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PubMed1992

[The prevalence of iron deficiency in pregnant women at their first consultation in health centers in a metropolitan area, Brazil. Etiology of anemia].

Three hundred and sixty-three pregnant women enrolled in the Pregnancy Medical Care Program of S. Paulo Health Department in the district of Butantan, S. Paulo city, Brazil, were studied at their first routine consultation between April and October, 1988. Their average age was 25 and 65.9% of them belonged to families with a monthly income below US$50.00 per capita. Only 3.1% presented an income above US$150.00 per capita. Taking the minimum transferrin saturation threshold of 15% as determining iron deficiency, a 4.6% prevalence of iron deficiency was observed in the first trimester, 17.3% in the second trimester and 42.8% in the third trimester, resulting in an overall prevalence of 12.4%. There was no significant difference between prevalences of iron deficiency according to the number of pregnancies. The prevalence of iron deficiency was higher in women presenting incomes below US$50.00 per capita.

Adult↗
PubMed1993

Folate deficiency increases genetic damage caused by alkylating agents and gamma-irradiation in Chinese hamster ovary cells.

The effect of folate deficiency on genetic damage caused by alkylating agents and gamma-irradiation was studied in Chinese hamster ovary (CHO) cells. Mutant frequencies of 6-thioguanine-resistant and diphtheria toxin-resistant cells were not significantly increased by incubation in low-folate medium. In contrast, folate deficiency increased the mutant frequencies of 6-thioguanine-resistant cells caused by N-ethyl-N-nitrosourea or ethyl methanesulfonate by about 3-fold. Folate deficiency was associated with a 70% increase of diphtheria toxin-resistant cells after exposure to ethyl methanesulfonate. Folate deficiency alone caused DNA strand breaks equivalent to 26 cGy, as monitored by alkaline filter elution. Following 400 cGy of gamma-irradiation, folate-deficient cells manifested strand breaks equivalent to a dose of 710 cGy. CHO cells in folate-containing medium repaired breaks within 3 h, while cells in low-folate medium had an increased break frequency (P = 0.02) at 3 h and were unable to fully repair radiation-induced damage even after 9 h. These studies indicate that folate deficiency acts synergistically with alkylating agents to increase somatic mutation and with gamma-irradiation to promote DNA strand breaks in CHO cells. Folate deficiency appears to potentiate the genetic damage caused by mutagens/carcinogens by limiting DNA repair.

Animals↗
PubMedDate not supplied

The relationship between maternal nutritional status and spontaneous abortion.

BACKGROUND: The incidence of pregnancy wastage is high among poor women. Though the aetiology of spontaneous abortion is multifactorial, nutritional deficiency is considered to be an important contributory factor. METHODS: A case-control study was conducted to assess the relationship between maternal vitamin status and spontaneous abortion. RESULTS: The incidence of anaemia (15%), and riboflavin (84%) and folate deficiency (24.5%) were similar among the cases and controls. Vitamin A levels were higher in the study group compared to those in controls. CONCLUSION: The results suggest that various nutrient deficiencies have no correlation with the occurrence of spontaneous abortion. The role of increased vitamin A levels needs to be studied further.

Abortion, Spontaneous↗
PubMed2003

Screening for vitamin B-12 and folate deficiency in older persons.

BACKGROUND: Vitamin B-12 deficiency is usually accompanied by elevated concentrations of serum total homocysteine (tHcy) and methylmalonic acid (MMA). Folate deficiency also results in elevated tHcy. Measurement of these metabolites can be used to screen for functional vitamin B-12 or folate deficiency. OBJECTIVE: We assessed the prevalence of vitamin B-12 and folate deficiency in a population-based study (n = 1562) of older persons living in Oxford City, United Kingdom. DESIGN: We postulated that, as vitamin B-12 or folate concentrations declined from adequate to impaired levels, tHcy (or MMA) concentrations would increase. Individuals were classified as being at high risk of vitamin B-12 deficiency if they had low vitamin B-12 (< 150 pmol/L) or borderline vitamin B-12 (150-200 pmol/L) accompanied by elevated MMA (> 0.35 micromol/L) or tHcy (> 15.0 micromol/L). Individuals were classified as being at high risk of folate deficiency if they had low folate (< 5 nmol/L) or borderline folate (5-7 nmol/L) accompanied by elevated tHcy (> 15 micromol/L). RESULTS: Cutoffs of 15.0 micro mol/L for tHcy and 0.35 micro mol/L for MMA identified persons with normal or elevated concentrations. Among persons aged 65-74 and >or= 75 y, respectively, approximately 10% and 20% were at high risk of vitamin B-12 deficiency. About 10% and 20%, respectively, were also at high risk of folate deficiency. About 10% of persons with vitamin B-12 deficiency also had folate deficiency. CONCLUSION: Use of tHcy or MMA among older persons with borderline vitamin concentrations may identify those at high risk of vitamin B-12 deficiency who should be considered for treatment.

