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Results for “FOLIC ACID DEFICIENCY”

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At least 1,117 records · Page 62Linked to original sources
PubMed2003

Anemia, serum vitamin B12, and folic acid in patients with rheumatoid arthritis, psoriatic arthritis, and systemic lupus erythematosus.

OBJECTIVE: Although anemia is frequent in inflammatory rheumatic diseases, data regarding vitamin B12 status is scarce. The purpose of this study was to analyze the incidence and nature of B12 and folic acid (FA) deficiencies in a cohort of rheumatic patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and systemic lupus erythematosus (SLE). METHODS: Levels of B12, FA, and parameters of anemia were recovered or examined in 276 outpatients. In those with recent findings of low serum B12 levels, further studies of serum homocysteine (Hcy) and urine methylmalonic acid (MMA) levels were performed. RESULTS: The incidence of anemia was high: 49%, 46%, and 35%, in RA, SLE, and PsA, respectively. Low levels of serum B12 were also frequent (24%), with almost similar occurrence in the three disease groups. Deficiency in FA was rare (<5%). Mean levels of both vitamins did not differ significantly among the three groups. No correlation between serum B12 levels and anemia was found. In the 15 patients with recently detected low B12 levels, Hcy and MMA were evaluated before and following B12 therapy. In ten of them, baseline Hcy levels were high, while MMA was increased in one patient only. Response to B12 administration, i.e., a decrease in Hcy and/or MMA levels, was noticed in four patients only, suggesting that only 26% of the low-serum-B12 patients had true B12 deficiency. CONCLUSIONS: The incidences of anemia and decreased serum B12 levels were high in these three groups of rheumatic patients. However, true tissue deficiency seems to be much rarer.

Adult↗
PubMed1965

Reversible absorptive defects in anticonvulsant megaloblastic anaemia.

Two cases of anticonvulsant megaloblastic anaemia are described, showing features of unusual interest. Though both cases were apparently deficient in folic acid, the Figlu tests were negative. One patient had an extremely low serum B(12) concentration apparently associated with defective B(12) absorption due to deficiency of intrinsic factor, and both showed impaired intestinal absorption of D-xylose. There was, however, no evidence of permanent gastro-intestinal dysfunction, and the absorptive defects disappeared completely after treatment with folic acid. Possible reasons for the findings are discussed. It is suggested that absorptive defects produced by the drugs may play some part in initiating anticonvulsant megaloblastic anaemia, and that once deficiencies of haemopoietic factors are established, a vicious circle may be set up owing to the effects of these deficiencies on the gastro-intestinal tract.

Adult↗
PubMed1982

Folic acid -- has it a role in the treatment of severe iron deficiency anaemia in pregnancy?

Forty-one pregnant patients with severe iron deficiency anaemia were treated with either intravenous iron-dextran (Imferon; Fisons) or intravenous iron plus folic acid. There was no difference in the rate of response or the eventual total response in the two groups, suggesting that iron therapy does not unmask or produce a relative folic acid deficiency.

Anemia, Hypochromic↗
PubMed1986

A comparison of the response of woodchucks and rats to variations in dietary lipotrope and protein content.

Juvenile woodchucks and weanling Fisher F344 rats were fed purified diets with or without supplemental lipotropic factors (choline, methionine, folic acid and vitamin B-12). The diets contained 10 or 20% protein. Lower weight gain due to low protein was observed in both species, while lipotrope depletion resulted in lower gain in male rats only. Urinary excretion of formimino-glutamic acid was higher due to low lipotrope in both species, as was relative liver weight. In rats, lipotrope depletion resulted in hepatic fatty metamorphosis at both levels of dietary protein with the low protein diet resulting in more severe lesions. No liver lesions were observed in woodchucks fed low lipotropes at the higher level of dietary protein, but fatty metamorphosis was observed in those fed the lower protein diets. The lesion was more severe in the low lipotrope group. The woodchuck appears to be less sensitive than the rat to induction of fatty liver by lipotrope deficiency, although the lesion was induced by lowering dietary protein.

