Vitamin deficiencies folic acid

No specific dietary restrictions are recommended for patients with IBD, but avoidance of high-residue foods in patients with strictures may help to prevent obstruction. Nutritional strategies in patients with long-standing IBD may include use of vitamin and mineral supplementation. Administration of vitamin B12, folic acid, fat-soluble vitamins, and iron may be needed to prevent or treat deficiencies. In severe cases, enteral or parenteral nutrition maybe needed to achieve adequate caloric intake. 

Macrocytic anemias Megaloblastic anemias Vitamin B12 deficiency Folic acid deficiency anemia Microcytic hypochromic anemias Iron-deficiency anemia Genetic anomaly Sickle cell anemia Thalassemia... 

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Alcoholics and patients with liver disease develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. There is also evidence that alcohol and liver disease interfere with absorption and metabolism 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. Folic acid deficiency is occasionally associated with cancer, leukemia, myeloproliferative disorders, certain chronic skin disorders, and other chronic debilitating diseases. Patients who require renal dialysis also develop folic acid deficiency, because folates are removed from the plasma each time the patient is dialyzed. 

Vitamin B12 is required by only two enzymes in human metabolism methionine synthetase and L-methylmalonyl-CoA mutase. Methionine synthetase has an absolute requirement for methylcobalamin and catalyzes the conversion of homocysteine to methionine (Fig. 28-5). 5-Methyltetrahydrofolate is converted to tetrahydrofolate (THF) in this reaction. This vitamin B12-catalyzed reaction is the only means by which THF can be regenerated from 5-methyltetrahydrofolate in humans. Therefore, in vitamin B12 deficiency, folic acid can become trapped in the 5-methyltetrahydrofolate form, and THF is then unavailable for conversion to other coenzyme forms required for purine, pyrimidine, and amino acid synthesis (Fig. 28-6). All folate-dependent reactions are impaired in vitamin B12 deficiency, resulting in indistinguishable hematological abnormalities in both folate and vitamin B12 deficiencies. 

Carbohydrates are more plentiful and constant in food supplies throughout the world when compared to other nutrients, such as proteins, vitamin A, folic acid, and iodine. A naturally occurring deficiency specifically in carbohydrates is im-known. However, deliberate omission of carbohydrates from the diet with continued consumption of fat as an energy source can lead to specific problems. Glucose is required as an energy source by the central nervous system. When there is a deficiency of glucose, the body adjusts its metabolism to provide ketone bodies, nutrients derived from fat, which can be utilized by the brain and other parts of the central nervous system. However, excessive production of the ketone bodies can result in acidosis, a lowering of the pH of the blood, which is potentially toxic. 

As with vitamin B13, folic acid deficiencies mainly result from malabsorption or alcoholism. No neurological abnormalities ore associated with folic acid deficiency. The resulting megaloblastic anemia is indistinguishable from that caused by vitamin B ] because both vitamins are involved in the critical biochemical step. Folic acid can correct the anemia cau.sed by vitamin B12 deficiency, but it has no effect on the neurological damage. Thus, only small amounts are found in over-the-counter preparations. 

Just having anemia doesn t mean you are deficient in iron. Anemia can be caused by a deficiency of vitamin Bj2, folic acid, copper, manganese, or a substance called intrinsic factor, a specialized protein that transports vitamin Bjo from the stomach to the bloodstream. If you believe you are anemic, go to your doctor and find out what is causing it. On the other hand, if you know you are not getting enough iron, then you are a good candidate for iron supplements. 

Vitamin and folic acid are essential vitamins the deficiency of either impairs DNA synthesis in any cell in which chromosomal replication and division are taking place. Since tissues with the greatest rate of cell turnover show the most dramatic changes, the hematopoietic system is especially sensitive to deficiencies of these vitamins. 

A. Role of Folic Acid Like vitamin Bp, folic acid is required for normal DNA synthesis, and its deficiency usually presents as megaloblastic anemia. In addition, deficiency of folic acid during pregnancy increases the risk of neural tube defects in the fetus. 

A thorough medical evaluation of an individual wifh anemia is necessary because fhe condition can result from a variefy of diseases as well as from nutritional deficiencies. Vitamin and folic acid deficiencies can also cause anemia. 

Water-Soluble Vitamins. Vitamin G (ascorbic acid) functions in the formation of collagen, wound healing, metabolic functions, and other roles. Foods high in vitamin G include citrus fruits, strawberries, cantaloupe, and cruciferous vegetables. B vitamins are important in energy metabolism. Thiamin (Bj) is called the antineuritic vitamin. Riboflavin (B ), rarely deficient in the diet, is found most abundantly in milk and dairy products. Niacin (Bj) is prevalent in meats, poultry, fish, peanut butter, and other foods. Other major B vitamins include folic acid (B ), B, and Bj2-... 

Treatment of CBS deficiency includes a low-methionine diet, vitamin Bs, folic acid, and betaine (N-trimethylglycine) [1]. Betaine works by (re)methy-lating homocysteine to methionine, and it is used in conjunction with folic acid in the treatment of MTHFR deficiency [3]. Hydroxycobalamin should be given to patients with methylmalonic aciduria protein restriction, folic acid, vitamin Bg, betaine and other measures may also be appropriate, depending on which mutant class (cblA through cblG) a patient is assigned to by complementation analysis [3, 6]. 

In cooperation with vitamin B12, folic acid methylates homocysteine to methionine. Therefore, homocysteine is a suitable marker for the supply of folate. In the case of a deficiency, the serum concentration of this marker is clearly raised compared with the normal value of 8-lOpmol/ml, resulting in negative effects on health because higher concentrations of homocysteine are toxic. 

