Folic acid deficiency anemia

Folic acid deficiency anemia is a common, slowly progressive, megaloblastic anemia. It usually occurs in infants, adolescents, pregnant and lactating females, alcoholics, elderly people, and people with malignant or intestinal diseases.

Causes and incidence

Folic acid deficiency anemia may result from:

❑ alcohol abuse (alcohol may suppress metabolic effects of folate)

❑ poor diet (common in alcoholics, elderly people living alone, and infants, especially those with infections or diarrhea)

❑ impaired absorption (due to intestinal dysfunction from disorders such as celiac disease, tropical sprue, regional jejunitis, or bowel resection)

❑ bacteria competing for available folic acid

❑ excessive cooking, which can destroy a high percentage of folic acids in foods (See Foods high in folic acid.)

❑ limited storage capacity in infants

❑ prolonged drug therapy (anticonvulsants and estrogens)

❑ increased folic acid requirements during pregnancy; during rapid growth in infancy (common because of recent increase in survival of premature 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).

It’s estimated that 10% of the United States population has low folate stores.

Signs and symptoms

Folic acid deficiency anemia gradually produces clinical features characteristic of other megaloblastic anemias, without the neurologic manifestations: progressive fatigue, shortness of breath, 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.

Diagnosis

The Schilling test and a therapeutic trial of vitamin B₁₂ injections distinguish between folic acid deficiency anemia and pernicious anemia. Significant findings include macrocytosis, decreased reticulocyte count, abnormal platelets, and serum folate less than 3 ng/ml.

Treatment

Treatment consists primarily of folic acid supplements and elimination of contributing causes. Folic acid supplements may be given orally or parenterally (to patients who are severely ill, have malabsorption, or are unable to take oral medication). Many patients respond favorably to a well-balanced diet. If the patient has combined B₁₂ and folate deficiencies, folic acid replenishment alone may aggravate neurologic dysfunction.

Special considerations

❑ Teach the patient to meet daily folic acid requirements by including a food from each food group in every meal. If he has a severe deficiency, explain that diet only reinforces folic acid supplementation and isn’t therapeutic by itself. Urge compliance with the prescribed course of therapy. Advise him not to stop taking the supplements when he begins to feel better.

❑ If the patient has glossitis, emphasize the importance of good oral hygiene. Suggest regular use of mild or diluted mouthwash and a soft toothbrush.

❑ Watch fluid and electrolyte balance, particularly in the patient who has severe diarrhea and is receiving parenteral fluid replacement therapy.

❑ Because anemia causes severe fatigue, schedule regular rest periods until the patient is able to resume normal activity.

❑ To prevent folic acid deficiency anemia, emphasize the importance of a well-balanced diet high in folic acid. Identify alcoholics with poor dietary habits and try to arrange for appropriate counseling. Tell mothers who aren’t breast-feeding to use commercially prepared formulas.

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Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

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Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2008 Williams & Wilkins.

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More About This Book: Title: Professional Guide to Diseases (Eighth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2005 ISBN: 1-58255-370-X

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