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Results for “FOLIC ACID DEFICIENCY”

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PubMedDate not supplied

Prevalence and type of anaemia in young Egyptian patients with type 1 diabetes mellitus.

Over a 2-month period, 200 type 1 diabetic patients attending a paediatric diabetic clinic in Cairo, Egypt were screened for anaemia and other complications of diabetes. The mean age was 11.2 years and the mean duration of diabetes was 4.0 years. Anaemia was diagnosed in 75 patients (37.5%) overall: 45 had microcytic hypochromic anaemia, 18 normocytic normochromic and 12 macrocytic hyperchromic. Of the 75, 41 patients (54.7%) had iron deficiency, 14 (18.7%) had folate deficiency and 14 (18.7%) had thalassaemia minor. Three patients (4%) had coeliac disease, and 18 patients (24%) had parasitic infections. None of the patients had hypothyroidism, renal failure or vitamin B12 deficiency.

Adolescent↗
PubMed2002

Folate deficiency, methionine metabolism, and alcoholic liver disease.

Methionine metabolism is regulated by folate, and both folate deficiency and abnormal hepatic methionine metabolism are recognized features of alcoholic liver disease (ALD). Previously, histological features of ALD were induced in castrated male micropigs fed diets containing ethanol at 40% of kilocalories for 12 months, whereas in male micropigs fed the same diets for 12 months abnormal methionine metabolism and hepatocellular apoptosis developed. Folate deficiency may promote the development of ALD by accentuating abnormal methionine metabolism. Intact male micropigs received eucaloric diets that were folate sufficient, folate deficient, or each containing 40% of kilocalories as ethanol for 14 weeks. Folate deficiency alone reduced hepatic folates by one half, and ethanol feeding alone reduced methionine synthase, S-adenosylmethionine (SAM), and glutathione (GSH) levels and elevated plasma malondialdehyde (MDA) levels. The combined regimen elevated plasma homocysteine, hepatic S-adenosylhomocysteine (SAH), urinary 8-hydroxy-2-deoxyguanosine (oxy(8)dG), an index of DNA oxidation, and serum aspartate aminotransferase (AST) levels. Terminal hepatic histopathologic characteristics included typical features of steatonecrosis and focal inflammation in pigs fed the combined diet, with no changes in the other groups. Hepatic SAM levels correlated with those of GSH, whereas urinary oxy(8)dG and plasma MDA levels correlated with the SAM:SAH ratio and to hepatic GSH. The results demonstrate the linkage of abnormal methionine metabolism to products of DNA and lipid oxidation and to liver injury. The finding of steatonecrosis and focal inflammation only in the combined diet group supports the suggestion that folate deficiency promotes and folate sufficiency protects against the early onset of methionine cycle-mediated ALD.

Animals↗
PubMed1992

Nutritional anaemias.

Nutritional anaemia is recognized as a major public health problem throughout the world, especially in developing countries. Infants, young children, menstruating women and, in particular, pregnant women are most frequently affected. Sufficient evidence suggests that iron deficiency is the most common cause of nutritional anaemia in the world. Folate deficiency is considered as the second most common cause. In this chapter we discuss the factors determining nutritional inadequacy in iron and folate requirements versus iron and folate intake, particularly in different age/sex categories; the amounts of iron and folate involved in daily exchange and the role of the diet and physiological and pathological variations in losses and requirements are reviewed. The consequences in terms of health of iron and folate deficiencies and methods for assessing iron and folate status of populations are also presented.

Adolescent↗
PubMed1977

Long-term of phenytoin: Effects on whole blood and red cell folate and haematological parameters.

Patients treated when phenytoin for periods of several months or years have slightly, but significantly lower whole blood and red cell folate values than comparable controls. This holds true irrespective of whether folate is determined microbiologically with Lactobacillus casei or by a radioligand method using the bovine milk binder. Haematological parameters including Hb, MCH, MCV and red blood cell counts did not show any alterations and no patient developed any signs of anaemia. This indicates that long-term use of phenytoin does not cause a clinically significant state of folate deficiency, unless some other contributing factors are present.

Adolescent↗
PubMed2003

Severe folate deficiency mimicking HELLP syndrome--report of two cases.

Severe folate deficiency in pregnancy may mimick HELLP syndrome as there are similar features in both. Proper diagnosis is important as far as the prognosis and management are concerned. Two cases of severe folate deficiency occuring in multigravid women mimicking HELLP syndrome are reported below with review of literature.

Adult↗
PubMed1979

[Granulocyte dysfunction in transcobalamin II deficiency].

