Hemoglobin, Hematocrit, MCV (mean corpuscular volume), MCH (mean corpuscular hemoglobin), MCHC (mean corpuscular hemoglobin concentration)

Strictly speaking, anemia is defined as a decrease in total body red cell mass. For practical purposes, however, anemia is typically defined as hemoglobin <12.0 g/dL and direct determination of total body RBC mass is almost never used to establish this diagnosis. Anemias are then classed by MCV and MCHC (MCH is usually not helpful) into one of the following categories:

• Microcytic/hypochromic anemia (decreased MCV, decreased MCHC)
  • Iron deficiency (common)
  • Thalassemia (common, except in people of Germanic, Slavonic, Baltic, Native American, Han Chinese, Japanese descent)
  • Anemia of chronic disease (uncommonly microcytic)
  • Sideroblastic anemia (uncommon; acquired forms more often macrocytic)
  • Lead poisoning (uncommon)
  • Hemoglobin E trait or disease (common in Thai, Khmer, Burmese,Malay, Vietnamese, and Bengali groups)
• Macrocytic/normochromic anemia (increased MCV, normal MCHC)
  • Folate deficiency (common)
  • B₁₂ deficiency (common)
  • Myelodysplastic syndromes (not uncommon, especially in older individuals)
  • Hypothyroidism (rare)
• Normochromic/normocytic anemia (normal MCV, normal MCHC) The first step in laboratory workup of this broad class of anemias is a reticulocyte count. Elevated reticulocytes implies a normo-regenerative anemia, while a low or “normal” count implies a hyporegenerative anemia:
  • Normoregenerative normocytic anemias (appropriate reticulocyte response)
    • Immunohemolytic anemia
    • Glucose-6-phosphate dehydrogenase (G6PD) deficiency (common)
    • Hemoglobin S or C
    • Hereditary spherocytosis
    • Microangiopathic hemolytic anemia
    • Paroxysmal hemoglobinuria
  • Hyporegenerative normocytic anemias (inadequate reticulocyte response)
    • Anemia of chronic disease
    • Anemia of chronic renal failure
    • Aplastic anemia*

*Drugs and other substances that have caused aplastic anemia include the following:

amphotericin    sulfonamides      phenacetin        trimethadione
silver          chlordiazepoxide  tolbutamide       thiouracil
carbamazepine   chloramphenicol   tetracycline      oxyphenbutazone
arsenicals      chlorpromazine    pyrimethamine     carbimazole
acetazolamide   colchicine        penicillin        aspirin
mephenytoin     bismuth           promazine         quinacrine
methimazole     chlorothiazide    dinitrophenol     ristocetin
indomethacin    phenytoin         gold              trifluoperazine
carbutamide     perchlorate       chlorpheniramine  streptomycin
phenylbutazone  primidone         mercury           meprobamate
chlorpropamide  thiocyanate       tripelennamine    benzene

The drugs listed above produce marrow aplasia via an unpredictable , idiosyncratic host response in a small minority of patients. In addition, many antineoplastic drugs produce predictable , dose-related marrow suppression; these are not detailed here.

Polycythemia

Polycythemia is defined as an increase in total body erythrocyte mass. As opposed to the situation with anemias, the physician may directly measure rbc mass using radiolabeling by ⁵¹chromium, so as to differentiate polycythemia (absolute erythrocytosis, as seen in polycythemia vera, chronic hypoxia, smoker’s polycythemia, ectopic erythropoietin production, methemoglobinemia, and high O₂ affinity hemoglobins) from relative erythrocytosis (as seen in stress polycythemia and dehydration). Further details of the work-up of polycythemias are beyond the scope of this monograph.

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