Age Factors↗
PubMed2002

Folic acid prevents exencephaly in Cited2 deficient mice.

Cited2 (also Mrg1/p35srj) is a member of a new conserved gene family that is expressed during mouse development and in adult tissues. In order to investigate the function of Cited2 during mouse embryogenesis, we introduced a null mutation into the Cited2 locus. Cited2(-/-) mutants died at late gestation and exhibited heart defects and exencephaly, arising from defective closure of the midbrain (MB) and hindbrain. Initiation of neural tube closure at the forebrain-midbrain (FB-MB) boundary, an essential step for closure of the cranial neural tube, was impaired in the Cited2(-/-) mutants. Gene marker analysis using in situ hybridization revealed that the patterning of the anterior neural plate and head mesenchyme was little affected or normal in the Cited2(-/-) embryos. However, Cited2 was required for the survival of neuroepithelial cells and its absence led to massive apoptosis in dorsal neuroectoderm around the FB-MB boundary and in a restricted transverse domain in the hindbrain. Treatment with folic acid significantly reduced the exencephalic phenotype in the Cited2(-/-) embryos both in vivo and in vitro. However, assessment of folate metabolism revealed no defect in the Cited2(-/-) mutants, and the elevated apoptosis observed in the neuroepithelium of the Cited2(-/-) mutants was apparently not decreased by folic acid supplementation. To our knowledge, the Cited2 mouse represents the first genetic model in which folic acid can prevent a defect in neural tube closure by a mechanism other than the neutralization of a defect in folate homeostasis.

Animals↗
PubMed2001

The utility of laboratory screening in medically III patients with psychiatric symptoms.

The presence of psychiatric illness in general hospital medical inpatients can complicate a patient's clinical course. Currently, there is no standard laboratory work-up recommended for this patient population. To begin to assess the utility of a routine panel of tests, the results of serum vitamin B12 (cobalamin) levels, folate levels, thyroid stimulating hormone levels, and syphilis serology of 349 patients were reviewed. These patients had been admitted to the hospital for nonpsychiatric conditions but either had preexisting psychiatric disturbances or developed a mood spectrum disorder or cognitive spectrum disorder during their hospitalization. The incidence of vitamin B12 and folate deficiencies in these patients was found to be higher than has been reported for the general population. Thus, routine screening for these vitamin deficiencies may be indicated because of their prevalence in this patient population.

Adolescent↗
PubMed1997

Folate deficiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal damage.

Folate deficiency causes massive incorporation of uracil into human DNA (4 million per cell) and chromosome breaks. The likely mechanism is the deficient methylation of dUMP to dTMP and subsequent incorporation of uracil into DNA by DNA polymerase. During repair of uracil in DNA, transient nicks are formed; two opposing nicks could lead to chromosome breaks. Both high DNA uracil levels and elevated micronucleus frequency (a measure of chromosome breaks) are reversed by folate administration. A significant proportion of the U.S. population has low folate levels, in the range associated with elevated uracil misincorporation and chromosome breaks. Such breaks could contribute to the increased risk of cancer and cognitive defects associated with folate deficiency in humans.

Chromosome Aberrations↗
PubMed1984

Low serum vitamin B12 in Alzheimer-type dementia.

Serum vitamin B12 levels (as determined by radio-immunoassay) were measured in 20 subjects aged 65 years and over with Alzheimer-type dementia, 20 age-matched subjects with non-Alzheimer type dementia and 20 age-matched subjects with no dementia. Serum vitamin B12 levels were significantly lower and serum vitamin B12 deficiency was significantly more frequent in subjects with Alzheimer-type dementia and were independent of age, sex, haematological abnormality or serum folate.

Aged↗
PubMed1994

Plasma homocysteine in relation to serum cobalamin and blood folate in a psychogeriatric population.

Plasma homocysteine, serum cobalamin and blood folate were analysed in 296 consecutive patients referred to a psychogeriatric department for diagnosis of mental disease. Plasma homocysteine correlated with positive significance with age and serum creatinine, and with negative significance with serum cobalamin and blood folate. Approximately 35-40% of the patients with low serum cobalamin (< 150 pmol l-1) or low blood folates (< 150 nmol l-1) exhibited normal values of plasma homocysteine (< 19.9 mumol l-1). Possibly, these patients do not have a deficiency of the vitamins in the tissue. At least 7.5% of the patients with serum cobalamin levels (> 150 pmol l-1) showed an inexplicably increased level of plasma homocysteine. These patients might have a deficiency of tissue cobalamin despite the normal serum cobalamin levels. The effect of cobalamin supplementation for 7-10 days on plasma homocysteine was tested in 62 patients with different levels of serum cobalamins. We found the most pronounced decrease of plasma homocysteine in the patients with lowest serum cobalamin levels and in the patients with highest plasma homocysteine, indicating that the percentage decrease of the initial concentration of plasma homocysteine could reflect the degree of cobalamin deficiency. Folate supplementation for 7-10 days reduced plasma homocysteine not only in patients with folate deficiency but also in those with a normal folate status, and even in patients with cobalamin deficiency. The latter patients further reduced their plasma homocysteine after additional cobalamin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2000

Hyperhomocyst(e)inemia, related vitamins and dementias.

