Iron preparations are used to treat the most common form of ane-mia—iron deficiency anemia. Iron preparations discussed in this section include ferrous fumarate, ferrous gluconate, ferrous sul-fate, iron dextran, and sodium ferric gluconate complex.
Iron is absorbed primarily from the duodenum and upper jejunum of the intestine. Different iron formulations don’t vary in absorp-tion, but they do vary in the amount of elemental iron supplied.
The amount of iron absorbed depends partially on the body’s stores of iron. When body stores are low or RBC production is ac-celerated, iron absorption may increase by 20% to 30%. On the oth-er hand, when total iron stores are large, the body absorbs only about 5% to 10% of the iron available.
Enteric-coated preparations decrease iron absorption because, in that form, iron isn’t released until after it leaves the duodenum. The lymphatic system absorbs the parenteral form after I.M. injec-tions.
Iron is transported by the blood and bound to transferrin, its carri-er plasma protein. About 30% of the iron is stored primarily as he-mosiderin or ferritin in the reticuloendothelial cells of the liver, spleen, and bone marrow. About 66% of the total body iron is contained in hemoglobin. Excess iron is excreted in urine, stool, sweat, and through intestinal cell-sloughing. It appears in breast milk and crosses the placenta.
Although iron has other roles, its most important role is the pro-duction of hemoglobin. About 80% of iron in the plasma goes to the bone marrow, where it’s used for erythropoiesis (production of RBCs).
Oral iron therapy is the preferred route for preventing or treating iron deficiency anemia. It’s used to prevent anemias in children ages 6 months to 2 years because this is a period of rapid growth and development. Pregnant women may need iron supplements to replace the iron used by the developing fetus.
Parenteral iron therapy is used for patients who can’t absorb oral preparations, aren’t compliant with oral therapy, or have bowel disorders (such as ulcerative colitis or Crohn’s disease). Patients with end-stage renal disease who are receiving hemodialysis may also receive parenteral iron therapy at the end of their dialysis ses-sion. While parenteral iron therapy corrects the iron store defi-ciency quickly, it doesn’t correct the anemia any faster than oral preparations would.
Iron preparations available for parenteral administration are iron dextran (given by I.M. injection or slow, continuous I.V. infu-sion) and iron sucrose. Iron sucrose is used for patients on he-modialysis. (See Testing for parenteral iron sen-sitivity.)
Iron absorption is reduced by antacids as well as by such foods as coffee, tea, eggs, and milk. Other drug interactions involving iron include:
§ Absorption of tetracyclines (demeclocy-cline, doxycycline, minocycline, oxytetracy-cline, and tetracycline), methyldopa, quinolones (ciprofloxacin, levofloxacin, lome-floxacin, moxifloxacin, norfloxacin, ofloxacin, and sparfloxacin), levothyroxine, and penicil-lamine may be reduced when taken with oral iron preparations.
§ Cholestyramine, cimetidine, proton-pump inhibitors, and colestipol may reduce iron ab-sorption in the GI tract. (See Adverse reac-tions to iron therapy.)