Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 11)

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Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 11)

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Protein Starvation Decreased dietary intake of protein may lead to mild to moderate hypoproliferative anemia; this form of anemia may be prevalent in the elderly. The anemia can be more severe in patients with a greater degree of starvation. In marasmus, where patients are both protein- and calorie-deficient, the release of EPO is impaired in proportion to the reduction in metabolic rate; however, the degree of anemia may be masked by volume depletion and becomes apparent after refeeding. Deficiencies in other nutrients (iron, folate) may also complicate the clinical picture but may not be apparent at diagnosis. Changes in...

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  1. Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 11) Protein Starvation Decreased dietary intake of protein may lead to mild to moderate hypoproliferative anemia; this form of anemia may be prevalent in the elderly. The anemia can be more severe in patients with a greater degree of starvation. In marasmus, where patients are both protein- and calorie-deficient, the release of EPO is impaired in proportion to the reduction in metabolic rate; however, the degree of anemia may be masked by volume depletion and becomes apparent after refeeding. Deficiencies in other nutrients (iron, folate) may also complicate the clinical picture but may not be apparent at diagnosis. Changes in the erythrocyte indices on refeeding should prompt evaluation of iron, folate, and B12 status. Anemia in Liver Disease
  2. A mild hypoproliferative anemia may develop in patients with chronic liver disease from nearly any cause. The peripheral blood smear may show spur cells and stomatocytes from the accumulation of excess cholesterol in the membrane from a deficiency of lecithin cholesterol acyltransferase. Red cell survival is shortened, and the production of EPO is inadequate to compensate. In alcoholic liver disease, nutritional deficiencies are common and complicate the management. Folate deficiency from inadequate intake, as well as iron deficiency from blood loss and inadequate intake, can alter the red cell indices. Hypoproliferative Anemias: Treatment Many patients with hypoproliferative anemias experience recovery of normal hemoglobin levels when the underlying disease is appropriately treated. For those in whom such reversals are not possible—such as patients with end- stage kidney disease, cancer, and chronic inflammatory diseases—symptomatic anemia requires treatment. The two major forms of treatment are transfusions and EPO. Transfusions Thresholds for transfusion should be altered based on the patient's symptoms. In general, patients without serious underlying cardiovascular or pulmonary disease can tolerate hemoglobin levels above 8 g/dL and do not require intervention until the hemoglobin falls below that level. Patients with more
  3. physiologic compromise may need to have their hemoglobin levels kept above 11 g/dL. A typical unit of packed red cells increases the hemoglobin level by 1 g/dL. Transfusions are associated with certain infectious risks (Chap. 107), and chronic transfusions can produce iron overload. Importantly, the liberal use of blood has been associated with increased morbidity and mortality, particularly in the intensive care setting. Therefore, in the absence of documented tissue hypoxia, a conservative approach to the use of red cell transfusions is preferable. Erythropoietin (Epo) EPO is particularly useful in anemias in which endogenous EPO levels are inappropriately low, such as the hypoproliferative anemias. Iron status must be evaluated and iron repleted to obtain optimal effects from EPO. In patients with chronic renal failure, the usual dose of EPO is 50–150 U/kg three times a week intravenously. Hemoglobin levels of 10–12 g/dL are usually reached within 4–6 weeks if iron levels are adequate; 90% of these patients respond. Once a target hemoglobin level is achieved, the EPO dose can be decreased. A fall in hemoglobin level occurring in the face of EPO therapy usually signifies the development of an infection or iron depletion. Aluminum toxicity and hyperparathyroidism can also compromise the EPO response. When an infection intervenes, it is best to interrupt the EPO therapy and rely on transfusion to correct the anemia until the infection is adequately treated. The dose needed to correct the
  4. anemia in patients with cancer is higher, up to 300 U/kg three times a week, and only about 60% of patients respond. Longer-acting preparations of EPO can reduce the frequency of injections. Darbepoetin alfa, a molecularly modified EPO with additional carbohydrate, has a half-life in the circulation that is 3–4 times longer than epoetin alfa, permitting weekly or every other week dosing. Acknowledgment Dr. Robert S. Hillman was the author of this chapter in the 14th edition, and material from his chapter has been retained Further Readings Bailie GR et al: Parenteral iron use in the management of anemia in end- stage renal disease patients. Am J Kidney Dis 35:1, 2000 [PMID: 10620537] Brugnara C: Iron deficiency and erythropoiesis: New diagnostic approaches. Clin Chem 49:1573, 2003 [PMID: 14500582] Fleming RE, Bacon BR: Orchestration of iron homeostasis. N Engl J Med 352:1741, 2005 [PMID: 15858181]
  5. Ganz T: Hepcidin, a key regulator of iron metabolism and mediator of inflammation. Blood 102:783, 2003 [PMID: 12663437] Hillman RS et al: Hematology in Clinical Practice, 4th ed. New York, McGraw-Hill, 2005 Stoltzfus RF: Iron deficiency: Global prevalence and consequences. Food Nutr Bull 24(Suppl 4):S99, 2003 Thomas C et al: The diagnostic plot: A concept for identifying different states of iron deficiency and monitoring the response to epoetin therapy. Med Oncol 23:23, 2006 [PMID: 16645227]

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