Folic acid deficiency anemia treatment

The male client at the outpatient client was diagnosed with folic acid deficiency anemia and was given a sample of oral folic acid. At the follow-up visit the nurse assesses the client to determine effectiveness of the treatment. ich data indicates the treatment is effective ... 

The anemias discussed in this chapter include iron deficiency anemia, anemia in patients witii chronic renal disease pernicious anemia, and anemia resulting from a folic acid deficiency. Table 45-1 defines these anemias. Drugp used in treatment of anemia are summarized in die Summary Drug Table Drugp Used in die Treatment of Anemia. 

The chemistry, metabolism, and clinical importance of folic acid have been the subject of many excellent reviews (A7, Gil, H14, H20, Rl). Folic acid deficiency leads to a macrocytic anemia and leucopenia. These symptoms are due to inadequate synthesis of nucleic acid. The synthesis of purine bases and of thymine, required for nucleic acid synthesis, is impaired in folic acid deficiency. Detection of folic acid activity in biologic fluids and tissues is of the utmost importance it distinguishes between the various anemias, e.g., those due to vitamin Bi2 or folic acid deficiency. Because morphology of the abnormal red cell does not help in diagnosing vitamin deficiency, one must rely on assay methods for differential diagnosis. Treatment of pernicious anemia with folic acid has led to subacute combined degeneration of the spinal cord despite... 

Parenteral Treatment of megaloblastic anemias due to folic acid deficiency when oral therapy is not feasible. 

Folic acid deficiency, a macrocytic anemia, results from in- adequate intake, decreased absorption, hyperutilization, or inadequate utilization. Treatment consists of the oral administration of folic acid, even in patients with absorption problems. Adequate folic acid intake is essential in women of childbearing years to decrease the risk of neural tube defects in their children. 

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. 

These types of anemias, which occur in infancy (megaloblastic anemia) and pregnancy (macrocytic anemia) and are usually due to simple folic acid deficiency, respond rapidly to treatment with folic acid, without vitamin B-12. It is possible that in some cases these anemias are due to an unknown metabolic defect in the production of the folacin enzymes. 

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. 

Megaloblastic anem/a.- Treatment of megaloblastic anemias due to a deficiency of folic acid as seen in tropical or nontropical sprue, anemias of nutritional origin, pregnancy, infancy, or childhood. 

Folic acid is used for the treatment of folate deficiency. Oral folic acid is usually the therapy of choice. For megaloblastic anemia doses of 5 mg daily for 4 months should be effective. Folinic acid is available in a parenteral formulation which may be indicated when oral therapy is not feasible and for rescue treatments following certain anti-cancer regimens. 

C. The only effective treatment of pernicious anemia is supplementation of vitamin B12.It is important to determine whether megaloblastic anemia is from a deficiency of folic acid or vitamin B12. Treatment of vitamin Bi2-deficient anemia with folic acid may result in neurological damage if vitamin Bi2 is not adequately supplemented. 

The treatment of folate deficiency in patients receiving anticonvulsant drugs is not without difiiculties. Chanarin (C3) described an epileptic patient who had developed a megaloblastic anemia due to folate deficiency. Treatment with folic acid apparently precipitated convulsions. Up to this time the patient had been free of seizures while on phenobarbital for 4 years. There have since been a number of reports of treatment with folic acid precipitating seizures in patients with epilepsy (D6, R3, W8). 

Many patients with infection have a reduced serum level of folate, particularly those with chronic bacterial infections. However, the development of a megaloblastic anemia is uncommon and when it does occur is perhaps more often associated with the treatment. It is probable that the folate deficiency is the result of a combination of fiictors including poor dietary intake, low reserves, an increased demand due to an increased cell turnover, impaired absorption, vomiting, and impaired metabolism due to the toxic state of the patient (C17, M16, W25). Pyrexia may also inhibit the reduction of folate. Panders and Rupert (P13) found that if folic acid was incubated with a chicken liver enzyme preparation at an elevated temperature the reduction of folic acid to tetrahydrofolic acid was inhibited. 

In humans, folic add avitaminosis is more often caused by faulty uptake and/or utilization, than by dietary deficiency. It usually results in blood ab-normtilities, e.g. megablastic anemia and thrombocytopenia. Antimetabolites of folic acid are aminop-terin and methopterin, which are used therapeutically in the treatment of leukemia. The sulfonamides are antimetabolites of p-aminobenzoic acid, and therefore act as inhibitors of bacterial folic acid synthesis. 

Such relapses can, however, be prevented by giving injections of vitamin B12 at the same time, and this measure should be adopted for those patients with megaloblastic anemia associated with a dual deficiency of vitamin B12 and folic acid, due to intestinal disorder, for example, who may need prolonged treatment with pteroylglutamic acid. In pernicious anemia, however, there is no need to give folic acid, for all the reversible manifestations of the disease are controlled by vitamin B12 alone. 

Pernicious anemia is primarily a deficiency of vitamin Bis due to permanent loss of Castle s intrinsic factor. Treatment with Bis is usually all that is required. In the initial stages there may be a temporary deficiency of folic acid or ascorbic acid, but there is seldom any need to administer these substances so long as enough Bis is given and the patient takes a good diet. 

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