Vitamin B12 and to a lesser extent folate deficiencies have been associated with dementias. Both these vitamins are determinants of plasma total homocysteine concentrations. In this review the frequency distributions of plasma vitamin B12, folate and homocysteine in South African males (# 51 yrs and > 51 yrs) illustrate the lower vitamin B12 levels in older subjects, and the shift toward elevated homocysteine concentrations in elderly people. Vitamin B12 deficiency appears to be associated with neuropsychiatric disorders, including dementias, but no causal relationship based on biochemical evidence has so far been established. Supplementation with vitamin B12 improves some neurological abnormalities and reverses only mild dementia of recent onset, but does not slow the progression of dementia. Elevated homocysteine levels appears to affect cognitive function, as measured by spatial copying skills and visual event-related potentials. Measurement of plasma homocysteine may help identify individuals with vitamin deficiencies and hyperhomocysteinemia. The relation between B-vitamins, homocysteine and dementia needs to explored further before vitamin supplementation is advocated to prevent or reverse neuropsychiatric disorders.

Aged↗
PubMed1990

Anterior ischemic optic neuropathy associated with macrocytic anemia.

A 37-year-old man experienced the acute onset of blurred vision, particularly in the inferior hemifield of his left eye. Neuro-ophthalmic examination showed a left afferent pupillary defect, a left inferior altitudinal visual field deficit, bilateral nerve fiber layer infarcts and hemorrhages, and left optic disc elevation with edema of the nerve fiber bundle. Complete examination and laboratory studies revealed only a severe folate deficiency anemia. This is the first well-documented report of anterior ischemic optic neuropathy associated with anemia in the absence of other systemic abnormalities.

Adult↗
PubMed1995

Cobalamin and folate deficiency in the elderly.

Elderly persons are more likely to have low values for serum and erythrocyte folate, and for serum cobalamin. Many of those with low vitamin levels have biochemical abnormalities consistent with true deficiency, including increased formiminoglutamic acid excretion, abnormal marrow deoxyuridine suppression, and raised serum levels of methylmalonic acid and homocysteine. Therapy with the appropriate vitamin reverses the biochemical defect. Despite this, the clinical consequences for most elderly persons are remarkably few. True megaloblastic anaemia is rare, and the small number of therapeutic trials to date have not improved the levels of haemoglobin in the treated subjects, although the mean corpuscular volume has decreased significantly. There has been recent concern that these low blood vitamin levels might be important causes of nervous system damage, but studies specifically of the elderly have not demonstrated overall improvements in neurological function following therapy. Vascular damage from high blood homocysteine levels secondary to cobalamin or folate deficiency remains a potential hazard. Dietary insufficiency, malabsorption of protein-bound vitamin B12 secondary to atrophic gastritis, and defective absorption of folyl polyglutamates seem the likeliest possible causes. Pernicious anaemia, although a common cause of severe megaloblastic anaemia in the elderly, is an infrequent cause for the low cobalamin levels in population studies. Although the benefits are uncertain, the balance of the evidence suggests that one should treat elderly persons with low values of cobalamin or folate. Crystalline vitamin B12 and folic acid are absorbed normally and are therefore suitable for replacement therapy, provided that pernicious anaemia is excluded.

Aged↗
PubMed2004

Alcohol and cancer: genetic and nutritional aspects.

Chronic alcohol consumption is a major risk factor for cancer of upper aero-digestive tract (oro-pharynx, hypopharynx, larynx and oesophagus), the liver, the colo-rectum and the breast. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol-associated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and protein, destroys the folate molecule and results in secondary cellular hyper-regeneration. Acetaldehyde is produced by mucosal and cellular alcohol dehydrogenase, cytochrome P450 2E1 and through bacterial oxidation. Its generation and/or its metabolism is modulated as a result of polymorphisms or mutations of the genes responsible for these enzymes. Acetaldehyde can also be produced by oral bacteria. Smoking, which changes the oral bacterial flora, also increases salivary acetaldehyde. Cigarette smoke and some alcoholic beverages, such as Calvados, contain acetaldehyde. In addition, chronic alcohol consumption induces cytochrome P450 2E1 enxyme activity in mucosal cells, resulting in an increased generation of reactive oxygen species and in an increased activation of various dietary and environmental carcinogens. Deficiencies of riboflavin, Zn, folate and possibly retinoic acid may further enhance alcohol-associated carcinogenesis. Finally, methyl deficiency as a result of multiple alcohol-induced changes leads to DNA hypomethylation. A depletion of lipotropes, including methionine, choline, betaine and S-adenosylmethionine, as well as folate, results in the hypomethylation of oncogenes and may lead to DNA strand breaks, all of which are associated with increased carcinogenesis.

