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A 27-year-old auto mechanic presents with a 1-month history of increasing fatigue, shortness of breath with strenuous exertion, easy bruising, and gum bleeding. His past history is negative, except for hepatitis A as a teenager. His occupation does involve the use of cleaning solvents on auto parts. Examination reveals a well-muscled male with pale conjunctiva, petechiae limited to the ankle areas, and hand and forearm bruises. No lymphadenopathy or hepatosplenomegaly.

CBC: Hematocrit/hemoglobin - 20%/6 g/dL

MCV - 91 fL MCH - 32 pg MCHC - 33 g/dL

RDW-CV - 13%


Normochromic/normocytic red cells with ± anisocytosis and the rare polychromatic macrocyte. Platelets and neutrophils markedly decreased without blast cells. Lymphocytes appear normal.

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Reticulocyte count/index - <1%/<0.5
White blood cell count - 1,600/μL
Absolute differential:

Neutrophils - <200/μL

Lymphocytes - 1,200/μL

Monocytes - 320/μL

Platelet count - 9,000/μL

  • How should the anemia be classified?

  • What tests should be ordered?

Disruption of the erythroid precursor pool or the structure of the marrow can produce a marrow-damage anemia. The severity of the anemia depends on the nature of the disorder. Relatively mild marrow-damage anemias are seen in association with drug toxicity and tumor infiltration. More severe anemias are typically seen in patients with acute leukemia and aplastic anemia.

The prevalence of marrow-damage anemias in any population is a function of the incidence of various disease states and environmental challenges. Impairment of red blood cell production is anticipated in most patients receiving tumor chemotherapy. In contrast, aplastic anemia characterized by a marked reduction in all hematopoietic precursors is a relatively rare event. Higher rates of aplastic anemia in the developing world are usually a result of the level of exposure to toxic drugs and chemicals in the workplace and environment.


Anatomical Distribution

The capacity of the erythroid marrow to compensate for anemia or hypoxia requires a normal pool of committed stem cells and a nurturing environment. The anatomical distribution of the marrow is illustrated in Figure 3-1. In normal adults, marrow is concentrated in the axial skeleton and proximal portions of the long bones. It can, however, extend out into more peripheral sites in response to long-standing anemia or as a result of myeloproliferative disease. Patients with thalassemia major can show extension of marrow even into the small bones of the hand.


Anatomical distribution of the marrow in the adult. At birth, the marrow is widely distributed throughout the skeleton. During childhood and early adult life, marrow in the more distal portions of the long bones is replaced by fat. Active marrow is limited to the axial skeleton and proximal ends of the long bones, as indicated by the shading of the skeleton.

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