Paul K. Schick, MD

Professor of Medicine, Emeritus, Thomas Jefferson Medical College, Philadelphia
Research Professor, Drexel University College of Medicine, Philadelphia
Adjunct Clinical Professor, Lankenau Hospital (LIMR), Wynnewood, PA

This case was reviewed and updated in September 2012 by Dr. Peter Marks and members of the Teaching Cases Subcommittee.

Copyright of the American Society of Hematology, 2006. ISSN: 1931-6860.


The etiology of an anemia should be established as early as possible so that appropriate management can be initiated. Classification according to morphological criteria (normocytic normochromic, microcytic hypochromic, or macrocytic) is an important first step.

  1. There are a number of tests that can be ordered to establish the diagnosis of iron deficiency: serum iron, TIBC, and serum ferritin. Bone marrow aspiration to evaluate iron stores is rarely required. The serum ferritin is the most important of these tests. The possibility of false positive and negative results should be recognized.
  2. It should be recognized that GI bleeding is the most common cause of blood loss and iron deficiency anemia in males and post-menopausal females. In the case presented here, a GI workup is not necessary because the cause of bleeding has been clearly established. However, a GI workup is mandatory if the source of bleeding has not been identified. Failure to evaluate the GI tract for lesions in men and in postmenopausal women can lead to severe consequences: failing to diagnose potentially resectable colon cancers before they metastasize and become incurable.
  3. Management of iron deficiency:
    1. Transfusions should be given only to avoid life-threatening complications of anemia. This will avoid the risks of transfusion therapy.
    2. Iron deficiency should be definitively documented prior to instituting replacement therapy, since thalassemia, and anemia of chronic disease (also known as anemia of inflammation) can present with a microcytic anemia. Anemia of chronic disease can be associated with microcytosis and low serum iron levels, but can be distinguished by other features.
    3. Oral iron is preferable to parenteral iron therapy and should be given at therapeutic doses and continued for several months in order to restore iron stores.
  4. There are several options for monitoring the response to therapy: The most helpful is obtaining serial Hgb levels. The Hgb level should begin to rise within a few weeks after patients with iron deficiency are placed on replacement therapy. Hemoglobin levels should increase about 2 to 3 g/dL a month while on therapy. Thus, even severe anemias due to iron deficiency can be corrected within 2 to 3 months. Any deviation from this rate of response should suggest ongoing bleeding or another cause for the anemia. In general, oral iron replacement therapy should be continued for 6 months after the hemoglobin has returned to normal in order to restore iron stores.
  5. Inappropriate iron therapy can lead to hemosiderosis. The complications of hemosiderosis can be avoided by definitively diagnosing iron deficiency prior to prescribing iron therapy and counseling patients appropriately regarding over-the-counter iron preparations. Hemosiderosis can also result from frequent blood transfusions, and iron chelation therapy can be used to manage this complication.

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