Granulocytes from a boy with congenital transcobalamin II (TC II) deficiency were found to have abnormally low antibacterial activity against Staphylococcus aureus. Transfusion of normal plasma supplemented with hydroxocobalamin temporarily restored granulocyte bactericidal activity to normal. Granulocyte function was also temporarily restored by oral leucovorin. The defect appears to be causally related to the patient's TC II deficiency and indirectly to an intracellular deficiency of cobalamin and folate coenzymes [1].

Blood Bactericidal Activity↗
PubMedDate not supplied

[The role of folates in the diverse biochemical processes that control mental function].

A variety of studies indicate that folate deficiency is associated with the appearance of problems of a neuromuscular or neurological nature such as depression, muscular and mental fatigue, states of confusion and non-senile dementia, and that these processes improve fully or partly when the deficiency is corrected. Because of the role of folates in the reactions in synthesis of neuro-transmitter and elements of neuron structure, it is not surprising that a deficiency is associated with depression and other mental problems. Folates are involved in the synthesis of S-adenosylmethionine (SAM) which is the main contributor of methyl groups in the nervous system and whose action as an antidepressive agent is confirmed. They are also involved in the synthesis of glutamate which is an excitant neurotransmitter, and in the formation of puric and pyrimidic bases. An alternative mechanism for explaining the etiopathogenesis of folate deficiency in depression and other mental disorders involves the regeneration of tetrahydrobiopterin (THB) which is an essential cofactor in hydroxylation process in the brains of mammals. Folate deficiency is a common nutritional problem in many groups of the Spanish population and, given the role of this vitamin in the operation of the nervous system, we might consider the possibility that, in some case, folate deficiency may cause or aggravate some alterations to mental function.

Brain↗
PubMed1998

Anaemia--more than meets the eye.

Anaemia is a commonly encountered medical condition, although associated ophthalmic manifestations are not often sought or recognised. The authors present a case report of a patient with severe vitamin B12 deficiency anaemia with florid retinal changes classical of anaemic retinopathy. A review of the ocular involvement in anaemia is also presented.

Adult↗
PubMed2000

Vitamin B(12) deficiency and depression in physically disabled older women: epidemiologic evidence from the Women's Health and Aging Study.

OBJECTIVE: It has been hypothesized that adequate concentrations of vitamin B(12) and folate are essential to maintain the integrity of the neurological systems involved in mood regulation, but epidemiologic evidence for such a link in the general population is unavailable. This study examined whether community-dwelling older women with metabolically significant vitamin B(12) or folate deficiency are particularly prone to depression. METHOD: Serum levels of vitamin B(12), folate, methylmalonic acid, and total homocysteine were assayed in 700 disabled, nondemented women aged 65 years and over living in the community. Depressive symptoms were measured by means of the Geriatric Depression Scale and categorized as no depression, mild depression, and severe depression. RESULTS: Serum homocysteine levels, serum folate levels, and the prevalences of folate deficiency and anemia were not associated with depression status. The depressed subjects, especially those with severe depression, had a significantly higher serum methylmalonic acid level and a nonsignificantly lower serum vitamin B(12) level than the nondepressed subjects. Metabolically significant vitamin B(12) deficiency was present in 14.9% of the 478 nondepressed subjects, 17. 0% of the 100 mildly depressed subjects, and 27.0% of the 122 severely depressed women. After adjustment for sociodemographic characteristics and health status, the subjects with vitamin B(12) deficiency were 2.05 times as likely to be severely depressed as were nondeficient subjects. CONCLUSIONS: In community-dwelling older women, metabolically significant vitamin B(12)deficiency is associated with a twofold risk of severe depression.

Age Factors↗
PubMed2003

Folate deprivation induces neurodegeneration: roles of oxidative stress and increased homocysteine.

Clinical studies suggest a relationship between folate deficiency and neurological and disorders including Alzheimer's disease (AD). To investigate mechanisms underlying this association, we examined the consequences of folate deprivation on neuronal cultures. Culturing embryonic cortical neurons and differentiated SH-SY-5Y human neuroblastoma cells in folate-free medium induced neurodegenerative changes characteristic of those observed in AD, including increased cytosolic calcium, reactive oxygen species (ROS), phospho-tau and apoptosis. In accord with clinical studies, generation of the neurotoxic amino acid homocysteine (HC) was likely to contribute to these phenomena, since (1) a significant increase in HC was detected following folate deprivation, (2) addition of the inhibitor of HC formation, 3-deazaadenosine, both prevented HC formation and eliminated the increase in ROS that normally accompanied folate deprivation, (3) direct addition of HC in the presence of folate induced the neurotoxic effects that accompanied folate deprivation, and (4) an antagonist of NMDA channels that blocks HC-induced calcium influx also blocked calcium influx following folate deprivation. Folate deprivation decreased the reduced form of glutathione, indicating a depletion of oxidative buffering capacity. This line of reasoning was supported by an increase in glutathione and reduction in ROS following supplementation of folate-deprived cultures with the cell-permeant glutathione precursor, N-acetyl-L-cysteine, or vitamin E. Folate deprivation potentiated ROS and apoptosis induced by amyloid-beta, while folate supplementation at higher concentrations prevented generation of ROS by amyloid-beta, suggesting that folate levels modulate the extent of amyloid-beta neurotoxicity. These findings underscore the importance of folate metabolism in neuronal homeostasis and suggest that folate deficiency may augment AD neuropathology by increasing ROS and excitotoxicity via HC generation.

