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At least 19 recordsLinked to original sources
PubMed1989

[Neurologic and psychologic disorders in folic acid deficiency].

Folic acid deficiency is the most common of all vitamin deficiencies in North America and in Western Europe, usually in association with other vitamin deficiencies. Alcoholism is considered to be the most frequent cause of folic acid deficiency, as far as the Western world is concerned. Severe neurological and mental disturbances can develop in case of folate deficiency probably long before the manifestation of macrocythaemia. Among the neurological sequelae of folic acid deficiency the main phenomena that are discussed as likely are polyneuropathy, funicular disease of the spine and restless legs. The psychic or mental symptoms that can be ascribed to folic acid deficiency are non-specific and correspond with the symptoms of a psychosis that can have physical causes. Administration of folic acid has repeatedly resulted in significant improvements of neurological and mental symptoms in folic acid deficiency. The exact mechanisms involved in a damage to the nervous system are not sufficiently clarified for folic acid deficiency. Diagnosis is effected mainly by determining the folic acid concentration in the serum. Daily administration of approx. 1.25-15 mg folic acid (oral and/or parenteral) is recommended. Mild side effects such as tiredness and irritability have been noted only with high folic acid dosage levels.

Folic Acid Deficiency↗
PubMed1977

The effect of aminopterin-induced folic acid deficiency on spermatogenesis.

Folic acid deficiency was produced by injecting aminopterin into adult male albino rats, resulting in inhibition of spermatogenesis. Bone marrow smears were studied to serve as an index of folic acid deficiency; however, changes in spermatogenesis were noticed earlier than the bone marrow changes. Meiotic division was affected more than mitotic division. The nuclei of spermatogenic cells showed degenerative changes. Chromosomal abnormalities, chiefly sticky chromosomes, were noticed in squashed preparations of seminiferous tubules.

Aminopterin↗
PubMed1977

Sparing effect of folic acid deficiency on the development of vitamin B12 deficiency in baboons fed a vitamin B12 deficient diet.

The effect of a vitamin B12 and folic acid deficient diet on juvenile and adolescent baboons (Papio cynocephalus anubis) was studied. The baboons developed clinical and hematological signs characteristics of folacin deficiency, although they were less severe in juvenile baboons. The signs disappeared when folic acid was replaced in the diet. The serum vitamin B12 levels increased in all baboons fed the vitamin B12 and folic acid deficient diet. When folic acid was added to the diet, the levels gradually decreased in adolescent baboons, liver vitamin B12 levels decreased to a lesser extent when fed a vitamin B12 and folic acid deficient diet than when fed a vitamin B12 deficient diet. In juvenile baboons fed a vitamin B12 and folic acid deficient diet, for 7 months and a vitamin B12 deficient diet for a further 11 months, liver vitamin B12 levels did not decrease at any time but were similar to those in baboons fed a vitamin B12 and folic acid supplemented diet.

Aging↗
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↗
PubMed1989

Pancytopenia--a rare manifestation of folic acid deficiency.

In the western world folic acid deficiency is a relatively rare cause of anaemia in the elderly population. A 79-year-old woman presented with pancytopenia (haemoglobin 3.4 mmol l-1, leucocytes 1.2.10(9)l-1, thrombocytes 22.10(9)l-1) due to folic acid deficiency. The deficiency was caused by an extremely low dietary intake. The case was complicated with infection and haemorrhagic manifestations. Administration of folic acid increased the number of erythrocytes, leucocytes and thrombocytes markedly. Beside vitamin B12 deficiency folic acid deficiency must be borne in mind in megaloblastic anaemias complicated with leucopenia and/or thrombocytopenia. Since the body stores of folic acid are low, rapid diagnosis and treatment are important.

Aged↗
PubMed1992

Treatment of iron-deficiency anemia complicated by scurvy and folic acid deficiency.

