Microcytic (low MCV) Iron deficiency Thalassemia Sideroblastic anemia Lead poisoning
Normocytic (normal MCV) Acute blood loss Hemolysis
Anemia of chronic disease Anemia of renal failure Myelodysplastic syndromes
Macrocytic anemia (high MCV) Folate deficiency Vitamin Br deficiency Drug toxicity, e.g., zidovudine Alcoholism/chronic liver disease after which the RBC circulates for approximately 120 days. The blood normally contains about one reticulocyte per 100 RBCs. The reticulocyte count, usually reported as a percentage of reticulocytes per 100 RBCs, may be falsely elevated in the presence of anemia. Therefore, a corrected reticulocyte percentage is calculated by multiplying the reported reticulocyte count by the patient's hematocrit divided by 45 (normal hematocrit). The reticulocyte may also be converted to an absolute number by multiplying the reported reticulocyte count by the RBC count and dividing by 100. The absolute reticulocyte count is normally 50.000-70,000 reticulocytes/mm3. If the reticulocyte count is low, causes of hypoproliferative bone marrow disorders should be suspected. A high reticulocyte count may reflect acute blood losses, hemolysis, or a response to therapy for anemia.
Iron studies are very helpful to confirm a diagnosis of iron deficiency anemia and to help in the differential diagnosis with other types of anemia, such as anemia of chronic disease and sideroblastic anemia (Table 25-3). Serum ferritin concentration is a reliable indication of iron deficiency. Serum ferritin values are increased with chronic inflammatory disease, malignancy, or liver injury; therefore, serum ferritin concentration may be above normal when iron deficiency exists with chronic diseases, such as rheumatoid arthritis, Hodgkin disease, or hepatitis, among many other disorders. Measurement of serum iron concentration, serum TIBC, and calculation of percent saturation of transferrin has been widely used for diagnosis of iron deficiency. True iron deficiency is strongly suspected on the basis of low serum iron level and normal or high binding capacity, which will result in a low calculated saturation. In anemia of chronic disease, serum iron concentration is low, but usually the TIBC is also reduced; therefore, percent transferrin saturation typically is normal in anemia of chronic disease. Chronic disease typically causes elevation in serum ferritin concentration. When chronic disease and iron-deficiency anemia coexist, serum ferritin concentration may be normal. Sideroblastic anemia is commonly microcytic and hypochromic. The iron studies in sideroblastic anemia include increases in serum iron and serum ferritin concentration and saturation of transferrin. An important clue to the presence of sideroblastic anemia is the presence of stippled RBCs in the peripheral blood smear. Iron stain in the bone marrow reveals pathognomonic feature of engorged mitochondria in the developing RBCs called ringed sideroblasts.
Evaluating the peripheral blood smear for specific abnormalities in RBC morphology may be very useful for determining the etiology of anemia. In iron-deficiency anemia, the peripheral blood smear shows RBCs smaller than normal (microcytes) and hypochromia.
Although the treatment of iron deficiency is straightforward, finding the underlying etiology is paramount. Treatment of iron-deficiency anemia consists of iron replacement therapy, typically with oral ferrous sulfate 325 mg two or three times daily. Correction of anemia usually occurs within 6 weeks, but therapy should continue for at least 6 months to replenish the iron stores.
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