Anemias folic acid deficiency causing

T8. Relationship between Folic Acid Deficiency and Anemia Folic acid deficiency, believed to be the most common vitamin deficiency, causes a type of anemia in which hemoglobin synthesis is impaired and erythrocytes do not mature properly. What is the metabolic relationship between hemoglobin synthesis and folic acid deficiency ... 

The answer is D. Several vitamin deficiencies can cause anemia due to reduced DNA synthesis in the erythropoietic cells of the bone marrow, especially folic acid and vitamin Bj2 (cobalamin), which are particularly prevalent among elderly patients due to poor diet and reduced absorption. In addition, deficiencies of either folic acid or vitamin Bj2 could produce the megaloblastic anemia seen in this patient. However, the absence of neurologic symptoms, a hallmark of vitamin Bj2 deficiency, makes that diagnosis less likely than folic acid deficiency. 

Alcohol indirectly affects hematopoiesis through metabolic and nutritional effects and may also directly inhibit the proliferation of all cellular elements in bone marrow. The most common hematologic disorder seen in chronic drinkers is mild anemia resulting from alcohol-related folic acid deficiency. Iron deficiency anemia may result from gastrointestinal bleeding. Alcohol has also been implicated as a cause of several hemolytic syndromes, some of which are associated with hyperlipidemia and severe liver disease. 

Once a diagnosis of megaloblastic anemia is made, it must be determined whether vitamin B12 or folic acid deficiency is the cause. (Other causes of megaloblastic anemia are very rare.) This can usually be accomplished by measuring serum levels of the vitamins. The Schilling test, which measures absorption and urinary excretion of radioactively labeled vitamin B12, can be used to further define the mechanism of vitamin Bi2 malabsorption when this is found to be the cause of the megaloblastic anemia. 

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. 

Folic acid deficiency can be caused by drugs. Methotrexate and, to a lesser extent, trimethoprim and pyrimethamine, inhibit dihydrofolate reductase and may result in a deficiency of folate cofactors and ultimately in megaloblastic anemia. Long-term therapy with phenytoin can also cause folate deficiency, but only rarely causes megaloblastic anemia. 

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. 

Folic acid Precursor of the coenzyme tetrahydrofolic acid. Deficiency causes anemias. 

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. 

There are many causes of folic acid deficiencies. Inadequate nutrition during periods of increased requirements is one of the main causes of megaloblastie anemia of pregnaney and neural tube defects. Alcoholism is considered the leading cause of folic acid deficiency... 

Cobalmin Deficiency. Pernicious anemia is the disease associated with vitamin Bi2 deficiency. It is usually caused by the inability to produce intrinsic factor. Indeed, many times the vitamin must be administered by injection. The blood picture, a megaloblastic anemia, is indistinguishable from that caused by folic acid deficiency. Indeed folic acid supplements can mask the blood picture. This is illustrated in Fig. 8.53. Removal of ad-enosyl cobalamin eliminates the regeneration of tetrahydrofolate during the methylation of homocysteine to methionine. Folic acid supplements provide a fresh source of tetrahydrofolate coenzymes. DNA synthesis can continue and new erythrocytes form. Excess folic acid also may compete for the available vitamin, further exacerbating vitamin deficiency. 

Anemias are classified by RBC size as macrocytic, normocytic, or microcytic. Vitamin B12 deficiency and folic acid deficiency are both macrocytic anemias. An example of a microcytic anemia is iron deficiency, whereas a normocytic anemia may be the result of recent blood loss or chronic disease. In many patients more than one anemia and etiology may occur at the same time. Inclusion of the underlying cause of the anemia makes diagnostic terminology easier to understand (e.g., microcytic anemia secondary to iron deficiency). 

D. Clinical Use and Toxicity Folic acid deficiency is most often caused by dietary insufficiency or by malabsorption. Anemia due to folic acid deficiency is readily treated by oral folic acid supplementation. Folic acid supplements will also correct the anemia but not the neurologic deficits of vitamin B, deficiency. Therefore, vitamin B 2 deficiency must be ruled out before one selects folic acid as the sole therapeutic agent in the treatment of a patient with megaloblastic anemia. Folic acid has no recognized toxicity. 

Crohn s disease is the second most common cause of folic acid deficiency anemia. Crohn s disease is a malabsorption syndrome of the small intestines. The client must receive the medication via the parenteral route. 

One of the main causes of folic acid deficiency anemia is chronic alcoholism, but abstaining from alcohol would not indicate the anemia is better. 

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. 

Disorders of Red Blood Cells. For the red blood cell to survive and function properly in the body, it must maintain a proper membrane, possess structurally correct and appropriately functioning hemoglobin, and have properly working metabolic pathways. Problems or defects in any of these areas will result in the red blood cell having a shortened life. Anemia results when the circulating red blood cells are unable to provide an adequate supply of oxygen to the tissues of the body. The many causes of anemia can be classified as nutritional deficiency (vitamin B12 or folic acid deficiency), blood loss, accelerated red cell destruction, hemoglobin defects (hereditary or acquired), and enzyme deficiencies. 

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. 

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. 

The underlying cause of anemia (e.g., blood loss iron, folic acid, or B12 deficiency or chronic disease) must be determined and used to guide therapy. 

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. 

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. 

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). 

Normal blood levels of vitamin B12 are 2 x 1(T10 M or a little more, but in vegetarians the level may drop to less than one-half this value. A deficiency of folic acid can also cause megaloblastic anemia, and a large excess of folic acid can, to some extent, reverse the anemia of pernicious anemia and mask the disease. 

Deficiencies of folic acid and vitamin B1 are relatively common. Whenever macrocytic anemia is present, evaluation of these two vitamins is necessary 10 determine the cause of the condition, The standard method of measuring folic acid has been the microbiological assay (Bailey et al.. 19821. which can be used to measure folic acid in serum, blood, tissues, and foods. Improved high performance liquid chromatography (HPLC) methods have... 

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