Animals↗
PubMed1982

The effect of folate analogues and vitamin B12 on provision of thymine nucleotides for DNA synthesis in megaloblastic anemia.

The role of vitamin B12 in the folate dependent biosynthesis of thymidine nucleotides is controversial. In an attempt to clarify this, three methods have been used to assess the relative efficacy of vitamin B12 (hydroxocobalamin) and various folate analogues in titrated concentrations at correcting 'de novo' thymidylate synthesis by megaloblastic human marrow cells: (1) The deoxyuridine (dU) suppression test which analyses the reduction in (3H)-thymidine labeling of DNA by unlabeled dU. Marrow cells were also labeled with (6-3H)-dU with assessment of (2) its incorporation into DNA and (3) the accumulation of (6-3H)-deoxyuridine monophosphate (3H-dUMP). The three methods gave similar results. In both, N6-formyl tetrahydrofolate (formyl-FH4) was the most effective agent at correcting thymidylate synthesis in megaloblastic anemia due to vitamin B12 or folate deficiency. Vitamin B12 corrected the lesion in vitamin B12 deficiency but not in folate deficiency. Tetrahydrofolate (FH4) and folic acid were effective in deficiency of vitamin B12 or folate, although in both deficiencies they were less effective than formyl-FH4. Methyl-FH4 was effective in folate deficiency but not in vitamin B12 deficiency. These results confirm the failure of methyl-FH4 utilisation in vitamin B12 deficiency. They suggest that if vitamin B12 is needed in the formylation of FH4, this is a minor role in provision of the correct coenzyme for thymidylate synthesis compared with its major role of provision of FH4 from methyl-FH4.

Anemia, Macrocytic↗
PubMed1976

Folic acid metabolism in normal, folate deficient and alcoholic man.

Folate metabolism was studied in normal, folate-deficient and alcoholic man by tracer measurements of plasma clearance, urinary excretion, tissue storage and release of folate using both [3H]pteroylglutamic acid (3H-PteGlu) and 14C-methyl-H4PteGlu. Alcohol ingestion did not adversely affect tissue uptake of folates. Whether in normal or folate deficient subjects, the relative clearance rates of 3H-PteGlu and 14C-methyl-H4PteGlu were maintained in the face of alcohol ingestion and there was no evidence of increased urinary loss of intact vitamin or labelled breakdown products. As measured by the flushing technique, the rate of storage or tissue binding of 3H-PteGlu was not influenced by folate deficiency, folate store depletion or alcohol ingestion. However, alcohol may retard the release of methyl-H4PteGlu from tissue stores to plasma. A significantly greater recovery of 14C-methyl-H4PteGly with flush was observed in those normal subjects who ingested alcohol for 6 d. A partial block in the rate of release of tissue folate stores would be a possible mechanism behind the rapid depression in serum methyl-H4PteGlu levels and early induction of megaloblastic erythropoiesis which has been observed following acute alcohol ingestion.

Alcoholism↗
PubMedDate not supplied

The effects of drugs on embryonic development.

A review of the literature demonstrated the difficulties in evaluating the teratogenic effect of drugs in man. Since epidemiologic studies provide suggestive rather than definitive data and results of the current drug testing in laboratory animals may not be applicable to man, the need to develop alternative methods of predicting teratogenicity was apparent. To develop such techniques by studying a possible mechanism of teratogenesis, experiments were performed using a teratogenic folic acid-deficiency and antagonism with 9-methyl pteroylglutamic acid in the pregnant rat. Embryos developing abnormally in response ot this regimen consumed oxygen at a significantly decreased rate. Similar significant reductions in oxygen consumption were found both in rat embryos malforming in response to maternal vitamin A acetate administration, and in mouse embryos in response to teratogenic doses of diphenylhydantoin. It was suggested that such measurements of oxidative metabolism or related techniques may have application in predicting drug teratogenicity and could aid present epidemiologic and empiric approaches to identification of human teratogens.

Animals↗