MEGALOBLASTIC ANEMIA

 

INTRODUCTION:  In the anemias caused by deficiencies of vitamin B12 or folic acid, identical bone marrow and peripheral blood changes occur because both vitamins are essential for normal DNA synthesis.

PATHOPHYSIOLOGY:  Folic Acid Deficiency: Folic acid is stored as compounds referred to as folates. The folate stores in the body are much smaller than those of vitamin B12, and they are quickly depleted when the dietary intake of folate is deficient ( usually within 4 months). Folate deficiency occurs in people who rarely eat uncooked vegetables. Alcohol increases folic acid requirements; folic acid requirements are also increased in patients with chronic hemolytic anemias and in women who are pregnant. Some patients with malabsorptive diseases of the small bowel may as well not absorb folic acid normally.

Vitamin B12 Deficiency: A deficiency of vitamin B12 can occur in several ways. Inadequate dietary intake is rare but can develop in strict vegetarians who consume no meat or dairy products.  Faulty absorption from the GI tract is more common, as with conditions such as Crohn’s disease or after ileal resection or gastrectomy. Another cause is the absence of intrinsic factor. A deficiency may also occur if disease involving the ileum or pancreas impairs absorption.  The body normally has large stores of vitamin B12, so years may pass before the deficiency results in anemia.

CLINICAL MANIFESTATIONS:  Symptoms of folic acid and vitamin B12 deficiencies are similar, and the two anemias may coexist. Symptoms are progressive, although the course of illness may be marked by spontaneous partial remissions and exacerbations.  Gradual development of signs of anemia (weakness, listlessness, and fatigue).  Possible development of a smooth, sore, red tongue and mild diarrhea (pernicious anemia).  Mild jaundice, vitiligo.  Confusion may occur; more often, paresthesias in the extremities and difficulty keeping balance; loss of position sense.  Lack of neurologic manifestations with folic acid deficiency alone.  Without treatment, patients die, usually as a result of heart failure secondary to anemia.  Heart failure

ASSESSMENT AND DIAGNOSTIC FINDINGS:  Schilling test (primary diagnostic tool).  Complete blood cell count (Hgb value as low as 4 to 5 g/dL, WBC count 2,000 to 3,000 per ml of blood, platelet count fewer than 50,000 per ml of blood; very high MCV).  Serum levels of folate and vitamin B12 (folic acid deficiency and deficient vitamin B12)

MEDICAL MANAGEMENT: Folic Acid Deficiency:  Increase intake of folic acid in patient’s diet and administer 1 mg folic acid daily.  Administer IM folic acid for malabsorption syndromes. Prescribe additional supplements as necessary, because the amount in multivitamins may be inadequate to fully replace deficient body stores.  Prescribe folic acid for patients with alcoholism as long as they continue to consume alcohol.

Vitamin B12 Deficiency:  Provide vitamin B12 replacement: Vegetarians can prevent or treat deficiency with oral supplements with vitamins or fortified soy milk; when the deficiency is due to the more common defect in absorption or the absence of intrinsic factor, replacement is by monthly IM injections of vitamin B12.  A small amount of an oral dose of vitamin B12 can be absorbed by passive diffusion, even in the absence of intrinsic factor, but large doses (2 mg/day) are required if vitamin B12 is to be replaced orally.  To prevent recurrence of pernicious anemia, vitamin B12 therapy must be continued for life.

RELATED;

1.  Anemia

2.  Iron deficiency anemia

3.  Medical conditions

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