Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 10)

Table 98-6 Diagnosis of Hypoproliferative AnemiasTestsIron Deficiency tionInflammaRenal DiseaseHypometa bolic StatesAnemiaMild to severeMild severeMild toMildMCV (fL) 9060–80–909090Morphol ogy mo-Nor cNormocyti yticNormocNormocyticmicrocyticSI360
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Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 10) Chapter 098. Iron Deficiency and Other Hypoproliferative Anemias (Part 10) Table 98-6 Diagnosis of Hypoproliferative Anemias Tests Iron Inflamma Renal Hypometa Deficiency tion Disease bolic States Anemia Mild Mild Mild to Mild to severe severe MCV 60– 80–90 90 90(fL) 90 Morphol Nor Normocyti Normoc Normocyticogy mo- c ytic microcytic SI the renal failure. Red cells are typically normocytic and normochromic, andreticulocytes are decreased. The anemia is primarily due to a failure to produceadequate amounts of EPO and a reduction in red cell survival. In certain forms ofacute renal failure, the correlation between the anemia and renal function isweaker. Patients with the hemolytic-uremic syndrome increase erythropoiesis inresponse to the hemolysis, despite renal failure requiring dialysis. Polycystickidney disease also shows a smaller degree of EPO deficiency for a given level ofrenal failure. By contrast, patients with diabetes or myeloma have more severeEPO deficiency for a given level of renal failure. Assessment of iron status provides information to distinguish the anemia ofrenal disease from the other forms of hypoproliferative anemia (Table 98-6) and toguide management. Patients with the anemia of renal disease usually present withnormal serum iron, TIBC, and ferritin levels. However, those maintained onchronic hemodialysis may develop iron deficiency from blood loss through thedialysis procedure. Iron must be replenished in these patients to ensure anadequate response to EPO therapy (see below). Anemia in Hypometabolic States Patients who are starving, particularly for protein, and those with a varietyof endocrine disorders that produce lower metabolic rates, may develop a mild tomoderate hypoproliferative anemia. The release of EPO from the kidney issensitive to the need for O2, not just O2 levels. Thus, EPO production is triggeredat lower levels of blood O2 content in disease states (such as hypothyroidism andstarvation) where metabolic activity, and thus O2 demand, is decreased. Endocrine Deficiency States The difference in the levels of hemoglobin between men and women isrelated to the effects of androgen and estrogen on erythropoiesis. Testosterone andanabolic steroids augment erythropoiesis; castration and estrogen administration tomales decrease erythropoiesis. Patients who are hypothyroid or have deficits inpituitary hormones also may develop a mild anemia. Pathogenesis may becomplicated by other nutritional deficiencies since iron and folic acid absorptioncan be affected by these disorders. Usually, correction of the hormone deficiencyreverses the anemia. Anemia may be more severe in Addisons disease, depending on the levelof thyroid and androgen hormone dysfunction; however, anemia may be maskedby decreases in plasma volume. Once such patients are given cortisol and volumereplacement, the hemoglobin level may fall rapidly. Mild anemia complicatinghyperparathyroidism may be due to decreased EPO production as a consequenceof the renal effects of hypercalcemia or to impaired proliferation of erythroidprogenitors.