Codocyte

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Codocytes in human blood ( Giemsa stain )

Codocyten , also known as target cells or Mexican Hutzellen ( "Mexican hat cells") are red blood cells, the appearance of a target have.

Under a light microscope , these cells appear to have a dark center (a central area with hemoglobin) surrounded by a white ring (an area that is relatively pale), followed by a dark outer ( peripheral ) second ring containing a strip of hemoglobin. In the electron microscope , on the other hand, the codocytes appear rather thin and bell-shaped. Because of their small thickness they are called leptocytic and because of the wave-shaped head they are called “Mexican hat cells”. On a routine morphological smear, some people prefer to distinguish between leptocytes and codocytes. They point out that in leptocytes the central point is not completely delimited from the peripheral ring; that is, the pallor is more C-shaped than a full ring.

The cells are characterized by a disproportionate increase in the ratio of surface membrane to volume. This is known as a "relative membrane excess". This is due to the increased red blood cell surface area (above normal) or decreased intracellular hemoglobin levels, which in turn can cause an abnormal decrease in cell volume without affecting the size of the membrane area. The increase in the surface-to-volume ratio gives the cell a reduced osmotic fragility since it can absorb more water for a given amount of osmotic stress.

In vivo the codocytes are bell-shaped. They only take on the target configuration when processed to create a blood film. In this film, these cells appear thinner than normal mainly due to their paleness, based on the thickness assessment using a microscope.

causes

The cells can be associated with the following symptoms:

  • Liver disease : Lecithin cholesterol acyltransferase (LCAT) activity can be reduced in obstructive liver disease. Decreased enzyme activity, in turn, increases the cholesterol to phospholipid ratio, which causes an increase in the surface area of ​​the red blood cell membranes.
  • Iron deficiency : The decrease in hemoglobin content in relation to area is possibly the reason for the appearance of codocytes. The same phenomenon occurs with thalassemia, hemoglobin C disease, etc.
  • α-thalassemia and β-thalassemia (hemoglobin pathology)
  • Hemoglobin C Disease
  • Post- splenectomy : An important function of the spleen is the elimination of opsonized , deformed and damaged erythrocytes by splenic macrophages . If the splenic macrophage function is disturbed or absent due to the removal of the spleen, altered erythrocytes are no longer efficiently removed from the circulation. Therefore, an increased number of codocytes can be observed.
  • Autosplenectomy caused by sickle cell anemia

In patients with obstructive liver disease, lecithin-cholesterol acyltransferase activity is weakened, which increases the cholesterol-phospholipid ratio and increases the surface area of ​​the red blood cell membranes. In contrast, membrane excess occurs correspondingly in patients with iron deficiency anemia and thalassemia due to the reduced amount of intracellular hemoglobin. When a cell membrane breaks, it becomes motionless and stops pulsing. The formation of codocytes decreases the amount of oxygen that circulates through the blood. They are unable to bind oxygen and transport it to all areas of the body.

Symptoms

An increase in codocytes results from a shift in the balance between red blood cells and cholesterol. The ratio between surface membrane and volume is also increased. Codocytes are more resistant to osmotic lysis , which is most often seen in dogs. Hypochromic cells in iron deficiency anemia also have the appearance of a target. Codocytes are unusually resistant to saline solution.

Individual evidence

  1. ^ Mexican Hat Cell ( Memento of March 2, 2012 in the Internet Archive )
  2. The Target Cell: An Overview ( Memento from September 14, 2006 in the Internet Archive )
  3. ^ Mary Louise Turgeon: Clinical hematology. Theory & procedures. Volume 936, Lippincott Williams & Wilkins, Dec. 7, 2004 - Chapter 6, p. 103.
  4. ^ A b Marshall A. Lichtman, William J. Williams, et al .: Williams Hematology . 7th edition. McGraw-Hill, New York 2006, ISBN 0-07-143591-3 .
  5. Lawrence M. Tierney, Stephen J. McPhee, Maxine A. Papadakis: Current Medical Diagnosis and Treatment 2007 . McGraw-Hill Professional, 2006, ISBN 0-07-147247-9 , pp. 498 .