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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.
When combined with Hemoglobin S (β^6Glu → Val) it causes a severe form of Sickle cell disease known as Hemoglobin S/O-Arab. Detection of Hb O-Arab can be carried out with a blood test, identifying the carries of hemoglobinopathies, so as to inform patients their chances of producing an affected child and ensure appropriate guidance is given.
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.
Sickle-cell disease was the genetic disorder to be linked to a mutation of a specific protein. Pauling introduced his fundamentally important concept of sickle cell anemia as a genetically transmitted molecular disease. [20] This vein (4) shows the interaction between the malaria sporozoites (6) with sickle cells (3) and regular cells (1).
Babies of such parents are born with no edema or major neurological defects, and eventually, this disease can be cured with Haematopoietic Stem Cell Transplantation. A newly developed diagnostic test, called Immunochromatography (IC) Strip Tests, uses monoclonal antibodies to detect Hemoglobin Barts in red blood cells' lysate.
With HbS, there can be mild sickle cell trait but no symptoms. [13] [14] Hemoglobin O-Arab causes sickle cell disease in heterozygous (HbS/HbO) individuals. However, the symptomatic anemia is mild and is not life-threatening. It is even milder than in heterozygous sickle cell trait (HbS/HbA). [15] A case of sickle cell retinopathy is documented ...