(4) Observe immediately and at intervals of 15 to 30 minutes after
preparation for signs of sickle cell information.
(1) The sickling phenomenon is a consequence of an inherited, abnormal
type of hemoglobin (hemoglobin S). The severity of the anemia as compared to the trait
will vary with the proportion of defective to normal hemoglobin. This abnormal
hemoglobin can be identified electrophoretically.
(2) When a fresh solution of sodium rnetabisulfite is used, positive cases
should show 10 to 75 percent sickling within 15 minutes. There is a positive correlation
between the degree of sickling and the severity of the disease.
Normal blood treated in this way shows no sickling.
6-13. HEMOGLOBIN ELECTROHORESIS (CELLULOSE ACETATE)
a. Principle. Hemoglobin fractions are separated by the rate of their protein
migration in an electrical medium. The fractions are stained with ponceau S and
quantitated on a densitometer. The order of mobility from the cathode toward the anode
is A3> AI> F> S-D>C-A2.
(1) A2 hemoglobin migrates identically to hemoglobin C. They are
distinguished by the quantity present. If this band is 40 percent or more of the total
hemoglobin, it is C. A2 hemoglobin should always be less than 20 percent.
(2) Two slow-moving, nonhemoglobin components are see using this
technique. These fractions are carbonic anhydrases I and II (CAI and CAII)
Hemoglobin A2 is elevated in thalassemia minor.
Genotype SS is found in patients with sickle cell anemia.
Genotype AS is found in patients with sickle cell trait.
(6) This method separates hemoglobin A2 in the presence of hemoglobin S
in patients manifesting sickle-thalassemia disease.
(7) Hemoglobin F is quantitated by the alkali denaturation test because it
migrates close to the hemoglobin A1 fraction on the electrophoretic pattern.
Include known A, S, and C controls in each analysis.