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An example of overdominance in humans is that of the sickle cell anemia.This condition is determined by a single polymorphism.Possessors of the deleterious allele have lower life expectancy, with homozygotes rarely reaching 50 years of age.
People with hemoglobin D trait do not have Hemoglobin D disease or sickle cell disease. They cannot develop these diseases later in life. They cannot develop these diseases later in life. While Hemoglobin D can be detected without a DNA test, one is needed to ascertain that a person who carries Hemoglobin D carries hemoglobin D-Punjab.
The underlying cause of sickle cell anemia is the synthesis of aberrant hemoglobin, which attaches to other aberrant hemoglobin molecules inside the red blood cell to undergo rigid deformation. [18] Sickle cell anemia symptoms usually appear around the age of six months. They can change over time and differ from person to person.
In addition, there is sickle cell trait (HbAS) which is defined by having HbA and HbS. This makes the individual heterozygous for sickle cell. Of the world population, it is estimated that there are about 300 million individuals with the sickle cell trait and about 100 million of those are in sub-Saharan Africa. [18]
Isosthenuria may be seen in disease states as chronic kidney disease and acute kidney injury in which the kidneys lack the ability to concentrate or dilute the urine and so the initial filtrate of the blood remains unchanged despite the need to conserve or excrete water based on the body's hydration status.
The ESR is decreased in polycythemia, hyperviscosity, sickle cell anemia, leukemia, chronic fatigue syndrome, [4] low plasma protein (due to liver or kidney disease) and congestive heart failure. Although increases in immunoglobulins usually increase the ESR, very high levels can reduce it again due to hyperviscosity of the plasma. [5]
Sickle cell-Hb Lepore Boston syndrome is a type of sickle cell disease (HbS) that differs from homozygous sickle cell disease where both parents carry sickle hemoglobin. In this variant one parent has the sickle cell hemoglobin the second parent has Hb Lepore Boston, the only one of the three variants described in association with HbS. [7]
Proliferative sickle retinopathy is the most severe ocular complication of sickle cell disease. Even though PSCR begins in the first decade of life, the condition remains asymptomatic and unnoticed until visual symptoms occur due to vitreous hemorrhage or retinal detachment.
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