and folate in children.
Cobalamin deficiency in the newborn usually results from cobalamin deficiency in the mother. Megaloblastic anaemia, pancytopenia and failure to thrive can be present, accompanied by neurological deficits if the diagnosis is delayed. Most cases of spina bifida and other neural tube defects result from maternal folate and/or cobalamin insufficiency in the periconceptual period. Polymorphisms in a number of genes involved in folate and cobalamin metabolism exacerbate the risk. Inborn errors of cobalamin metabolism affect its absorption, (intrinsic factor deficiency, Imerslund-Gräsbeck syndrome) and transport (transcobalamin deficiency) as well as its intracellular metabolism affecting adenosylcobalamin synthesis (cblA and cblB), methionine synthase function (cblE and cblG) or both (cblC, cblD and cblF). Inborn errors of folate metabolism include congenital folate malabsorption, severe methylenetetrahydrofolate reductase deficiency and formiminotransferase deficiency. The identification of disease-causing mutations in specific genes has improved our ability to diagnose many of these conditions, both before and after birth.
Diet↗
Red cell or serum folate? Results from the National Pathology Alliance benchmarking review.
AIMS: The National Pathology Alliance benchmarking review has completed five years of data collection and analysis of the workload and organisation of haematology laboratories in the UK. This study analyses variation in practice in how laboratories respond to a request to determine whether or not a patient has folate deficiency. METHODS: A three year analysis of workload data on the number of serum/plasma folate and red cell folate assays performed on an annual basis for the period 1 April 1999 to 31 March 2002. RESULTS: Three diagnostic testing strategies were found, namely: serum/plasma folate only, red cell folate only, and both serum/plasma folate and red cell folate. CONCLUSION: Evidence from the literature indicates that serum folate measurements provide equivalent information to red cell folate measurements when attempting to determine whether folate deficiency is present. There seems to be no basis for the routine testing of all samples for serum/plasma folate and a red cell folate.
Benchmarking↗
Low serum folate levels as a risk factor for depressive mood in patients with chronic epilepsy.
This study takes into consideration whether low serum folate levels may contribute to depressive mood in patients with chronic epilepsy. The serum folate levels and the score on the Self-Rating Depression Scale (SDS) were examined in 46 patients with chronic epilepsy. Patients with a score indicating at least minor depression on the SDS had a significantly lower serum folate level than patients with a normal score on SDS. There was a significant negative correlation between the serum folate levels and the SDS score. A serum folate level below 7.5 ng/ml was significantly associated with a pathological score on SDS. Because a serum folate level of 7.5 ng/ml is in the normal range for many laboratories, further studies using total plasma homocysteine as a sensitive measure of functional folate deficiency are required to elucidate the impact of folate metabolism on depressive mood in patients with chronic epilepsy.
Adult↗
Folate deficiency in operated terminal ileitis (Crohn's disease).
In a series of 39 subjects previous results for serum folate levels were confirmed while intraglobular folate did not differ from those in a control group. To verify the hypothesis that SASP administration could be responsible for serum folate deficiency three different sub-groups were considered. 11 patients had never taken SASP (sub-group I), 16 patients had taken SASP in the past but the treatment had been withheld at least 2 months before (sub-group II), 12 patients were still taking the drug at the time of the study (sub-group III). Differences in serum folate levels between each one of the three sub-groups and the control group were significant. The same was not true for the differences between each one of the three sub-groups and the other. These findings seem to confirm that SASP treatment is not the major cause of serum folate deficiency, but a multifactorial pathogenesis might account for it.
Adolescent↗
Oral methionine loading as a cause of acute serum folate deficiency: its relevance to parenteral nutrition.
Oral methionine supplements (8.0 g daily for 4 days) were given to five normal volunteers who continued to eat their usual diet. This treatment resulted in a significant fall in serum folate concentration. Three days after the end of treatment concentrations had not completely returned to control values. The fall in concentration was prevented by giving oral folic acid supplements. It is suggested that folic acid supplements should be given to patients who are receiving intravenous infusions of amino acid mixtures.