We present a case of a child with iron-deficiency anemia, folic acid deficiency, and scurvy. His anemia proved refractory to treatment with iron until he received both folic acid and vitamin C supplementation. This case illustrates the importance of the evaluation of ascorbic acid and folate status in treating iron-deficiency anemia initially refractory to iron supplementation, because multiple nutrient deficiencies may coexist.

Anemia, Hypochromic↗
PubMed1977

[Manifest and latent folic acid deficiency in the aged (author's transl)].

The serum folate level of 100 aged persons (after 70) was decreased (less than 4 ng/ml) in 41% of the cases (manifest deficiency of folic acid). In the group of aged persons having normal folate values, in 41% of the cases the clearance method proved a latent folic acid deficiency, being the 15 minute value after 15 gamma/kg folic acid i.v., less than 25 ng/ml.

Adult↗
PubMed1976

Effect of vitamin B12 and folic acid deficiencies on neutrophil function.

Morphological and quantitative neutrophil abnormalities are common in the megaloblastic anemias of vitamin B12 and folic acid deficiency. Little is known, however, about the role of these vitamins in normal leukocyte function. Seven patients with megaloblastic bone marrows, four with vitamin B12 deficiency and three with folic acid deficiency, were studied to determine the effect, if any, of these deficiencies on leukocyte function. Phagocytosis of staphylococci, hexose monophosphate shunt activation with phagocytosis, and microbicidal capacity against Staphylococcus aureus were determined prior to the institution of specific therapy. In two instances, these studies were repeated following treatment. There was no impairment of phagocytosis per se, and resting metabolism was not significantly decreased. With phagocytosis, however, metabolic activation was decreased to 35%-36% of control values in the leukocytes of patients with vitamin B12 deficiency but not in the leukocytes of patients with folic acid deficiency. Bacterial killing was slightly decreased in vitamin B12 but not in folic acid deficiency. These abnormalities of function were reversed after specific therapy. These findings suggested a specific role for vitamin B12 in the production of intermediates necessary for normal cell function.

Blood Bactericidal Activity↗
PubMed1975

[Frequent and rare forms of vitamin B 12 and folic acid deficiency anemias].

The common and rarer causes of vitamin B12 and folic acid deficiency are discussed with special reference to pathophysiological aspects and conditions in Switzerland. The overall incidence of Addisonian pernicious anemia was found to be 80 per 100,000 patients, whereas the incidence of other B12 deficiency states was 18 per 100,000 patients. Folic acid deficiency was found in 23 of 100,000 patients, though this figure appears to be an underestimate. Nutritional (latent) folate deficiency seems to be the most frequent vitamin deficiency in Switzerland.

Anemia, Pernicious↗
PubMed1978

[Effect of chronic alcohol administration and of folic acid deficiency on iron absorption].

The influence of chronic alcohol ingestion and artificially induced folic acid deficiency on iron absorption has been measured in rabbits by whole body counter. Results show that chronic alcohol ingestion does not modify iron absorption. Folic acid deficiency increases iron absorption by two probable mechanisms: first by increased plasma iron turnover (PIT), which parallels ineffective erythropoiesis, and second by a probable direct effect on the intestinal mucous membranes. This second mechanism appears to be independent of PIT: concomitant deficiency of folic acid and alcohol ingestion produces an increase in iron absorption without modification of PIT. Experience with drugs inhibiting protein synthesis suggests that this increase may be mediated by decreased protein synthesis.

Alcoholism↗
PubMed1990

Anaemia in rheumatoid arthritis: the role of iron, vitamin B12, and folic acid deficiency, and erythropoietin responsiveness.

