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PubMed1965

FOLIC ACID.

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Anemia↗
PubMed2026

Neuroimaging in cerebral folate deficiencies.

Cerebral folate deficiency refers to neurological disorders associated with a reduced cerebrospinal fluid (CSF) concentration of 5-methyltetrahydrofolate (5-MTHF), arising from primary defects in folate transport or metabolism, or secondarily from acquired or other inherited conditions. Clinical presentation ranges from infancy to adulthood, with manifestations including developmental delay, seizures, cognitive impairment, and neuropsychiatric symptoms. Folate plays a central role in one-carbon metabolism, requiring interaction with other B-vitamins, most notably vitamin B12, to support nucleotide synthesis, methylation reactions, and myelin production. Disruption of folate-dependent pathways contributes to the imaging findings of cerebral folate deficiencies, which include abnormal white matter, calcifications, cerebral or cerebellar atrophy, and in some cases, stroke, or stroke-like lesions. This review outlines folate biochemistry, transport mechanisms into the central nervous system, and associated genetic defects, followed by a discussion of imaging features in primary and secondary cerebral folate deficiencies. Relevant differential diagnoses, particularly cobalamin-related disorders, are also examined. Importantly, many cerebral folate deficiencies are potentially reversible with timely recognition and therapy, underscoring the important role of neuroimaging in diagnosis and follow-up of these disorders.

Humans↗
PubMed1979

Serum folate and folic acid binding proteins in iron deficiency anaemia.

Serum and red cell folate and folic acid binding protein (FABP) concentrations were determined on 20 iron deficiency anaemic children of both sexes aged 6--12 years. All cases had haemoglobin level less than 12 gm% or haematocrit less than 36% with low serum iron and elevated unsaturated iron binding capacity. Serum folate levels in the anaemic group was not significantly different from that of normal subjects while red cell folate level was significantly lower in the anaemic group. However, all cases had red cell folate levels higher than 100 ng/ml. There was a direct relationship between the haemoglobin concentration and serum folate level. Serum FABP level in the anaemic group was found to be significantly higher than that of normal subjects and showed no correlation with haemoglobin, haematocrit, serum or red cell folate levels. The significance of elevated serum FABP was discussed.

Anemia, Hypochromic↗
PubMed1971

Associations between drugs administered during pregnancy and congenital abnormalities of the fetus.

In a retrospective study to compare the drug consumption during pregnancy of mothers of infants with congenital abnormalities and of those without, over 97% of 1,369 mothers took prescribed drugs and 65% self-administered drugs. Significantly more mothers of infants with congenital abnormalities took aspirin, antacids, dextroamphetamine, phenobarbitone, sodium amytal, other barbiturates, cough medicines, iron, sulphonamides, and nicotinamide than mothers in the control group. However, most mothers taking analgesics, antacids, appetite suppressants, barbiturates, cough medicines, iron, sulphonamides, and vitamins produced normal infants. Any teratogenic effect of these drugs is therefore one of low potency. On the other hand, deficiencies such as those of ascorbic acid and folic acid may have a teratogenic effect. There is need for caution in presuming teratogenic effects on the basis of the associations shown here. During pregnancy, however, it would appear wise to avoid the administration of any drug which carries a suspicion of teratogenicity unless that drug is specifically indicated, and self-medication with common household remedies such as aspirin and antacids should be avoided. These recommendations would also apply to any woman of childbearing age in whom conception is likely.

Abnormalities, Drug-Induced↗
PubMed2001

Prevention of pathologies associated with oxidative stress and dietary intake deficiencies: folate deficiency and requirements.

Folate (folic acid, folacin) is an essential vitamin that is found in nature. Folates contain the core chemical structure of pteroylglutamic acid, but vary in their state of reduction, the single carbon moiety they bear and/or the length of the glutamate chain. At least 50% of whole body folate is stored in the liver. The influence of intracellular folate concentration depends largely on dietary intake. The supply of folate depends primarily on the quantity and bioavailability of ingested folate and the rate of loss by urinary and fecal routes and through catabolism.

Animals↗
PubMed1989

[Megaloblastic anemia and gastrointestinal manifestations in Lima. The tip of the iceberg?].

UNLABELLED: The records of the last three years from the Hematology service are reviewed and twenty patients (6.23%) fulfilling the inclusion criteria were chosen out of a total of 316. RESULTS: pallor and malaise 100%, change in bowel movements 75%, nausea, vomiting and hemorrhage 40%, jaundice 25%, nausea aroused by food 20%, infection 10%. Severe hyporegenerative anemia 100%, thrombocytopenia 75%, pancytopenia 60%. We found as associated conditions: gynecological and obstetric history 25%, enteric and peritoneal tuberculosis 15%, and without an apparent cause (primary) 40%. Levels of vitamin B12 and folic acid were measured in eleven patients and the finding were: B12 deficiency in six (54.5%), folic acid deficiency in three (27.2%) and deficiency of both in two (18.1%). With the exception of one patient who died from sepsis, all the other patients had a favorable outcome with vitamin treatment. We found folic acid deficiency associated with ferropenia mainly in those patients with obstetric history; the combined deficit in those patients with an associated pathological process, and B12 deficiency in the group without any apparent cause. From the available national information and our observations we can conclude that we are facing an outbreak of megaloblastic anemia that frequently goes on with gastrointestinal manifestations and for which the cause has not been elucidated.

Adolescent↗
PubMed1997

[Folates and the neural tube. Review of the literature].

There are two types of neural tube fusion abnormality (NTFA)--craniorachischisis and rachischisis--with a prevalence of 11.2/10,000 in continental Europe. Their prevalence varies widely and is influenced by many factors, including geographical, racial and seasonal components. The transmission of NTFAs is usually polygenic and affected by many factors, and far more rarely of the mendelian monogenic type. The occurrence of NTFAs has been shown to be due to folic acid (FA) deficiency. First suspected in 1965, FA deficiency was proved to be a cause of NTFAs both occurring and recurring in the 1980s. FA deficiency might act by preventing the remethylation of homocysteine to methionine, the latter is known to play an essential role in fusion of the neural tube in animals. Primary prevention of NTFAs therefore requires that FA supplementation be given to women planning a pregnancy and after conception. Two possible ways of preventing FA deficiency can be envisaged, ie. via folic acid supplementation or systemic enrichment of the basic diet. Neither of the two alternatives is sufficient by itself and probably a combination of the two would provide the best means of preventing neural tube defects.

Animals↗
PubMed1978

[Folic acid and vitamin B 12 in chronic alcoholics].

In 64 chronic alcoholics folic acid and vitamin B12 in plasma and folic acid in erythrocytes were determined. The mean values of folic acid in plasma and in erythrocytes were significantly below normal. The determination of vitamin B12 showed normal results in a group of 20 cases treated with vitamin B12 containing drugs, whereas in the group of untreated alcoholics significantly reduced values were found. Comparison of folic acid and vitamin B12 concentrations in plasma revealed a more frequent deficiency of folic acid than of vitamin B12, which was combined with anemia in half the alcoholics investigated. The need to treat chronic alcoholics with folic acid and vitamin B12 is pointed out.

Adult↗