Administration, Oral↗
Folate deficiency is a common finding in psychogeriatric patients.
BACKGROUND AND AIMS: In previous studies we observed a high frequency of elevated total plasma homocysteine (tHcy) concentrations in psychogeriatric patients. The objective of the present study was to obtain detailed information on folate status in psychogeriatric patients and its association with elevated tHcy concentration. METHODS: We measured serum and blood folate, tHcy, serum cobalamin, and serum methylmalonic acid in a study population consisting of 141 psychogeriatric patients, 49 of whom had elevated tHcy concentration. RESULTS: The concentrations of serum and blood folate showed a high correlation and were significantly lower, and age significantly higher, in patients with elevated tHcy compared to patients with normal concentrations of tHcy. A stepwise multiple regression analysis including age, serum and blood folate, serum cobalamin, serum methylmalonic acid and serum creatinine showed that only serum creatinine (p<0.001), age (p<0.01), serum folate (p<0.05) and blood folate (p<0.05) independently predicted tHcy concentration. Only one patient of those with serum folate above 12 nmo/L had an elevated tHcy concentration. No such clear limit was observed for the relation between tHcy and blood folate. Thirty-two of the patients with elevated tHcy had decreased serum folate concentrations (<7.0 nmol/L), and seven of these patients also had signs of cobalamin deficiency. Ten patients had only signs of cobalamin deficiency. CONCLUSIONS: Folate deficiency appears to be common in psychogeriatric patients, and serum folate seems to reflect folate deficiency better than blood folate. Our findings suggest the use of tHcy, serum cobalamin and serum folate to evaluate cobalamin-folate status in psychogeriatric patients.
Aged↗
Acute onset of folate deficiency in patients under intensive care.
Four patients with ruptured abdominal aortic aneurysm developed thrombocytopenia and marked megaloblastic changes within 3-10 days of surgery. In 2 patients, direct evidence of folate deficiency within marrow cells was obtained by measuring deoxyuridine suppression in short-term bone marrow cultures. The results suggest that folate deficiency was limited to marrow tissue. Folate deficiency localized to the bone marrow offers an explanation for the extremely rapid onset of thrombocytopenia in these patients. The significance of these findings with regard to folate metabolism is discussed. The importance of recognizing this potentially fatal complication of critical illness is emphasized, because it should be readily prevented by folic acid therapy.
Acute Disease↗
Atypical cobalamin deficiency. Subtle biochemical evidence of deficiency is commonly demonstrable in patients without megaloblastic anemia and is often associated with protein-bound cobalamin malabsorption.
We performed studies in 25 patients with low serum cobalamin levels who had few if any clinical or hematologic findings of cobalamin deficiency. All but three had morphologically normoblastic hematopoiesis, and 15 were not even anemic. None of those tested excreted methylmalonic acid or homocystine. Nevertheless, the dUST identified metabolic abnormalities in 18 of the 25 cases. In vitro additives were essential in the dUST. Especially noteworthy was MTHF, whose addition unmasked an otherwise undetectable dUST abnormality in four cases. Why MTHF appears to act as a "stress test" in this setting is unknown but deserves further attention. Seven patients had early forms of classical malabsorptive states such as pernicious anemia, defined by abnormal Schilling test results. Among the rest, seven of 13 patients displayed malabsorption of protein-bound cobalamin despite normal absorption of free cobalamin by the Schilling test. In two patients, initially normal Schilling test results became abnormal the following year. These findings demonstrate that seemingly falsely low serum cobalamin levels often indicate subtle biochemical cobalamin deficiency. Early stages of pernicious anemia or other classical malabsorptive states are sometimes responsible for such subtle deficiency. However, malabsorption confined to protein-bound cobalamin is an equally common cause. Current concepts of cobalamin deficiency and the absorptive defects that can cause it should be expanded to include atypical defects requiring newer methods of identification.
Adult↗
Haemolysis and erythropoiesis. II. Reticulocytosis and rate of haemoglobin rise in haemolytic and deficiency anaemias.