Thirty six patients with rheumatoid arthritis (RA) (25 with anaemia) were studied to establish the role of iron, vitamin B12, and folic acid deficiency, erythropoietin responsiveness, and iron absorption in the diagnosis and pathogenesis of anaemia in RA. Iron deficiency, assessed by stainable bone marrow iron content, occurred in 13/25 (52%), vitamin B12 deficiency in 7/24 (29%), and folic acid deficiency in 5/24 (21%) of the anaemic patients. Only 8/25 (32%) had just one type of anaemia. The iron deficiency of anaemia of chronic disease (ACD) was distinguished by ferritin concentration, which was higher in that group. Mean cell volume (MCV) and mean cell haemoglobin (MCH) were lower in both anaemic groups, but most pronounced in iron deficient patients. Folic acid, and especially vitamin B12 deficiency, masked iron deficiency by increasing the MCV and MCH. Iron absorption tended to be highest in iron deficiency and lowest in ACD, suggesting that decreased iron absorption is not a cause of ACD in RA. No specific causes were found for vitamin B12 or folic acid deficiency. Haemoglobin concentration was negatively correlated with erythrocyte sedimentation rate in the group with ACD. Erythropoietin response was lower in ACD than in iron deficient patients. It was concluded that generally more than one type of anaemia is present simultaneously in anaemic patients with RA. The diagnosis of each type may be masked by another. Studies on pathogenesis of the anaemia are difficult as deficiencies generally coexist with ACD. Disease activity and, possibly, erythropoietin responsiveness are major factors in ACD pathogenesis.

Aged↗
PubMed1992

Disturbed reproductive performance in extreme folic acid deficient golden hamsters.

We studied the effects of folic acid-deficient diets on maternal red blood cell folate level and reproductive performance in golden hamsters (Mesocricetus auratus, Waterhouse). Animals on the same day of oestrous cycle were put together and finally divided into three groups. Each group comprised at least 12 mature female hamsters. The animals were given three different diets, which were commenced before mating. The feeding regimens comprised a standard diet (group 1), or a folic acid-deficient diet which started either 2 weeks (group 2) or 16 weeks (group 3) prior to mating. The regimens were continued until sacrifice of the animals on day 9 of pregnancy. Pregnancy was realized by caging a male with a selected female during the night of ovulation. Just prior to sacrifice, blood samples were drawn to measure maternal folic acid levels in red blood cells. The pregnant uteri were removed and the embryonic sacs were carefully dissected away from the uterus. The number of sacs per pregnant animal was noted. Extreme folic acid deficiencies were confirmed in the pregnant golden hamsters on a folic acid-deficient diet which started 16 weeks prior to mating as compared to those on a standard diet and on a folic acid-deficient diet which started 2 weeks prior to mating. This deficiency appears to interfere with normal reproductive performance. It caused early embryonic loss several days after mating and resulted, finally, in restoration of the oestrous cycle.

Animals↗
PubMed1975

Folic acid deficiency in the United States: folate assays in a prenatal clinic.

Tissue deficiency of folic acid, as measured by a red cell folate level below 150 ng. per milliliter, was present in 16 per cent of 110 sequential pregnant women at the time of their first prenatal visit to a municipal clinic. A further 14 per cent of subjects had red cell folate levels in the range "suggestive but not conclusive for tissue folate depletion" (150 to 199 ng. per milliliter). All of the subjects were from low-income families in New York City and most were black or of Puerto Rican origin. Serum folate levels showed good general correlation with red cell folate but were of less value as a diagnostic test, since they were below the lower limit of normal in 64 per cent of subjects, including many subjects who did not yet have low tissue folate. In contrast to their value in other folate deficiency states, neutrophil lobe counts showed no correlation with serum or red cell folate levels in pregnancy and thus appeared of little diagnostic value in pregnancy. It is suggested that surveys of folate deficiency in other pregnant population groups in the United States be carried out. These results support the recommendations of the Committee on Maternal Nutrition and the Committee on Dietary Allowances of the Food and Nutrition Board, National Research Council (U.S.A.) that folic acid supplements (200 to 400 mug per day) should be taken throughout pregnancy.

Black or African American↗
PubMed1977

Folate-responsive neurological and mental disorders: report of 16 cases. Neuropsychological correlates of computerized transaxial tomography and radionuclide cisternography in folic acid deficiencies.

