Hypoproliferative or Decreased Production Anemias Nutritional

Deficiencies in nutrients such as folic acid and vitamin B12 may hinder the process of erythrocyte maturation.4,5 Folic acid and vitamin B12 are required for the formation of DNA. When these nutrients are decreased, DNA synthesis is inhibited, and consequently, erythrocyte maturation also is inhibited.4,5 Poor diet can be a contributor to the deficiencies in these nutrients. Similarly, patients with a condition called pernicious anemia are unable to absorb B12 via their GI tract due to a lack in a glycoprotein called intrinsic factor. This glycoprotein binds to vitamin B12 and facilitates its absorption in the ileum. This condition results in B12 deficiency despite adequate dietary B intake.6

Iron is also a vital nutrient in the development of functioning erythrocytes as it is essential for the formation of Hgb. Lack of iron leads to a decrease in Hgb synthesis and ultimately RBCs. Normal homeostasis of iron transport and metabolism is depicted in Figure 66-2.7 Approximately 1 to 2 mg of iron is absorbed through the duodenum each day, and the same amount is lost via blood loss, desquamation of mucosal cells, or menstruation.

Since there is no true "excretion" of iron from the body, iron-deficiency anemia (IDA) typically occurs because of either inadequate absorption of iron or excess blood loss. Inadequate absorption may occur in patients who have congenital or acquired intestinal diseases, such as inflammatory bowel disease, celiac disease, or bowel resection. Achlorhydria and diets poor in iron also may contribute to iron deficiency states. In contrast, iron deficiency also may occur in patients who exhibit a higher rate of iron loss from the body. This is manifested in blood loss, either from the GI system, menstruation, cancer, or trauma.7

Hfe Hereditary Hemochromatosis
FIGURE 66-2. The distribution of iron use in adults. (From Ref. 7.)

Hypoproliferative Marrow

Patients with chronic diseases exhibit a different patho-physiologic mechanism of disease. For example, patients with cancer may suffer from anemia because of chemotherapy and/or the tumor effects on the marrow itself. Chemotherapy may cause destruction of highly proliferating stem cells, thereby decreasing the production of mature erythrocytes.8 In addition, cancer can cause anemia via hemorrhage, replacing normal bone marrow with malignant cells, and releasing cytokines that lead to decreased EPO production. Both of these scenarios can lead to anemia from a hypopro-liferative marrow.8

Decreased EPO Production or Response

Patients with CKD suffer from a decrease in erythropoietin production because EPO is produced mainly in the kidneys.4,5 In patients with anemia of chronic disease, there is a blunted EPO production as well as a diminished response to EPO.9 Anemia of chronic disease also affects iron homeostasis, causing iron sequestration into storage sites and decreasing the amount available to the rest of the body.9

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