Animals↗
PubMed1981

Folate deficiency and in vitro palatogenesis I: effects of a folate-deficient culture on rabbit palate fusion and folate pools.

Folate compounds are essential for nucleic acid metabolism and data from in vitro experiments have shown that folatee deficiency during pregnancy induced by dietary deprivation or folate antagonists is teratogenic. The craniofacial complex is a main target of this teratogen, with the lip and palate being especially vulnerable. The direct effect of folate deficiency on a target teratogenic tissue was, therefore, examined in vitro using fetal rabbit palates in an organ culture system. Folate pool sizes in the palates on the 4 days preceding fusion were determined by competitive binding assay. There was a sharp decrease in folate levels from 2.63 +/- 0.86 ng/mg wet wt on Day 15 of gestation to 1.23 +/- 0.35 ng/mg on Day 16 and 0.59 +/- 0.12 ng/mg on Day 17. The folat pool size on Day 14 was found to be quite variable with a mean of 1.93 ng/mg wet wt. Comparable results were obtained when the folate pool sizes were expressed as nanograms of folate per milligram of protein. The effect of a folate-deficiency culture medium on in vitro fusion and folate pool sizes was examined. The results of incubating palatal shelves excised on Days 14, 15, 16, and 17 of gestation for 5, 4, 3, and 2 days, respectively, show that a folate-depleted medium neither prevented nor delayed fusion. An examination of the palatal pool size after incubation in folate-deficient media revealed that while there was some decrease in folate levels, the palates apparently retained sufficient folate to support cellular activity.

Abnormalities, Drug-Induced↗
PubMed2002

Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson's disease.

Although the cause of Parkinson's disease (PD) is unknown, data suggest roles for environmental factors that may sensitize dopaminergic neurons to age-related dysfunction and death. Based upon epidemiological data suggesting roles for dietary factors in PD and other age-related neurodegenerative disorders, we tested the hypothesis that dietary folate can modify vulnerability of dopaminergic neurons to dysfunction and death in a mouse model of PD. We report that dietary folate deficiency sensitizes mice to MPTP-induced PD-like pathology and motor dysfunction. Mice on a folate-deficient diet exhibit elevated levels of plasma homocysteine. When infused directly into either the substantia nigra or striatum, homocysteine exacerbates MPTP-induced dopamine depletion, neuronal degeneration and motor dysfunction. Homocysteine exacerbates oxidative stress, mitochondrial dysfunction and apoptosis in human dopaminergic cells exposed to the pesticide rotenone or the pro-oxidant Fe(2+). The adverse effects of homocysteine on dopaminergic cells is ameliorated by administration of the antioxidant uric acid and by an inhibitor of poly (ADP-ribose) polymerase. The ability of folate deficiency and elevated homocysteine levels to sensitize dopaminergic neurons to environmental toxins suggests a mechanism whereby dietary folate may influence risk for PD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2001

Homocysteine and methylmalonic acid as indicators of folate and vitamin B12 deficiency in pregnancy.

Deficiency of folate during pregnancy is associated with megaloblastic anaemia. Lower levels of folate and vitamin B12 have been reported in mothers whose offspring had neural tube defects compared to unaffected controls. Increased methylmalonic acid levels are a sensitive indicator of mild vitamin B12 deficiency and elevated homocysteine levels denote vitamin B12 or folate deficiency. We have investigated the relationship between serum concentration of total homocysteine, methylmalonic acid, vitamin B12 and folate in pregnancy. A significant inverse correlation was found between homocysteine and red cell folate and, to a lesser extent, serum folate. In addition, a significant inverse correlation was found between methylmalonic acid and vitamin B12. No significant relationship was found between homocysteine and vitamin B12. The relationship between red cell folate and serum folate and homocysteine may be useful for detecting borderline folate deficiency in pregnancy and indicate pregnancies at risk of neural tube defect. These sensitive assays are useful tools for the further investigation of folate vitamin B12 and metabolism in normal and abnormal pregnancy.

Adult↗