7.3: Sickle Cell Trait (Hemoglobin AS)

A Laboratory Guide to Clinical Hematology · LibreTexts

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    Cause(s):

    β globin chain amino acid substitution in the 6th position from glutamic acid (Glu) to valine (Val). Only one β globin genes is affected.1,2

    Inheritance:

    Heterozygous state where one normal β globin gene and one affected β globin gene are inherited.3

    Clinical Findings:1-3

    Due to the presence of Hb A and reduced concentration of HB S, polymerization of Hb S and sickling of red blood cells does not normally occur. As a result, condition is mostly benign and asymptomatic.

    Sickling can still occur under extremely low hypoxic conditions.

    Laboratory Features:1-3

    CBC:

    All parameters (Even Hb) are normal

    PBS:

    Absence of sickle cells

    PBS appears normal

    (may see a slight increase in target cells)

    BM:

    N/A

    Hemoglobin Electrophoresis:

    Hb S: 35-45%

    Hb A: 50-65%

    Hb A2: Normal

    Hb F: Normal

    Hb A:Hb S is ~60:40

    Other Tests:

    Solubility Screen: Positive

    Metasulfite Sickling Test: Positive

    HPLC

    Hemoglobin Electrophoresis

    		  

    References:

    1. Laudicina RJ. Hemoglobinopathies: qualitative defects. In: Clinical laboratory hematology. 3rd ed. New Jersey: Pearson; 2015. p.231–50.

    2. Harmening DM, Yang D, Zeringer H. Hemolytic anemias: extracorpuscular defects. 5th ed. Philadelphia: F.A. Davis Company; 2009. p. 250-79).

    3. Randolph TR. Hemoglobinopathies (structural defects in hemoglobin). In: Rodak’s hematology clinical applications and principles. 5th ed. St. Louis, Missouri: Saunders; 2015. p. 426-453.

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