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Results for “FOLIC ACID DEFICIENCY”

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At least 1,315 records · Page 73Linked to original sources
PubMed1998

Prevalence of folate deficiency and macrocytosis in patients with and without alcohol-related illness.

BACKGROUND: This study was done to determine the prevalence of folate deficiency and macrocytosis in patients admitted to the hospital medicine service with alcohol and nonalcohol-related illnesses. METHODS: Two groups of patients, with and without alcohol-related illnesses, were included. Patients were excluded if they received folate therapy, medications known to alter folate concentrations, or if they had an uncertain diagnosis. Complete blood count and erythrocyte folate concentrations were determined from each patient. A Fisher's Exact Test and odds ratio were used to determine the prevalence of macrocytosis and correlation between folate deficiency and macrocytosis in the alcoholic group, respectively. RESULTS: Of the 36 alcoholic patients, 11.1% were folate deficient, and 33.3% had macrocytosis. Only 2 of 12 patients with macrocytosis were folate deficient. No control patient had macrocytosis or folate deficiency. CONCLUSION: The prevalence of folate deficiency among patients with alcohol-related illness is low. There is no correlation detected between macrocytosis and folate deficiency. Our findings suggest that it may be inappropriate to routinely supplement all alcoholics with folic acid, but certainly a small minority may benefit from it.

Adolescent↗
PubMed2005

Vitamin B12 deficiency is the dominant nutritional cause of hyperhomocysteinemia in a folic acid-fortified population.

Prevalence rates for folate deficiency and hyperhomocysteinemia have been markedly reduced following the introduction of folic acid fortification in the United States. We report the prevalence of hyperhomocysteinemia in a population of community-dwelling elderly Latinos in the post-folic acid fortification era. We measured homocysteine, total vitamin B12, holotranscobalamin, red blood cell folate, and serum creatinine in 1096 subjects aged > or =60 years. Hyperhomocysteinemia (>13 micromol/L) was observed in 16.5% of the subjects. The population attributable risk percentages for hyperhomocysteinemia were 29.7% for total B12 <148 pmol/L, 36.4% for holotranscobalamin <35 pmol/L, and 41.4% for creatinine >115 micromol/L. In contrast, the population attributable risk percentage for hyperhomocysteinemia was only 0.3% for red blood cell folate <365 nmol/L. We conclude that in the post-folic acid fortification era, low vitamin B12 status has become the dominant nutritional determinant of hyperhomocysteinemia. Steps to either reduce the prevalence of vitamin B12 deficiency or to identify and treat individuals with vitamin B12 deficiency could further reduce the prevalence of hyperhomocysteinemia.

Aged↗
PubMed1999

Brain function in the elderly: role of vitamin B12 and folate.

Vitamin B12 (cobalamin) deficiency associated neuropathy, originally called subacute combined degeneration, is particularly common in the elderly. The potential danger today is that with supplementation with folic acid of dietary staples such as flour, that the incidence of this disease could rise as folic acid, as opposed to natural folate (N5CH3HFGlu1), enters the cell and the metabolic cycle by a cobalamin independent pathway. This chapter briefly describes the clinical presentation of the disease, which unless treated will induce permanent CNS damage. The biochemical basis of the interrelationship between folate and cobalamin is the maintenance of two functions, nucleic acid synthesis and the methylation reactions. The latter is particularly important in the brain and relies especially on maintaining the concentration of S-adenosylmethionine (SAM) which, in turn, maintains the methylation reactions whose inhibition is considered to cause cobalamin deficiency associated neuropathy. SAM mediated methylation reactions are inhibited by its product S-adenosylhomocysteine (SAH). This occurs when cobalamin is deficient and, as a result, methionine synthase is inhibited causing a rise of both homocysteine and SAH. Other potential pathogenic processes related to the toxic effects of homocysteine are direct damage to the vascular endothelium and inhibition of N-methyl-D-aspartate receptors.

Aged↗
PubMed2006

High frequency of maternal vitamin B12 deficiency as an important cause of infantile vitamin B12 deficiency in Sanliurfa province of Turkey.

BACKGROUND: Vitamin B12 deficiency in infancy may cause failure to thrive, severe neurological disorders and megaloblastic pancytopenia. It is well known that infants born with deficient vitamin B12 storage have increased the risk of vitamin B12 deficiency. Vitamin B12 deficiency is more prevalent in infancy in Sanliurfa province (at the southeast region of Turkey). AIM OF THE STUDY: The aim of this study was to determine the frequencies of vitamin B12, folic acid and iron deficiencies in pregnants and their babies at birth and to what extend the mothers' deficiency becomes effective on babies' deficiencies. METHODS: The study groups were constituted by 180 pregnant women and their single and term babies. Venous blood samples of pregnants were obtained 1-3 h before delivery and babies' cord bloods were collected at birth. Vitamin B12 and folic acid levels were measured with electro chemiluminiscence method; serum iron and iron binding capacities were measured by colorimetric method and complete blood counts were performed by automatic blood counter. RESULTS: Mean vitamin B12 levels in maternal and cord blood serum were 130 +/- 61.7 pg/ml and 207 +/- 141 pg/ml; mean folic acid levels were 8.91 +/- 6.46 ng/ml and 17.8 +/- 11.8 ng/ml; mean serum iron levels were 56.9 +/- 37.5 microg/dl and 147 +/- 43.2 microg/dl; and mean transferrin saturations were 11.8 +/- 8% and 65.6 +/- 24%, respectively. There were vitamin B12 deficiency (<160 pg/ml) in 72% of the mothers and 41% of the babies, and severe deficiency (<120 pg/ml) in 48% of the mothers and 23% of the babies. Folic acid deficiency was found in 12% of the mothers, but was not found in the babies. There were iron deficiency in 62% of the mothers and 1% of the babies. There were statistically significant correlation between maternal and cord blood serum vitamin B12 levels (r = 0.395, P < 0.001) and folic acid levels (r = 0.227, P = 0.017), while there were no correlation between maternal and cord blood iron levels and transferrin saturations. CONCLUSION: The study results showed that vitamin B12 deficiency is prevalent in pregnants in this region and that 41% of infants have born with deficient vitamin B12 storages. Therefore, prophylactic use of vitamin B12 by pregnant women in Sanliurfa and other poor communities could have considerable benefits to prevent vitamin B12 deficiency and its complications in infants.

Adult↗
PubMed1970

Mental deterioration in epilepsy due to folate deficiency.

Folate deficiency in 50 epileptic children aged 5 to 18 years was treated with a combination of folic acid and vitamin B(12). Improvement in mental condition occurred from five to eight weeks after beginning treatment in some of the younger children; no change was noticed, however, in 31. Similarly, in 19 children fits became less frequent and less severe. It is recommended that both folic acid and vitamin B(12) should be given as soon as a patient is started on anticonvulsant drugs to prevent mental deterioration.

Adolescent↗