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Results for “FOLIC ACID DEFICIENCY”

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At least 1,477 records · Page 82Linked to original sources
PubMed2004

Are hematinic deficiencies the cause of anemia in chronic heart failure?

BACKGROUND: Anemia in chronic heart failure (CHF) is common, varying in prevalence between 14.4% and 55%, and is more frequent in patients with more severe heart failure. Patients with CHF who have anemia have a poorer quality of life, higher hospital admission rates, and reduced exercise tolerance. We explored the relation between hematinic levels and hemoglobin (Hb) levels and exercise tolerance in a group of patients with CHF. METHODS: We analyzed data from 173 patients with left ventricular systolic dysfunction (LVSD), 123 patients with symptoms of heart failure, but preserved left ventricular (LV) systolic function ("diastolic dysfunction"), and 58 control subjects of similar age. Each underwent echocardiography, a 6-minute walk test, and blood tests for renal function and Hb and hematinic levels (vitamin B12, iron, and folate). We classified patients as having no anemia (Hb level >12.5 g/dL), mild anemia (Hb level from 11.5-12.5 g/dL), or moderate anemia (Hb level <11.5 g/dL). RESULTS: Of patients with LVSD, 16% had moderate anemia and 19% had mild anemia. Of patients with preserved LV function, 16% had moderate anemia and 17% had mild anemia. Four control subjects had a Hb level <12.5 g/dL. Of all patients, 6% were vitamin B12 deficient, 13% were iron deficient, and 8% were folate deficient. There was no difference between patients with LVSD and the diastolic dysfunction group. In patients with LVSDS, the average Hb level was lower in New York Heart Association class III than classes II and I. The distance walked in 6 minutes correlated with Hb level in both groups of patients with CHF (r = 0.29; P <.0001). Patients with anemia achieved a lower pVO2 (15.0 [2.3] vs 19.5 [4.4], P <.05). Peak oxygen consumption correlated with Hb level (r = 0.21, P <.05) in the patients, but not in the control subjects. In patients with anemia, the mean creatinine level was higher than in patients with a Hb level >12.5 g/dL, but there was no clear relationship with simple regression. Hematocrit level and mean corpuscular volume were not different in the patients with diastolic dysfunction, patients with LV dysfunction, or the control subjects. Hematocrit levels were not influenced by diuretic dose. Patients with anemia were not more likely to be hematinic deficient than patients without anemia. CONCLUSIONS: Patients with symptoms and signs of CHF have a high prevalence of anemia (34%) whether they have LV dysfunction or diastolic dysfunction, but few patients have hematinic deficiency. Hemoglobin levels correlate with subjective and objective measures of severity and renal function.

Aged↗
PubMed1976

Folate-responsive neuropathy: report of 10 cases.

Ten patients with severe neurological disease that was clinically indistinguishable from subacute combined degeneration of the spinal cord were found to have normal serum vitamin B12 levels. All were folate deficient. Specific folate treatment led to significant reversal of the neuropathy. These findings indicate the need to review orthodox concepts of the role of folic acid in maintaining the integrity of the nervous system.

Aged↗
PubMed1995

Vitamin B12, folic acid, ferritin and haematological variables among Thai construction site workers in urban Bangkok.

Serum vitamin B12, folic acid, ferritin and haematological variables were investigated in eighty-seven male and nineteen female construction site workers in Bangkok. Haemoglobin concentration, haematocrit and MCHC were found to be higher in male than in female workers. Serum ferritin was slightly higher in males than in females. Serum B12 was found to be higher in male than in female workers and serum folic acid level were significantly higher in female than in male workers. Vitamin B12 deficiency was found in 2.3 per cent and folic acid deficiency in 6.9 per cent of the male workers. Serum vitamin B12 and folic acid levels were normal for female workers. The adequate serum levels of vitamin B12 and folic acid might be the result of the habit of the workers to consume tonic drinks which contain glucose, caffeine, and vitamins especially vitamins B6, and B12.

Adolescent↗
PubMed1995

Morphology, biology and biochemistry of cobalamin- and folate-deficient bone marrow cells.

