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Folic acid supplemental

Methyl-tetrahydro folic acid is furthermore, together with vitamin B12 and B6, required to regenerate homocysteine (see Vitamin B12, Fig. 1). Homocysteine results when methionine is used as a substrate for methyl group transfer. During the last few years, homocysteine has been acknowledged as an independent risk factor in atherosclerosis etiology. Folic acid supplementation can help reduce elevated homocysteine plasma levels and is therefore supposed to reduce the risk of atherosclerosis as well [2]. [Pg.509]

It is recommended that women of childbearing age take 400 pg/d synthetic folic acid as a supplement in order to reduce the risk of neural tube defects of the embryo when they later become pregnant (periconcep-tional folic acid supplementation) [2]. When supplementing folic acid, it should be considered that this vitamin can mask the simultaneous presence of vitamin B12 deficiency. The typical symptom of vitamin B12 deficiency, megaloblastic (= macrocytic) anemia, will be reduced by high doses of folic acid, yet the nervous system will - in the long run - be irreversibly damaged (= funicular myelitis) when vitamin B12 is not provided as well. [Pg.509]

Folic Acid Supplements Reduce the Risk of Neural Tube Defects Hyperhomocysteinemia... [Pg.494]

Elevated homocysteine concentrations have been associated with an increased risk for cardiovascular disease in both epidemiologic and clinical studies.43 Several studies have evaluated the benefit of lowering homocysteine levels with folic acid supplementation. One study reported a reduction in major cardiac events with the combination of folic acid, vitamin B12, and vitamin B6 following PCI.44 However, a more recent study found an increased risk of instent restenosis and the need for target-vessel revascularization with folate supplementation following coronary stent placement.45 The role of folate in the management of IHD is currently unclear. [Pg.79]

Folic acid supplementation with 1 mg daily generally is recommended in adult SCD patients, women considering pregnancy, and any SCD patient with chronic hemolysis.6 Because of accelerated erythropoiesis, these patients have an increased need for folic acid. There are conflicting studies in the SCD population, especially among infants and children, but if the child has chronic hemolysis, supplementation is recommended.21... [Pg.1012]

Administer prophylactic folic acid supplementation to SCD patients receiving hydroxyurea because folate deficiency may be masked by the use of hydroxyurea. [Pg.1013]

Folic acid supplementation, 1 mg twice daily, should be given. [Pg.305]

Patients receiving sulfasalazine should receive oral folic acid supplementation since sulfasalazine inhibits folic acid absorption. [Pg.305]

All women with epilepsy should take a folic acid supplement, 0.4 to 5 mg daily. [Pg.372]

Cyanocobalamin, or vitamin B12, is in small amounts required for red blood cell production and for the formation of nucleoproteins and proteins. It is also needed for the proper functioning of the nervous system. Folic acid supplements can correct the anemia associated with vitamin B12 deflciency. Unfortunately, folic acid will not correct changes in the nervous system that result from vitamin B12 deficiency. Vitamin B12 is only found in animal sources such as liver and other organs. Some vitamin B12 is obtained from fish, eggs and milk. Folic acid and cyanocobalamin have been discussed in more detail in Chapter 22. [Pg.475]

Folic acid supplements are given to pregnant women to decrease the risk of neural tube defects such as spina bifida. Prenatal vitamin preparations that contain higher concentrations of folic acid must be dispensed under a health care worker s guidance because high folate intakes can mask the symptoms of pernicious anemia. [Pg.781]

E. Folic acid supplements should be given to all pregnant women. In addition, phenytoin use is associated with lowered folate levels. [Pg.784]

Bailey, L. B., Rampersaud, G. C., Kauwell, G. P. (2003). Folic acid supplements and fortification affect the risk for neural tube defects, vascular disease and cancer evolving science. J. Nutr., 133,1961S-1968S. [Pg.417]

Morgan SL, Baggott IE, Vaughn WH et al. The effect of folic acid supplementation on the toxicity of low-dose methotrexate in patients with rheumatoid axthiitis. Arthritis Rheum 1990 33 9-18. [Pg.172]

Reduced forms of folic acid are required for essential biochemical reactions that provide precursors for the synthesis of amino acids, purines, and DNA. Folate deficiency is not uncommon, even though the deficiency is easily corrected by administration of folic acid. The consequences of folate deficiency go beyond the problem of anemia because folate deficiency is implicated as a cause of congenital malformations in newborns and may play a role in vascular disease (see Folic Acid Supplementation A Public Health Dilemma). [Pg.739]

Folic Acid Supplementation A Public Health Dilemma... [Pg.739]

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Patients with alcohol dependence and patients with liver disease can develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. Pregnant women and patients with hemolytic anemia have increased folate requirements and may become folic acid-deficient, especially if their diets are marginal. Evidence implicates maternal folic acid deficiency in the occurrence of fetal neural tube defects, eg, spina bifida. (See Folic Acid Supplementation A Public Health Dilemma.) Patients with malabsorption syndromes also frequently develop folic acid deficiency. Patients who require renal dialysis develop folic acid deficiency because folates are removed from the plasma during the dialysis procedure. [Pg.741]

Parenteral administration of folic acid is rarely necessary, since oral folic acid is well absorbed even in patients with malabsorption syndromes. A dose of 1 mg folic acid orally daily is sufficient to reverse megaloblastic anemia, restore normal serum folate levels, and replenish body stores of folates in almost all patients. Therapy should be continued until the underlying cause of the deficiency is removed or corrected. Therapy may be required indefinitely for patients with malabsorption or dietary inadequacy. Folic acid supplementation to prevent folic acid deficiency should be considered in high-risk patients, including pregnant women, patients with alcohol dependence, hemolytic anemia, liver disease, or certain skin diseases, and patients on renal dialysis. [Pg.741]

Gamble MV Folate and arsenic metabolism A double-blind, placebo-controlled folic acid supplementation trial in Bangladesh. Am J Clin Nutr 2006 84 1093. [PMID 17093162]... [Pg.1245]

Yerby MS (2003) Clinical care of pregnant women with epilepsy neural tube defects and folic acid supplementation. Epilepsia 44 33-40... [Pg.723]

NRC Campbell. How safe are folic acid supplements Arch Intern Med 156 1638-1644, 1996. [Pg.474]

Hence, women taking antiepileptic drugs should discuss the potential risks with their family members and physician, and consider whether they will continue taking their medication(s).38 If an expectant mother continues to take her medication(s), using one drug (monotherapy) at the lowest effective dose will help reduce the risk of harmful effects on the fetus.1,43 In addition, mothers should receive optimal prenatal care (folic acid supplementation, proper amounts of exercise, rest, and so forth) to help ensure the baby s health.27,43 After delivery, the baby should be monitored initially for drug-related effects such as withdrawal symptoms, and should be subsequently evaluated for developmental delays that might become apparent later in childhood.27... [Pg.113]


See other pages where Folic acid supplemental is mentioned: [Pg.727]    [Pg.20]    [Pg.336]    [Pg.419]    [Pg.83]    [Pg.432]    [Pg.404]    [Pg.739]    [Pg.739]    [Pg.739]    [Pg.739]    [Pg.739]    [Pg.1264]    [Pg.119]    [Pg.373]    [Pg.751]    [Pg.752]   
See also in sourсe #XX -- [ Pg.494 ]




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