Interrelationship of Folic Acid, Vitamin B12and Ascorbic Acid in Patients with Megaloblastic Anemia

Abstract

Folic acid and vitamin B₁₂ deficiency states are associated with defects in nucleoprotein metabolism characterized biochemically by increased ratios of ribosenucleic acid to desoxyribosenucleic acid, and uracil to thymine. These biochemical changes can be correlated with the degree of megaloblastosis. In pernicious anemia, folic acid therapy will temporarily correct the defect in nucleoprotein metabolism by mass action. Eventually, a greater deficiency of vitamin B₁₂ occurs, resuiting in hematologic relapse and progressive neurologic disease. Folic acid is inactive at the erythroid cellular level, while vitamin B₁₂ is active at the erythroid cellular level. Pernicious anemia of pregnancy and vitamin B₁₂-refractory megaloblastic anemia also occur because of defects in nucleoprotein metabolism. These abnormalities arise because of conditioned deficiencies of folinic acid coenzyme, rather than a deficiency of vitamin B₁₂. Ascorbic acid metabolism may be altered in patients with megaloblastic anemias. Thse plasma ascorbic acid level is subnormal as compared to a group of patients with similar dietary background but without macrocytic anemia. Vitamin C is capable of producing reticulocytosis and improvement in the anemia of some of these patients. The alteration in ascorbic acid metabolism may reflect changes in redox potentials associated with vitamin B₁₂ deficiency.