Two groups of patients with folic acid responsive neurological and psychiatric disorders are reported. The first group (7 patients) had well-established acquired folate deficiency due either to defective absorption (4 cases with atrophy of jejunal mucosa) or to a deficient diet (3 cases). One patient had a subacute combined degeneration of the spinal cord while others were depressed and had weight loss, permanent muscular and intellectual fatigue, restless legs syndrome, depressed ankle jerks, diminution of the sense of vibration in the knees and a stocking-type tactile hypoesthesia. The second group (9 patients) comprised idiopathic cases of folic acid deficiency. Their main subjective complaints were chronic fatigability and familial restless legs syndrome. The neurological findings were similar to those of the patients with acquired disorders. Neuropsychological testing procedures revealed an abnormal intellectual functioning in all 16 patients. Abnormal patterns of radionuclide cisternograms and computerized transaxial tomography (CTT) were found in 11 patients. After 6-12 months of folic acid therapy a striking improvement regarding their intellectual functioning was noticed: the IQ, Kohs Block Design and Category tests were significantly improved. The correlation of neuropsychological findings with CTT and radionuclide cisternograms led to the conclusion that chronic folate deficiency could induce cerebral atrophy.

Adult↗
PubMed1989

Homocysteinemia in rats induced by folic acid deficiency.

The effect of folate deficiency on homocysteine metabolism was examined in rats given a folate-deficient diet. Total homocysteine was determined in serum stored at -22 degrees C for 3 wk. All animals in the control group had more than 20 ng.ml-1 of serum folate and more than 1000 pg.ml-1 of serum cyanocobalamin throughout the experimental period. In contrast, serum folate in animals given the folate-deficient diet decreased to less than 3 ng.ml-1 after 4 wk and to less than 2 ng.ml-1 (a subnormal level) after 10 wk of the experiment while serum cyanocobalamin remained at more than 1000 pg.ml-1 throughout the experiment. In the control group, mean serum total homocysteine +/- SD was 4.04 +/- 1.07 nmol.ml-1 during the 20 wk of experiment. At the 10th wk before serum folate reached subnormal levels, the animals given the folate-deficient diet had a mean serum total homocysteine of 7.67 +/- 1.53 nmol.ml-1, demonstrating a significant increase (P less than 0.001). No further significant increase of mean serum total homocysteine concentrations was observed after serum folate became subnormal. This study demonstrated for the first time that a selective deficiency of folic acid caused a 2-4 fold increase in serum total homocysteine when serum folate was at low normal and at subnormal levels in rats.

Animals↗
PubMed1975

Trypanosoma lewisi, Trypanosoma rhodesiense: mitotic activity in normal and folic acid deficient rats.

Ten experiments were performed to compare mitotic activity in livers of rats infected with Trypanosoma rhodesiense and Trypanosoma lewisi. The host dietary groups were: (1) complete of full complement; (2) folic acid deficient, and (3) pair-fed or calorically restricted. Liver mitotic counts of T. lewisi-infected rats fed complete and pair-fed control diets showed a high degree of significance over that of control rats. From days 35 to 55, liver mitotic counts of T. lewisi-infected rats deficient in folic acid showed an average of 16 +/- 2 mitotic phases as compared to 9 +/- 2 for livers of uninfected animals. Liver mitotic counts of T. rhodesiense-infected and non-infected rats fed complete and pair-fed control diets showed that there were essentially no differences in the mitotic counts from that seen in liver from control, uninfected animals. On day 25 (day 5 of infection), folic acid-deficient infected rats showed a significantly higher number of dividing cells than the controls. Folate was measured in isolated, washed T. lewisi and T. rhodesiense cells. T. lewisi and T. rhodesiense contained 9.6 ng folate per 10(8) cells and 6.2 ng of folate per 10(8) cells respectively. Metabolic products of T. lewisi contained an average of 0.51 ng of folate per 10(8) trypanosomes. T. rhodesiense metabolic products contained 0.3 ng of folate per 10(8) trypanosomes.

Animals↗