Medication Summary
Documentation of the etiology of anemia is essential in the selection of therapy. Not all microcytic anemias are caused by iron deficiency; some are iron-overloading disorders. Similarly, not all megaloblastic anemias are associated with either vitamin B12 deficiency or folic acid deficiency.
Iron Products
Class Summary
Mineral supplements are used to provide adequate iron for hemoglobin synthesis and to replenish body stores of iron. Iron is administered prophylactically during pregnancy because of the anticipated requirements of the fetus and the losses that occur during delivery.
Ferrous sulfate (Fer-In-Sol, Fer-Iron, Slow Iron, Slow-Fe)
Ferrous sulfate is the mainstay treatment for treating patients with iron deficiency anemia. It should be continued for about 2 months after correction of the anemia and its etiologic cause in order to replenish body stores of iron. Ferrous sulfate is the most common and cheapest form of iron used. Tablets contain 50-60 mg of iron salt. Other ferrous salts are used and may cause less intestinal discomfort because they contain a smaller dose of iron (25-50 mg). Oral solutions of ferrous iron salts are available for use in pediatric populations.
Carbonyl iron (Feosol, Iron Chews, Ircon)
Carbonyl iron is used as a substitute for ferrous sulfate. It has a slower release of iron and is more expensive than ferrous sulfate. The slower release affords the agent greater safety if ingested by children. On a milligram-for-milligram basis, it is 70% as efficacious as ferrous sulfate. Claims are made that there is less gastrointestinal (GI) toxicity, prompting use when ferrous salts are producing intestinal symptoms and in patients with peptic ulcers and gastritis.
Iron dextran (Infed)
Dextran-iron replenishes depleted iron stores in the bone marrow, where it is incorporated into hemoglobin. Parenteral use of iron-carbohydrate complexes has caused anaphylactic reactions, and its use should be restricted to patients with an established diagnosis of iron deficiency anemia whose anemia is not corrected with oral therapy.
The required dose can be calculated (3.5 mg iron/g of hemoglobin) or obtained from tables in the Physician's Desk Reference. For intravenous (IV) use, this agent may be diluted in 0.9% sterile saline. Do not add to solutions containing medications or parenteral nutrition solutions.
Iron sucrose (Venofer)
Iron sucrose is used to treat iron deficiency (in conjunction with erythropoietin) due to chronic hemodialysis. Iron deficiency is caused by blood loss during the dialysis procedure, increased erythropoiesis, and insufficient absorption of iron from the GI tract. Iron sucrose has shown a lower incidence of anaphylaxis than other parenteral iron products.
Ferric gluconate (Ferrlecit)
Ferric gluconate replaces iron found in hemoglobin, myoglobin, and specific enzyme systems. It allows transportation of oxygen via hemoglobin.
Ferric maltol (Accrufer)
An oral iron replacement that delivers iron for uptake across the intestinal wall and transfer to transferrin and ferritin. It is indicated for iron deficiency in adults.
Ferric derisomaltose (Monoferric)
Complex of iron (III) hydroxide and derisomaltose, an iron carbohydrate oligosaccharide that releases iron. Iron binds to transferrin for transport to erythroid precursor cells to be incorporated into hemoglobin. Ferric derisomaltose is administered IV and is indicated for iron deficiency anemia in adults who are intolerant to or have had unsatisfactory response to oral iron.
Vitamins
Class Summary
Vitamins are used to meet necessary dietary requirements and are used in metabolic pathways, as well as in DNA and protein synthesis.
Cyanocobalamin (vitamin B-12) and folic acid are used to treat megaloblastic and macrocytic anemias secondary to deficiency. Both vitamin B-12 and folic acid are required for the synthesis of purine nucleotides and the metabolism of some amino acids. Each is essential for normal growth and replication. Deficiency of either cyanocobalamin or folic acid results in defective DNA synthesis and cellular maturation abnormalities. Consequences of deficiency are most evident in tissues with high cell turnover rates (eg, hematopoietic system).
Vitamin K deficiency causes elevation of prothrombin time and is commonly seen in patients with liver disease.
Cyanocobalamin (Nascobal)
Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B-12 in humans. Microbes synthesize vitamin B-12, but humans and plants do not. Vitamin B-12 deficiency may result from intrinsic factor (IF) deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum.
Folic acid (FA-8)
Folic acid is an essential cofactor for enzymes used in the production of red blood cells (RBCs).