In addition to direct effects of chemical compounds on the fetus, metabolic disturbances in the mother, such as diabetes or hyperthermia, or deficiencies of calories or specific nutrients such as vitamin A, zinc, and folic acid may lead to teratogenesis. Compounds that inhibit placental functions may also induce malformations, e.g., by inhibiting placental circulation. For example, hydroxyurea disrupts the placental circulation and induces malformations. In addition, it also induces DNA damage. 

In terms of amino acids bacterial protein is similar to fish protein. The yeast s protein is almost identical to soya protein fungal protein is lower than yeast protein. In addition, SCP is deficient in amino acids with a sulphur bridge, such as cystine, cysteine and methionine. SCP as a food may require supplements of cysteine and methionine whereas they have high levels of lysine vitamins and other amino acids. The vitamins of microorganisms are primarily of the B type. Vitamin B12 occurs mostly hi bacteria, whereas algae are usually rich in vitamin A. The most common vitamins in SCP are thiamine, riboflavin, niacin, pyridoxine, pantothenic acid, choline, folic acid, inositol, biotin, B12 and P-aminobenzoic acid. Table 14.4 shows the essential amino acid analysis of SCP compared with several sources of protein. 

Macrocytic or magaloblastic anemia is caused by disturbances of DNA synthesis. It occurs, for example, in both folic acid and vitamin B12 deficiencies. Hematopoesis is slowed down due to reduced DNA synthesis and a reduced number of abnormally large (macrocytic) and hemaglobin-rich (hyperchromic) erythrocytes is released. 

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. 

Bile acid sequestrants may interfere with die digestion of fats and prevent die absorption of die fat-soluble vitamins (vitamins A, D, E, and K) and folic acid. When die bile acid sequestrants are used for long-term therapy, vitamins A and D may be given in a water-soluble form or administered parenterally. If bleedingtendencies occur as die result of vitamin K deficiency, parenteral vitamin K is administered for immediate treatment, and oral vitamin K is given for prevention of a deficiency in the futum... 

Anemias, reductions in the number of red blood cells or of hemoglobin in the blood, can reflect impaired synthesis of hemoglobin (eg, in iron deficiency Chapter 51) or impaired production of erythrocytes (eg, in folic acid or vitamin Bjj deficiency Chapter 45). Diagnosis of anemias begins with spectroscopic measurement of blood hemoglobin levels. 

The water-soluble vitamins comprise the B complex and vitamin C and function as enzyme cofactors. Fofic acid acts as a carrier of one-carbon units. Deficiency of a single vitamin of the B complex is rare, since poor diets are most often associated with multiple deficiency states. Nevertheless, specific syndromes are characteristic of deficiencies of individual vitamins, eg, beriberi (thiamin) cheilosis, glossitis, seborrhea (riboflavin) pellagra (niacin) peripheral neuritis (pyridoxine) megaloblastic anemia, methyhnalonic aciduria, and pernicious anemia (vitamin Bjj) and megaloblastic anemia (folic acid). Vitamin C deficiency leads to scurvy. 

Pernicious anemia arises when vitamin B,2 deficiency blocks the metabohsm of folic acid, leading to functional folate deficiency. This impairs erythropoiesis, causing immature precursors of erythrocytes to be released into the circulation (megaloblastic anemia). The commonest cause of pernicious anemia is failure of the absorption of vitamin B,2 rather than dietary deficiency. This can be due to failure of intrinsic factor secretion caused by autoimmune disease of parietal cells or to generation of anti-intrinsic factor antibodies. 

Water-soluble vitamins removed by hemodialysis (HD) contribute to malnutrition and vitamin deficiency syndromes. Patients receiving HD often require replacement of water-soluble vitamins to prevent adverse effects. The vitamins that may require replacement are ascorbic acid, thiamine, biotin, folic acid, riboflavin, and pyridoxine. Patients receiving HD should receive a multivitamin B complex with vitamin C supplement, but should not take supplements that include fat-soluble vitamins, such as vitamins A, E, or K, which can accumulate in patients with renal failure. 

Anemia from vitamin B12 or folic acid deficiency is treated effectively by replacing the missing nutrient. 

A decrease in erythrocyte production can be multifactorial. A deficiency in nutrients (such as iron, vitamin B12, and folic acid) is a common cause that often is easily treatable. In addition, patients with cancer and CKD are at risk for developing a hypoproductive anemia. Furthermore, patients with chronic immune-related diseases (such as rheumatoid arthritis and systemic lupus erythematosus) can develop anemia as a complication of their disease. Anemia related to these chronic inflammatory conditions is typically termed anemia of chronic disease. 

Deficiencies in nutrients such as folic acid and vitamin B12 may hinder this process of erythrocyte maturation.4,5 Folic acid and vitamin B12 are important nutrients required for the formation of DNA. In a setting where these nutrients are decreased, DNA synthesis is inhibited, and consequently, erythrocyte maturation also is inhibited.4,5 Poor diet can be a contributor to the deficiencies in these... 

The underlying cause of anemia (e.g., blood loss iron, folic acid, or vitamin B12 deficiency or chronic disease) must be determined and used to guide therapy. As discussed previously, patients should be evaluated initially based on laboratory parameters to determine the etiology of the anemia (see Fig. 63-3). Subsequently, the appropriate pharmacologic treatment should be initiated based on the cause of anemia. 

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