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Home :: Folic Acid Deficiency Anemia

Folic Acid Deficiency Anemia

Folic acid is known by a number of names. More commonly today, it is called folacin; but, as far as anemia is concerned, the two most popular names still used are "folic acid deficiency anemia" and "folate deficiency anemia."

A common, slowly progressive megaloblastic anemia, folic acid deficiency anemia is most prevalent in infants, adolescents, pregnant and lactating females, alcoholics, elderly people, and people with malignant or intestinal diseases


Folic acid deficiency anemia results from a decreased level or lack of folate, a vitamin that is essential for red blood cell production and maturation. Causes include:

  • alcohol abuse (alcohol prevents absorption of several nutrients especially the B vitamins)
  • poor diet (common in alcoholics, elderly people who live alone, and infants, especially those with infections or diarrhea)
  • impaired absorption because of intestinal dysfunction from such disorders as celiac disease, tropical sprue, regional jejunitis, Crohn's disease, or bowel resection
  • overcooking of food, destroying valuable water-soluble nutrients, including a high percentage of folic acid
  • limited storage capacity in infants
  • prolonged drug therapy (with anticonvulsants and estrogens)
  • increased folic acid requirement during pregnancy, during rapid growth in infancy (common because of increased survival rate of pre term infants), during childhood and adolescence (because of general use of folate-poor cow's milk), and in patients with neoplastic diseases and some skin diseases (chronic exfoliative dermatitis).

Signs and symptoms

Folic acid deficiency anemia gradually produces clinical features that are characteristic of other megaloblastic anemias without the neurologic manifestations. They include progressive fatigue, dyspnea, palpitations, weakness, glossitis, nausea, anorexia, headache, fainting, irritability, forgetfulness, pallor, and slight jaundice.

Folic acid deficiency anemia does not cause neurologic impairment unless it's associated with vitamin B12 deficiency, as in pernicious anemia.


The Schilling test and a therapeutic trial of vitamin B12 injections distinguish between folic acid deficiency anemia and pernicious anemia. Significant findings include macrocytosis, a decreased reticulocyte count, low platelet count, and a serum folate level less than 4 mg/ml.


Folic acid supplements and the elimination of contributing causes are the primary treatments. Supplements may be given orally (usually 1 to 5 mg/day) or parenterally (to patients who are severely ill, have malabsorption, or are unable to take oral medication).

Oral or intravenous folic acid supplements may be taken on a short-term basis until the anemia has been corrected, or -- in the case of poor absorption by the intestine -- replacement therapy may be lifelong.

Dietary treatment consists of increasing the intake of green, leafy vegetables and citrus fruits.


Eating raw or lightly cooked vegetables every day will help maintain normal folic acid levels, as will taking a folic acid supplement containing at least 400 mcg of this vitamin. Because folic acid deficiency can cause birth defects, all women of childbearing age who can become pregnant should consume at least 400 mcg of folic acid daily; a woman who is pregnant should have regular medical checkups, and take a good prenatal vitamin.

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