Polychromasia refers to a condition in which red blood cells (RBCs) appear grayish-blue in color when examined on a blood smear slide under a microscope. Polychromasia occurs when RBCs are released prematurely from the bone marrow, where they are produced. RBCs are released prematurely in response to a certain type of hormone stimulation usually resulting from anemia or possibly due to structural damage to the bone marrow from a variety of causes.
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Normal Red Blood Cell Development
Most RBCs are made and mature in the bone marrow. Developing RBCs still need to make proteins, so they still have a nucleus and protein-making structures called ribosomes. Since the only function of a mature RBC is to carry oxygen, normally when an RBC is released from the bone marrow, the nucleus and ribosomes are absent. RBCs released from the bone marrow prematurely still have some ribosomes left, and that is what causes the grayish-blue color when exposed to Wright-Giemsa stain on a slide.
- Most RBCs are made and mature in the bone marrow.
- Since the only function of a mature RBC is to carry oxygen, normally when an RBC is released from the bone marrow, the nucleus and ribosomes are absent.
Hormonal Control of RBC Release
Causes of Low HCT and HGB
A hormone called erythropoietin (EPO), produced by the kidneys, controls the rate of RBC production and release from the bone marrow. When EPO levels rise, more immature RBCs are released from the bone marrow, resulting in polychromasia. EPO is usually released in response to anemia (a lowered number of RBCs in the blood), so anemia should be considered a cause of polychromasia.
- A hormone called erythropoietin (EPO), produced by the kidneys, controls the rate of RBC production and release from the bone marrow.
- When EPO levels rise, more immature RBCs are released from the bone marrow, resulting in polychromasia.
Anemia from Decreased RBC Production
Cause of anemia are decreased production of RBCs and production of RBCs that are defective in some way 1. Dietary deficiencies in iron, folate or vitamin B12 can cause production of fewer RBCs and cause those that are produced to have less of the oxygen-carrying protein, hemoglobin. Aplastic anemia is a generalized failure of the bone marrow to produce sufficient blood cells, including RBCs. A genetic condition called thalassemia causes production of RBCs with defective hemoglobin that cannot survive.
- Cause of anemia are decreased production of RBCs and production of RBCs that are defective in some way 1.
- Dietary deficiencies in iron, folate or vitamin B12 can cause production of fewer RBCs and cause those that are produced to have less of the oxygen-carrying protein, hemoglobin.
Anemia from Increased RBC Loss
Causes of High MPV Blood
Another cause of anemia is the increased loss or destruction of RBCs 1. An obvious example of this is loss of blood from bleeding, which can cause severe anemia. There are other conditions that can cause destruction of RBCs without loss of blood, which is known as hemolytic anemia. Hemolytic anemia can be caused by autoimmune disorders, genetic biochemical defects (glucose-6-phosphate dehydrogenase deficiency) or through mechanical trauma, such as occurs in heart surgery. Sickle cell anemia is a combination of defective production and increased destruction, in that genetic defects in RBC production cause hemolytic anemia under certain circumstances.
Damage to Bone Marrow
Polychromasia can also occur when the bone marrow is damaged, leading to the premature release of RBCs. The most common cause of widespread bone marrow damage is infiltration by malignant (cancer) cells, either from the marrow itself (leukemia) or as the result of metastasis from other tissue. Another cause is bone marrow fibrosis, in which uncontrollable growth of immature blood cells of various types leads to the formation of scar tissue that damages the bone.
Causes of Low HCT and HGB
Causes of High MPV Blood
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- "Harrison’s Principles of Internal Medicine;" Dennis L. Kasper; 2005
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- American Society of Hematology. Common types of anemia.
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Based in Los Angeles, Marie Miller worked 15 years as a newspaper reporter in New Jersey and California. Her articles have appeared in the Asbury Park Press, the Star Ledger and the Del Mar Sun. She holds a Bachelor of Arts in journalism from Boston University