Iron
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.)
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