The Risks of Sickle-Cell Trait

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Abstract
For many decades, it has been well known that sickle cell anemia is due to the homozygous inheritance of a hemoglobin variant (hemoglobin S) rather than hemoglobin A in the red cells. Sickle cell anemia is associated with a wide array of complications, including recurrent painful episodes ("crises") affecting almost every part of the body, thromboembolic phenomena, recurrent infections, and a shortened life expectancy.1 Sickle hemoglobin is a spectacular example of the effect that a single point mutation can exert. Sickle hemoglobin is the result of the substitution of valine for glutamic acid at position 6 on the beta-chain of . . .

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