![]() Rarely, with hematologic malignancy, you can see acquired thalassemia. Thalassemia is usually obvious because of the normal iron studies and chronic microcytosis with or without anemia. This is often obvious due to severe/worsening microcytosis or worsening anemia. this is more likely in the patients with thalassemia trait with history of chronic blood loss. ![]() It is possible to have both iron deficiency and thalassemia in the same patient. A low ferritin is always iron deficiency (except in the very rare congenital aferritinemia). In inflammatory states the ferritin is often normal with a microcytic, iron-responsive anemia suggested by a saturation under 10%. When evaluating iron studies in hospitalized or ill patients, some authors will recommend checking ferritin, iron and transferrin or total iron binding capacity (TIBC). If the hemoglobinopathy panel is “normal” then it must be alpha-thalassemia trait which does not show up on that study. Note that normal iron studies with an MCV under 77 is almost certainly thalassemia. So a well maintained hemoglobin with microcytosis is likely to be thalassemia trait.Īlways check the iron studies first since iron deficiency may mask beta-thalassemia trait. In thalassemia however, even a patient with the trait and a normal hemoglobin will have severe microcytosis. In iron deficiency, the MCV falls progressively as the anemia worsens. A quick review of patient’s hemoglobin and MCV can guide further workup when differentiating between thalassemia or iron deficiency as a cause of microcytic anemia. This is most likely iron deficiency or thalassemia. Particularly in patients with a severe anemia, a normal MCV may reflect a combined macrocytic and microcytic process. Diagnostic approach to hypo-proliferative anemias Similarly, a normal MCV in a chronic alcoholic or a patient with liver disease may reflect new iron deficiency or a different microcytic process. ![]() An “improved” MCV of 75 with a new anemia reflects a macrocytic process (e.g. For example, a patient with a thalassemia trait may have a very low MCV (e.g. We are interested not only in the absolute MCV but in the change in the MCV. The approach to a hypo-proliferative anemia depends on the MCV with a few wrinkles. ![]() This is less overwhelming than it sounds since the diagnosis is usually in the bone marrow biopsy. Intrinsic bone marrow disease including: myeloma, aplastic anemias, lymphoma, infections and metastatic non-hematologic malignancies. B12 with atrophic gastritis causing iron deficiency) Mixed macrocytic and microcytic process (e.g. Normocytic anemia is by far the most complex anemia to sort out and may be: Other “artefacts” including cold agglutinins (red cell clumping) or the missed diagnosis of severe reticulocytosis. Specific dyslipidemias which enlarge the RBC lipid bilayer membrane – liver disease, ethanol use, severe hypothyroidism. azathioprine, cytoxan) or myelodysplasia. B12 / Folate deficiency, chemotherapy-like agents (myelosuppressive chemotherapy), immunosuppressive drugs (e.g. Something interfering with normal nuclear maturation, e.g. Usually due to either iron deficiency or a thalassemia although lead poisoning, congenital sideroblastic anemia, severe chronic disease anemia, or rare hereditary fragmentation syndromes can present this way. The MCV is tightly regulated and even modest variation of this commonly ignored lab result is of clinical significance. Bone marrow failures can be segregated by red cell size – the mean cellular volume (MCV). If the reticulocyte count is inappropriately low then the bone marrow production of red blood cells (RBCs) is inadequate. Hyperproliferative anemias is discussed in a separate section. due to the underlying lymphoma causing the hemolysis). autoimmune hemolytic anemia) but not as elevated as one would expect (e.g. The reticulocyte count may be elevated, consistent with a shortened red cell survival (e.g. Low reticulocytes or inappropriately normal reticulocyte count as seen with a bone marrow failure.īoth. A high reticulocyte count or rapidly falling hemoglobin as seen with shortened red cell survival
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