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Adolescent↗
Folate deficiency in Crohn's disease: incidence, pathogenesis, and treatment.
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Adolescent↗
Megaloblastic anemia secondary to folate deficiency associated with hypothyroidism.
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Adult↗
Folate status during pregnancy in women is improved by long-term high vegetable intake compared with the average western diet.
The effect of increasing dietary folate on folate status during pregnancy is controversial. The aim of this study was to compare folate intake and folate status during pregnancy of women with high long-term vegetable intake and those eating an average Western diet. In a prospective study that included 109 participants, pregnant women adhering to a predominant vegetarian diet with high vegetable intake for 8 +/- 0.5 y with subgroups of ovo-lacto vegetarians (n = 27) and low meat eaters (n = 43) and women eating an average Western diet (control group, n = 39) were compared with regard to dietary intake and plasma and red blood cell (RBC) folate concentrations during wk 9-12, 20-22 and 36-38 of gestation. Plasma and RBC folate concentrations were highest in ovo-lacto vegetarians, followed by low meat eaters and lowest in the controls. Ovo-lacto vegetarians and low meat eaters showed a lower risk for folate deficiency, with RBC folate concentrations of <320 nmol/L resulting in odds ratios of 0.10 (95% confidence interval, 0.01-0.56) and 0.52 (95% confidence interval, 0.20-1.34), respectively. In ovo-lacto vegetarians, the RBC folate concentration was positively related to the intake of vitamin B-12 (r = 0.51, P: < 0.0001). The results of the study suggest that long-term high vegetable intake favorably affects plasma folate as well as RBC folate concentrations throughout pregnancy and reduces the risk of folate deficiency if an adequate vitamin B-12 supply is ensured.
Adult↗
[Maternal iron and folate deficiencies. Effects on the newborn infant].
Three studies of materno-fetal iron and folate status are analyzed. Repercussions of maternal iron and folate deficiencies on neonates are investigated. The incidence of iron deficiency is high during pregnancy and increases in multiparous and alien women. Although no correlation was found between mothers' and neonates' ferritinemia, maternal iron deficiency was shown to influence fetal hemoglobin synthesis and iron stores. Folate deficiency in mothers had no obvious incidence on hematological parameters in neonates. However it does influence gestation duration and therefore birthweight.
Female↗
The serum vitamin B12 level: its assay and significance.
1. Low serum B12 levels can be measured with considerable precision by microbiological assay with the Euglena gracilis assay and B12 deficiency can be recognised with a high level of consistency by either the Euglena or L. leichmannii assays. Either method is ideally suited for the assay of large numbers of specimens. The Lactobacillus leichmanii technique requires preliminary extraction of protein and it has been suggested that this may be a source of inaccuracy. 2. The radioisotope dilution assay should be the ideal method of measuring B12 levels in small or moderate numbers of specimens for it is a simple method that can be carried out in any laboratory with suitable counting equipment. After many false starts the conditions required for accurate assay are now understood. Each of 40 to 50 radioisotopic dilution techniques that have been introduced claims to be capable of differentiating B12 deficiency from control subjects but the reported correlations between the actual levels found in the two different assays are variable and the levels may be much higher with some radioisotopic methods. 3. The subnormal serum levels which are found in pernicious anaemia with all these techniques indicate severe reduction of the liver B12 level. A low serum B12 level in other conditions has, in the absence of associated folate or iron deficiency, the same significance. If the fall in the serum B12 level is associated with folate or iron deficiency, the tissue B12 levels are usually reduced but not to the low levels found in B12 deficiency states. 4. In practice, a subnormal B12 level is a valuable pointer not only to unsuspected pernicious anaemia but also to other gastrointestinal or nutritional disorders. The significance of a fall in the B12 level can only be understood if its cause is defined by a full clinical and gastroenterological investigation. 5. Falsely low serum B12 levels are found under certain iatrogenic conditions and B12 levels may be normal in spite of cellular deficiency of B12 under the rare circumstances of pernicious anaemia being associated with chronic myeloid leukaemia or when there is deficiency of TC 2.
Anemia, Megaloblastic↗