B12- or folate-deficient haemopoietic cells display abnormalities in their morphology under both the light and electron microscope, their cell kinetics and their capacity to synthesize protein. These abnormalities are maximal in the last dividing cell class and in non-dividing cells, presumably because B12 and folate uptake is largely confined to the most immature erythroid and granulocyte precursors. In patients with moderate or severe anaemia due to B12 or folate deficiency, erythropoiesis is markedly ineffective; intramedullary cell death occurs mainly in the early and late polychromatic megaloblasts. The damaged erythroblasts appear to display neoantigens or normally-hidden antigens at their cell surface and these react with naturally occurring antibodies. The opsonised erythroblasts are then recognised by macrophages via their IgG-Fc receptors and phagocytosed. Marrow cells from B12- or folate-deficient patients show a subnormal suppression of 3H-thymidine incorporation after pre-incubation with nonradioactive deoxyuridine, suggesting that such cells suffer from an impairment of the 5,10-methylene-THF-dependent methylation of deoxyuridylate to thymidylate. However, the exact mechanism by which B12 deficiency causes a reduced supply of this folate coenzyme is uncertain. Methylcobalamin is required for the 5-methyl-THF-dependent methylation of homocysteine to methionine and an impairment of this reaction will result in both reduced conversion of 5-methyl-THF to THF and in reduced methionine synthesis. There is controversy as to whether the reduced supply of THF or methionine is responsible for the reduced availability of 5,10-methylene-THF. Currently, the balance of evidence favours the hypothesis that the reduced supply of methionine leads to reduced synthesis of formyl-THF and, eventually, of 5,10-methylene-THF. Despite the evidence for impaired thymidylate synthesis, the duration of the S phase of megaloblasts appears to be normal or only modestly increased. Data on rates of DNA strand elongation are inconsistent, with subnormal rates reported in PHA-stimulated B12- or folate-deficient lymphocytes and normal rates in B12- or folate-deficient bone marrow cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Apoptosis↗
PubMed1984

Anaemia in young primigravidae in the guinea savanna of Nigeria: sickle-cell trait gives partial protection against malaria.

Haematological indices, malarial parasitaemia, serum and red cell folate (SFA, RCF), serum vitamin B12 and haemoglobin (Hb) electrophoretic patterns were studied in 228 non-elite young Hausa primigravidae at less than 24 weeks of gestation. The study was conducted in the guinea savanna of Nigeria, where malaria is hyperendemic. Ninety-nine (43%) were anaemic (Hb less than 11.0 g dl-1). The commonest cause of anaemia was malaria, in 28% of all and 40% of anaemic subjects. Plasmodium falciparum was predominant; P. malariae was seen in 1.3% and P. ovale was not recorded. Parasitaemia was more frequent and more dense in the wet than the dry season. Iron deficiency was diagnosed in 18% of all and 25% of anaemic women; 14% of all patients were folate-deficient; high MCV and MCH correlated with anaemia, and low SFA was associated weakly with anaemia and malaria. Serum vitamin B12 was normal or high in all 145 in whom it was measured; 3% had congenital elliptocytosis, but this did not contribute to the anaemia. Sickle-cell trait was present in 26% and Hb-AC in less than 1%. Hb-AS was associated with significantly lower frequency and density of P. falciparum; this has not been demonstrated in pregnancy in Africa previously. However, the parasitological advantage was not reflected in any haematological advantage. The roles of malaria, folate-deficiency and iron-deficiency in the causation of anaemia in Hausa primigravidae will be defined further by a double-blind trial of antimalarial prophylactics, iron supplements and folic acid supplements.

Adolescent↗
PubMed1989

Hematologic complications of gastric bypass for morbid obesity.

Of 530 patients who have had a gastric bypass operation for morbid obesity at Allegheny General Hospital, 41 had decreases in serum iron, vitamin B12, and/or folate levels. These abnormalities were detected eight months to eight years (median, two years) after the operation. The hemoglobin level ranged from 7.4 to 14.1 gm/dl at the time of detection, and mean corpuscular volume (MCV) ranged from 58 to 119 cu microns. The most common problem was combined iron and vitamin B12 deficiencies. Physicians should be aware that folate, vitamin B12, and iron deficiencies occur after gastric bypass, though the time to development is variable. Hemoglobin level and MCV are not predictive of these deficiencies.

Anemia, Hypochromic↗
PubMed1984

Effect of folate deficiency on local cerebral glucose utilization in the rat.

There is considerable debate on the role of folate in CNS function. Recent work indicates that folate deficiency may affect CNS serotonin metabolism, and clinical studies describe many consequences of such a deficiency. On the other hand some workers maintain that folate deficiency alone causes CNS abnormalities. We maintained rats, through dietary deprivation, at folate levels below 4 ng/ml for more than 6 weeks and showed that at that time both their liver and brain folate levels were significantly reduced. We then studied their local cerebral glucose utilization (LCGU) using the [14C]deoxyglucose technique. This method assesses cerebral function by measuring regional metabolic activity. We also determined LCGU in rats given the same diet but replenished with folate (folate control) and in others given free access to commercially available food (normal controls). Our results show that this degree of folate deficiency has no effect on cerebral function. This contrasts with the focal suppression of LCGU we previously reported in a model of vitamin B12 deficiency.

Animals↗