Folic acid deficiency malabsorption

When treating folic acid deficiency, an initial daily dose of 1 mg/day by mouth typically is effective. Absorption of folic acid generally is rapid and complete. However, patients with malabsorption syndromes may require larger doses (up to 5 mg/day). Similar to vitamin B12 deficiency, resolution of symptoms and reticulocytosis is prompt, occurring within days of commencing therapy. Hgb will start to rise after 2 weeks of therapy and may take from 2 to 4 months to resolve the deficiency completely. Afterwards, if the underlying deficiency is corrected, folic acid replacement can be discontinued. However, in cases where folic acid is consumed rapidly or absorbed poorly, chronic replacement may be required. 

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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. 

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. 

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. 

The effectiveness of pancreatic enzyme supplementation in treating malabsorption is measured by improvement in body weight and stool consistency or frequency. The 72-hour stool test for fecal fat may be used when there is concern regarding the adequacy of treatment. Serum uric acid and folic acid concentrations should be monitored yearly in patients prone to hyperuricemia or folic acid deficiency. Blood glucose must be closely monitored in the diabetic patient. 

Folic acid deficiency can occur due to pregnancy, malabsorption syndromes or inadequate diet. Some drugs, for example phenytoin (used in epilepsy), oral contraceptives and isoniazid (used in treating tuberculosis), can cause reduced absorption of folic acid. Oral replacement therapy with folic acid is effective. 

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. 

Folic acid deficiency leading to a megaloblastic anaemia, which requires oral folic acid (bottom right), may occur in pregnancy (folate requirement is increased) and in malabsorption syndromes (e.g. sieai-orriioea and sprue). 

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. 

Therapy malabsorption of vitamin B12, i.e., in pernicious or other macrocytic anemias, sprue, gastrointestinal pathology or surgery, enteropathy concomitant with folic acid deficiency, stimulation of hematopoiesis... 

The L. casei method described here can also be used to determine absorption of folic acid. Five milligrams of folic acid is given by mouth samples are obtained at 0, 2, 4, 6, and 8 hours. In cases of deficient folic acid absorption, normal peak levels are not obtained in the malabsorption syndrome, a flat curve indicates no absorption. Normal peak levels are maintained during 2-4 hour intervals (B3). 

Megaloblastic anemia is characterized by the appearance of large cells in the bone marrow and blood due to defective maturation of hematopoietic cells. Folic acid or vitamin B12 deficiency will result in this type of anemia. Malabsorption, impaired use, chronic infections, and drugs can lead to folic acid or vitamin B12 deficiency. 

Deficiencies of vitamin B12 can result from either low dietary levels or, more commonly, from poor absorption of the vitamin due to the failure of gastric parietal cells to produce intrinsic factor (as in pernicious anemia) or to a loss of activity of the receptor needed for intestinal uptake of the vitamin.5 Nonspecific malabsorption syndromes or gastric resection can also cause vitamin B12 deficiency. The vitamin may be administered orally (for dietary deficiencies), or intramuscularly or deep subcutaneously (for pernicious anemia). [Note Folic acid administration alone reverses the hematologic abnormality and thus masks the B12 deficiency, which can then proceed to severe neurologic dysfunction and disease. Therefore, megaloblastic anemia should not be treated with folic acid alone, but rather with a combination of folate and vitamin B12.] Therapy must be continued for the remainder of the life of a patient suffering from pernicious anemia. There are no known adverse effects of this vitamin. 

Folic acid is a nutritional supplement frequently used during periods of deficiency. Folic acid needs increase during chronic diseases, such as malabsorption liver disease, alcoholism, and anticonvulsant or oral contraceptive use. Folic acid supplementation during pregnancy is strongly recommended to prevent neural tube defects to the unborn child. The active form of folic acid, folinic acid, is used in the management of certain medical diseases (e.g., patients taking methotrexate, and 5-fluorouracil). 

Folic acid, or its various equivalents, is used to treat megaloblastic anaemia due to deficiency, which may be due to poor diet, malabsorption syndrome or to the use of certain drugs (e.g. methotrexate or antiepileptics). It is given prophylactically to pregnant women, neonates and in chronic haemolytic anaemia, including sickle-cell anaemia. 

Therapy for fohc acid deficiency consists of the administration of exogenous folic acid in order to induce hematologic remission, replace body stores, and resolve signs and symptoms. In the majority of cases, 1 mg daily is sufficient to replace stores except in cases of deficiency due to malabsorption, in which case doses up to 5 mg daily may be necessary. Synthetic fohc acid is almost completely absorbed by the gastrointestinal tract and is converted to tetrahydrofolate with-... 

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