Monday, May 29, 2017

Folic acid 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’s essential for red blood cell production and maturation. 
Causes include:
  • alcohol abuse (may suppress metabolic effects of folate)
  • inadequate diet (common in alcoholics, elderly people who live alone, and infants, especially those with infections or diarrhea)
  • impaired absorption (due to intestinal dysfunction from such disorders as celiac disease, tropical sprue, and regional jejunitis and from bowel resection)
  • bacteria competing for available folic acid
  • overcooking, which can destroy a high percentage of folic acids in foods
  • 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 preterm 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. These include progressive fatigue, dyspnea, palpitations, weakness, glossitis, nausea, anorexia, headache, fainting, irritability, forgetfulness, pallor, and slight jaundice.
Folic acid deficiency anemia doesn’t 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 help 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).

Many patients also respond favorably to a well-balanced diet.
If the patient has combined vitamin B12 and folate deficiencies, folic acid replenishment alone may aggravate neurologic dysfunction.

No comments:

Post a Comment