Acetaldehyde↗
PubMed1985

Clinical role of pteridine therapy in tetrahydrobiopterin deficiency.

In most patients with deficiency of tetrahydrobiopterin (BH4) continuous administration of BH4 or of a synthetic analogue such as 6-methyltetrahydropterin (6-MPH4) lowers plasma phenylalanine concentrations to the therapeutic range. The effective dose of BH4 varies from 1 to 2 mg kg-1 daily in patients with defective biopterin synthesis, to 5 mg kg-1 or more in patients with dihydropteridine reductase (DHPR) deficiency. The cost of 2 mg kg-1 day-1 of BH4 is comparable to the cost of a low phenylalanine diet. Higher doses of pterins given orally (20 mg kg-1) raise the levels of tetrahydropterin in cerebrospinal fluid (CSF) to normal in patients with defective biopterin synthesis in whom initial concentration of biopterin species are low. In some, but not all, such patients pterin therapy also raises CSF amine metabolite concentrations and ameliorates symptoms. High dose therapy does not appear to be effective in raising CSF pterin levels in patients with DHPR deficiency who already accumulate dihydrobiopterin (BH2) in CSF. Central folate deficiency is an additional cause of neurological deterioration in patients with DHPR deficiency who require supplementation with folate as folinic acid. It is suggested that the accumulation of BH2 in such patients competitively interferes with folate metabolism.

Amino Acid Metabolism, Inborn Errors↗
PubMed2000

Etiology and diagnostic evaluation of macrocytosis.

BACKGROUND: Elevation of mean cell volume (MCV) is a common clinical problem, but the etiologic spectrum and optimal diagnostic evaluation of macrocytosis are not well defined. METHODS: We studied 300 consecutive hospitalized adult patients with MCV values > or = 100 fL. Assessment included complete blood counts, morphologic review, liver function tests, and levels of serum cobalamin (Cbl), methylmalonic acid, and total homocysteine. RESULTS: The most common cause of macrocytosis was drug therapy, followed by alcohol, liver disease, and reticulocytosis. Megaloblastic hematopoiesis accounted for less than 10% of cases. MCV values > 120 fL were usually caused by Cbl deficiency. Anisocytosis, macro-ovalocytosis, and teardrop erythrocytes were most prominent in megaloblastic hematopoiesis. Elevated levels of serum methylmalonic acid and total homocysteine were useful in the diagnosis of Cbl deficiency. CONCLUSIONS: Drugs and alcohol are the most common causes of macrocytosis in hospitalized patients in a New York City teaching hospital. We have formulated tentative guidelines for the evaluation of high MCV values in this setting.

Adult↗
PubMed1982

The metabolism of [3',5',9(n)-3H] pteroylglutamic acid by chicken liver in vivo. Effects of folate deficiency and vitamin B12 supplementation.

1. Control, folate-deficient and vitamin B12-supplemented chickens were given [3', 5', 9 (n)-3H] pteroylglutamic acid by intraperitoneal injection. After various time intervals (1.5 h-8d) the incorporation of radioactivity into hepatic folate derivatives was measured. 2. The results confirm that avian species have a faster assimilation of folate than most mammalian species. 3. Folate deficiency increased the incorporation and retention of [3H] pteroylglutamic acid. The degree of folate conjugation was unaffected by folate deficiency but the formyl to methyl folate ratio was decreased. 4. Vitamin B12 supplementation had no effect on the uptake or conjugation of [3H] pteroylglutamic acid, but increased the formyl to methyl folate ratio.

Animals↗
PubMed2002

Folate and Vitamin B(12) deficiency presenting as pancytopenia in pregnancy: a case report and review of the literature.

We present a case of extreme pancytopenia in a 27-year-old pregnant woman. The initial picture was compatible with a severe hematological problem in the category of aplastic anemia, paroxysmal nocturnal hemoglobinuria or even acute leukemia. The further biochemical investigations revealed, however, a folate deficiency. Nowadays this is a very rare cause of pancytopenia. Next to this she also had a Vitamin B(12) deficiency due to intrinsic factor failure. The recent literature is discussed.

Adult↗

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