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Sickle cell disease (SCD), also simply called sickle cell, is a group of hemoglobin-related blood disorders typically inherited. The most common type is known as sickle cell anemia. It results in an abnormality in the oxygen-carrying protein haemoglobin found in red blood cells.
Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene (is heterozygous), but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele (is homozygous).
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 – The gene for HbS associated with sickle-cell is today distributed widely throughout sub-Saharan Africa, the Middle East, and parts of the Indian subcontinent, where carrier frequencies range from 5–40% or more of the population.
Sickle cell-beta thalassemia is an inherited blood disorder. The disease may range in severity from being relatively benign and like sickle cell trait to being similar to sickle cell disease.
Hemoglobin electrophoresis is a blood test that can detect different types of hemoglobin. The test can detect hemoglobin S, the form associated with sickle cell disease, as well as other abnormal types of hemoglobin, such as hemoglobin C.
Sickle cell nephropathy is a type of nephropathy associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels.
Some well-known hemoglobin variants, such as sickle-cell anemia, are responsible for diseases and are considered hemoglobinopathies. Other variants cause no detectable pathology, and are thus considered non-pathological variants.
Transfusion therapy for sickle-cell disease entails the use of red blood cell transfusions in the management of acute cases of sickle cell disease and as a prophylaxis to prevent complications by decreasing the number of red blood cells (RBC) that can sickle by adding normal red blood cells.
Sickle Cell Anemia, a Molecular Disease" is a 1949 scientific paper by Linus Pauling, Harvey A. Itano, Seymour J. Singer and Ibert C. Wells that established sickle-cell anemia as a genetic disease in which affected individuals have a different form of the metalloprotein hemoglobin in their blood.
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