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...
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Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 11) Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 11) Protein Starvation Decreased dietary intake of protein may lead to mild to moderatehypoproliferative anemia; this form of anemia may be prevalent in the elderly. Theanemia can be more severe in patients with a greater degree of starvation. Inmarasmus, where patients are both protein- and calorie-deficient, the release ofEPO is impaired in proportion to the reduction in metabolic rate; however, thedegree of anemia may be masked by volume depletion and becomes apparent afterrefeeding. Deficiencies in other nutrients (iron, folate) may also complicate theclinical picture but may not be apparent at diagnosis. Changes in the erythrocyteindices on refeeding should prompt evaluation of iron, folate, and B12 status. Anemia in Liver Disease A mild hypoproliferative anemia may develop in patients with chronic liverdisease from nearly any cause. The peripheral blood smear may show spur cellsand stomatocytes from the accumulation of excess cholesterol in the membranefrom a deficiency of lecithin cholesterol acyltransferase. Red cell survival isshortened, and the production of EPO is inadequate to compensate. In alcoholicliver disease, nutritional deficiencies are common and complicate themanagement. Folate deficiency from inadequate intake, as well as iron deficiencyfrom blood loss and inadequate intake, can alter the red cell indices. Hypoproliferative Anemias: Treatment Many patients with hypoproliferative anemias experience recovery ofnormal 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—symptomaticanemia requires treatment. The two major forms of treatment are transfusions andEPO. Transfusions Thresholds for transfusion should be altered based on the patientssymptoms. In general, patients without serious underlying cardiovascular orpulmonary disease can tolerate hemoglobin levels above 8 g/dL and do not requireintervention until the hemoglobin falls below that level. Patients with morephysiologic compromise may need to have their hemoglobin levels kept above 11g/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 chronictransfusions can produce iron overload. Importantly, the liberal use of blood hasbeen associated with increased morbidity and mortality, particularly in theintensive care setting. Therefore, in the absence of documented tissue hypoxia, aconservative approach to the use of red cell transfusions is preferable. Erythropoietin (Epo) EPO is particularly useful in anemias in which endogenous EPO levels areinappropriately low, such as the hypoproliferative anemias. Iron status must beevaluated and iron repleted to obtain optimal effects from EPO. In patients withchronic renal failure, the usual dose of EPO is 50–150 U/kg three times a weekintravenously. Hemoglobin levels of 10–12 g/dL are usually reached within 4–6weeks if iron levels are adequate; 90% of these patients respond. Once a targethemoglobin level is achieved, the EPO dose can be decreased. A fall inhemoglobin level occurring in the face of EPO therapy usually signifies thedevelopment of an infection or iron depletion. Aluminum toxicity andhyperparathyroidism can also compromise the EPO response. When an infectionintervenes, it is best to interrupt the EPO therapy and rely on transfusion to correctthe anemia until the infection is adequately treated. The dose needed to correct theanemia in patients with cancer is higher, up to 300 U/kg three times a week, andonly 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 ahalf-life in the circulation that is 3–4 times longer than epoetin alfa, permittingweekly or every other week dosing. Acknowledgment Dr. Robert S. Hillman was the author of this chapter in the 14th edition, andmaterial 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 diagnosticapproaches. Clin Chem 49:1573, 2003 [PMID: 14500582] Fleming RE, Bacon BR: Orchestration of iron homeostasis. N Engl J Med352:1741, 2005 [PMID: 15858181] Ganz T: Hepcidin, a key regulator of iron metabolism and mediator ofinflammation. 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. FoodNutr Bull 24(Suppl 4):S99, 2003 Thomas C et al: The diagnostic plot: A concept for identifying differentstates of iron deficiency and monitoring the response to epoetin therapy. MedOncol 23:23, 2006 [PMID: 16645227]